Serum cTnI Concentrations Research Articles

Seric Concentration of Troponin I and Electrocardiographic Tracing in Dogs Submitted to Long-Term Sedation during 24 Hours

Background: General anesthetics and sedatives are commonly used for long-term sedation in veterinary medicine; however, they can lead to cardiac suppression. Cardiac troponin I is a biomarker used to detect myocardial pathology, monitor treatment, and assess outcomes in veterinary patients. The aim of this study was to evaluate the serum concentration of troponin I (cTnI), the electrocardiographic (ECG) tracing, and the ventricular stroke work index in dogs undergoing two long-term sedation protocols over 24 h.Materials, Methods & Results: Twelve healthy mongrel dogs with an average weight of 13.2 ± 2.3 Kg were admitted for this study. Twenty-four h before the experiment began (M-24), venous blood samples were collected for chemiluminescent cTnI evaluation and ECG data were obtained, specifically heart rate (HR); P, PR, QRS and T wave duration; P, R, T wave amplitude; and ST segment depression. On the day of the experiment, the animals were anaesthetized with propofol and isoflurane, and instrumented. After instrumentation, right and left ventricular stroke work index (RVSWI and LVSWI respectively) and intrapulmonary shunt (Qs/Qt) were performed as baseline parameters. The isoflurane was then discontinued and the animals randomly allocated to two groups (n = 6 each): Midazolam and fentanyl group (GMF), in which the animals received a bolus and continuous rate infusion (CRI) of midazolam (0.5 mg/kg and 0.5 mg/kg/h) and fentanyl (5 µg/kg and 10 µg/kg/h) or ketamine and morphine group (GKM), in which the animals received a bolus and CRI of ketamine (1 mg/kg and 0.6 mg/kg/h) and morphine (0.5 mg/kg and 0.26 mg/kg/h). Both groups also received propofol as a bolus and CRI (3 mg/kg and 0.3 mg/ kg/min) over 24 h. The ECG and cTnI parameters were evaluated at 6, 12, and 24 h during CRI (M6, M12, and M24) and 12 and 24 h after the end of infusion (T12 and T24). The hemodynamic parameters RVSWI, LVSWI, and Qs/Qt were evaluated every 2 h until the end of CRI. There was a non-significant increase in cTnI from M6 in both groups; however, a significant increase was only observed in GMF between M-24 and T12. During sedation, HR decreased an average of 46% in GKM and 51% in GMF compared to M-24. The QT interval (milliseconds) increased in both groups after CRI started, returning to baseline values at T24. There were no differences in P, QRS, and T wave amplitude or ST segment depression in either group.Discussion: The serum concentration of cTnI increased in GMF at T12, more probably due to hemodynamic changes during sedation rather than myocardial lesions, since the increase was relatively mild. A greater hemodynamic change was observed in GMF, with a greater increase in RVSWI compared to baseline than GKM, which may reflect an increase in cardiac effort and possibly cTnI release; however, in both groups, the cTnI values remained within the acceptable values for the species. Bradycardia was reported during long-term sedation, which may be due to the synergism between opioids as a result of vagal stimulation, central sympathetic inhibition, and a possible action on cardiac receptors, and propofol due to the inhibitory effect on the sympathetic nervous system. Increases in QT interval did not lead to marked changes in this study. T wave amplitude and ST segment depression remained unchanged and within acceptable values for the species, and thus agreed with cTnI data, implying that no myocardial lesions were produced by these protocols. It has been established that for both protocols, cTnI remained within physiological ranges for healthy dogs, and therefore, these methods could be used safely for long-term sedation without producing hypoxia/ischemia of the myocardium or ST-segment depression.

Cardioprotective and anti-inflammatory effects of combined α7 nicotinic acetylcholine receptor agonist and limb remote ischemic postconditioning in rats with myocardial ischemia/reperfusion injury

Objective To assess the cardioprotective and anti-inflammatory effects of combined α7 nicotinic acetylcholine receptor(α7nAChR) agonist and limb remote ischemic postconditioning in rats with myocardial ischemia/reperfusion injury(I/RI). Methods Sixty male SD rats were randomly divided equally into six groups(n=10): sham group(S group), control group(C group), ischemia preconditioning group(IPC group), special α7nAChR agonist PNU282987 postconditioning group(P group), lime remote ischemic postconditioning group(L group), combined PNU282987 and lime remote ischemic postconditioning group(P+L group). Throughout the experiment, HR, MAP, and a lead Ⅱ electrocardiogram were continuously monitored. Blood samples were taken at 120 min of reperfusion for measuring serum concentrations of troponin I(TnI), myocardial-bound creatine kinase(CK-MB), TNF-α, high mobility group box 1 protein(HMGB-1), IL-6 and IL-10 by the kits specifically for rats. At the end of experiment, the infarct size(IS) was assessed using excised hearts by Evans blue and triphenyltetrazolium chloride staining. Results Compared with C group, the IS,serum cTnI and CK-MB concentrations were significantly decreased in IPC, P, L and P+L groups. Compared to IPC group, the IS and serum cTnI concentration were significantly higher in P, L and P+L groups. Compared to P and L groups, the IS, serum cTnI and CK-MB concentrations were significantly decreased in P+L group. At 120 min of reperfusion, serum TNF-α concentration was significantly increased in C, IPC and L groups. Also, serum IL-6 and HMGB1 concentrations were significantly increased in C, IPC, P and L groups compared with S group. Compared to C group, serum TNF-α, IL-6 and HMGB1 concentrations were significantly decreased in IPC, P, L and P+L group. Compared to IPC and L groups, serum TNF-α, IL-6 and HMGB1 concentrations were significantly decreased in P and P+L groups. Conclusions Combined α7nAChR agonist and limb remote ischemic postconditioning can provide an improved cardioprotection, but not an enhanced anti-inflammatory effect. Key words: Myocardial; Ischemia/reperfusion injury; Inflammation; Cholinergic anti-inflammatory pathway; Limb remote ischemic postconditioning

Relationship between failed mechanism of sevoflurane postconditioning-induced myocardial protection and dynamin-related protein 1 activity in diabetic rats

Objective To evaluate the relationship between the failed mechanism of sevoflurane postconditioning-induced myocardial protection and the activity of dynamin-related protein 1(Drp1)in diabetic rats. Methods Pathogen-free healthy adult male Sprague-Dawley rats, weighing 220-280 g, in which diabetes mellitus was induced by combination of high-fat and high-sucrose diet and intraperitoneal injection of streptozotoein 30 mg/kg, were studied.Sixty rats with diabetes mellitus were divided into 5 groups(n=12 each)using a random number table: sham operation group(group Sham), myocardial ischemia/reperfusion(I/R)group(group I/R), sevoflurane postconditioning group(group SP), Drp1 inhibitor mitochondrial division inhibitor-1(Mdivi-1)group(group M)and Mdivi-1 plus sevoflurane postconditioning group(group M-SP). Myocardial I/R was induced by occluding the left anterior descending branch of the coronary artery for 30 min followed by 120 min reperfusion except for group Sham.Mdivi-1 1.2 mg/kg was intraperitoneally injected at 15 min before ischemia in M and M-SP groups, and 2.5% sevoflurane was inhaled starting from 5 min of reperfusion in SP and M-SP groups.Blood samples were collected from the right internal jugular vein at 120 min of reperfusion for measurement of serum cardiac troponin I(cTnI)concentrations(by enzyme-linked immunosorbent assay). Rats were then sacrificed and myocardial specimens were obtained for determination of the myocardial infarct size(by TTC), cell apoptosis(by TUNEL), expression of Bax, Bcl-2 and activated caspase-3(by Western blot)and nicotinamide adenine dinucleotide(NAD+ )content(by spectrophotometry). Apoptosis index(AI)and Bax/Bcl-2 ratio were calculated. Results Compared with group Sham, the percentage of myocardial infarct size, serum concentration of cTnI, AI and Bax/Bcl-2 ratio were significantly increased, the expression of activated caspase-3 was up-regulated, and the NAD+ content was decreased in the other four groups(P 0.05). Compared with group SP, the percentage of myocardial infarct size, serum concentration of cTnI, AI and Bax/Bcl-2 ratio were significantly decreased, the expression of activated caspase-3 was down-regulated, and the NAD+ content was decreased in group M-SP(P 0.05). Conclusion The failed mechanism of sevoflurane postconditioning-induced myocardial protection may be related to the activity of Drp1 in diabetic rats. Key words: Diabetes mellitus; Myocardial reperfusion injury; Anesthetics, inhalation; Apoptosis

Impact of a Soccer Game on Cardiac Biomarkers in Adolescent Players.

Biochemical markers such as cardiac troponin I (cTnI) and N-terminal pro B-type natriuretic peptide (NT-proBNP) have become indispensable tools for the diagnosis of myocardial injury, providing highly sensitive and specific information about cardiac cell damage and wall stress. The purpose of the present research was to examine the response of cardiac biomarkers to a soccer game in adolescent male soccer players. Twenty-two trained adolescent male soccer players (14-16y) were selected in a purposive manner. Blood samples were taken before, immediately after, and 2 and 24 hours after the game for the determination of cTnI and NT-proBNP. Serum concentration of cTnI and NT-proBNP increased immediately and 2 hours after the soccer game (P < .001). After 24 hours, the levels of cTnI dropped but remained above baseline (P = .002), whereas serum NT-proBNP levels returned to baseline. At no time point did any of the values exceed the upper reference value. This is the first study to investigate the acute responses of cardiac biomarkers to a soccer game in adolescent male players. The postgame elevation of cardiac biomarkers and their rapid recovery are indicative of a physiological rather than a pathological response.

Comparison of effects of oxycodone and morphine on myocardial ischemia-reperfusion injury in rats

Objective To compare the effects of oxycodone and morphine on myocardial ischemia-reperfusion (I/R) injury in rats. Methods Forty-eight SPF healthy adult male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, were randomized into 4 groups (n=12 each) using a random number table: sham operation group (S group), myocardial I/R injury group (I/R group), morphine group (M group) and oxycodone group (O group). Myocardial I/R was produced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by 120 min of reperfusion.In group S, the anterior descending branch of the left coronary artery was only exposed but not ligated.In M and O groups, morphine 1.5 mg/kg and oxycodone 0.5 mg/kg were injected, respectively, via the internal jugular vein at 5 min before ischemia.At the end of reperfusion, arterial blood samples were collected via cardiac puncture for determination of the serum creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) concentrations.Myocardial infarct size was measured by 2, 3, 5-triphenyltetrazolium chloride staining.Apoptosis in cardiomyocytes was determined by TUNEL, and apoptosis index (AI) was calculated. Results Compared with S group, serum CK-MB and cTnI concentrations and AI were significantly increased, and myocardial infarct size was enlarged in I/R, M and O groups (P<0.05). Compared with I/R group, serum CK-MB and cTnI concentrations and AI were significantly decreased, and myocardial infarct size was decreased in M and O groups (P<0.05). Serum CK-MB and cTnI concentrations and AI were significantly lower, and myocardial infarct size was smaller in O group than in M group (P<0.05). Conclusion Oxycodone produces better efficacy than morphine in reducing myocardial I/R injury in rats. Key words: Oxycodone; Morphine; Myocardial reperfusion injury

Sevoflurane ameliorates doxorubicin-induced myocardial injury by affecting the phosphorylation states of proteins in PI3K/Akt/mTOR signaling pathway.

The effect of sevoflurane on the doxorubicin-induced myocardial injury was explored by investigating the phosphorylation states of proteins in phosphatidylinositol 3-kinase (PI3K)/Akt/mam-malian target of rapamycin (mTOR) signaling pathway. Myocardial injury rat models were induced by doxorubicin and evenly assigned into five groups according to different treatment: Doxorubicin group (DG, 200-μL saline solution), sevoflurane group (SevG, inhaled with 2.4% sevoflurane for 2 h), LY294002 group (LYG, Akt inhibitor, 0.3 mg/kg in 200-μL Dimethyl Sulfoxide [DMSO]), solvent DMSO control group (SG) and autophagy inhibitor 3-methyladenine (3-MA) group (MG, 30 mg/kg in 200-μL DMSO). The healthy rats were assigned to a contro1 group (CG, 200-μL saline solution). Myocardial apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The concentration of cardiac troponin I (cTnI) was detected by ELISA. The levels of total Akt (t-Akt), phosphorylated Akt (p-Akt), mammalian target of rapamycin (mTOR), phosphorylated-mTOR (p-mTOR) and autophagy marker LC3-II was detected by Western Blot. The experiments were also repeated at the cell level. Terminal deoxynucleotidyl transferase dUTP nick end labeling analysis showed that the ap-optosis rates were high in DG and SG, reached the highest level in LYG, reduced in SevG and MG, and reached the lowest level in CG. The levels of p-Akt p-mTOR were low in groups DG and SG, reached the lowest level in LYG, increased in SevG and MG, and reached the highest level in CG. In contrast, LC3-II expression, apoptosis index and serum cTnI concentration were high in DG and SG, reached the highest level in LYG, reduced in SevG and MG, and reached the lowest level in CG (p < 0.05). Cell experiment showed similar results as with animal experiments. Sevoflurane ameliorates myocardial injury by affecting the phosphorylation states of the proteins in PI3K/Akt/mTOR signaling pathway and reducing the injury biomarker. (Cardiol J 2017; 24, 4: 409-418).

Role of JAK2-STAT3 signaling pathway in sevoflurane postconditioning-induced inhibition of mPTP opening during myocardial ischemia-reperfusion in rats

Objective To evaluate the role of Janus kinase 2-signal transducer and activator of transcription 3(JAK2-STAT3)signaling pathway in sevoflurane postconditioning-induced inhibition of mitochondrial permeability transition pore(mPTP)opening during myocardial ischemia-reperfusion(I/R)in rats. Methods Sixty pathogen-free healthy male Sprague-Dawley rats, weighing 250-300 g, were divided into 4 groups(n=15 each)using a random number table: I/R group, sevoflurane postconditioning group(group SP), AG-490 group(group AG)and sevoflurane postconditioning plus AG-490 group(group SP+ AG). Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of coronary artery followed by 120 min reperfusion.In group SP, 2.8% sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.JAK2 inhibitor AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion in group AG.In group SP+ AG, AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion, and 2.8% sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.At 15 min of reperfusion, 5 rats were sacrificed and myocardial specimens were obtained for determination of the expression of JAK2, phosphorylated JAK2(p-JAK2), STAT3 and phosphorylated STAT3(p-STAT3)in myocardial tissues by Western blot.The ratios of p-JAK2 to JAK2 expression(p-JAK2/JAK2)and p-STAT3 to STAT3 expression(p-STAT3/STAT3)were calculated.Five rats were sacrificed at the end of reperfusion for measurement of myocardial infarct size.The left 5 rats were selected and sacrificed, myocardial specimens were obtained, and the opening of mPTP was detected by a calcein-cobalt quenching method. Results Compared with group I/R, the myocardial infarct size and mPTP opening were significantly decreased, and JAK2/p-JAK2 and STAT3/p-STAT3 were increased in group SP(P 0.05). Compared with group SP, the myocardial infarct size was significantly enlarged, the extent of mPTP opening was aggravated, and JAK2/p-JAK2 and STAT3/p-STAT3 were decreased in SP+ AG and AG groups(P<0.05). Conclusion The mechanism by which sevoflurane postconditioning inhibits the opening of mPTP during myocardial I/R is related to activation of JAK2-STAT3 signaling pathway in rats. Key words: Aesthetics, inhalation; Janus kinase 2; STAT3 transcription factor; Mitochondrial membrane transport proteins; Myocardial reperfusion injury; Ischemic postconditioning

Effect of sufentanil postconditioning on level of cathepsin B in myocardium during ischemia-reperfusion in rats

Objective To evaluate the effect of sufentanil postconditioning on the level of cathepsin B in the myocardium during ischemia-reperfusion(I/R)in the rats. Methods Eighteen healthy adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 3 groups(n=6 each)using a random number table: sham operation group(group S), group I/R and sufentanil postconditioning group(group SP). The rats were anesthetized with intraperitoneal 20% urethane 5 ml/kg.Myocardial I/R was induced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120 min reperfusion.At 5 min before reperfusion, sufentanil 1.0 μg/kg was intravenously injected in group SP, and the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion, blood samples from the abdominal aorta were collected for determination of serum cardiac troponin I(cTnI)and creatine kinase-MB(CK-MB)concentrations, and myocardial specimens were obtained for examination of the ultrastructure of cardiomyocytes(using transmission electron microscopy)and for determination of Beclin-1, microtubule-associated protein 1 light chain 3Ⅱ(LC3Ⅱ)and cathepsin B expression(by Western blot)and cathepsin B activity(by fluorometric assay). Results Compared with group S, the serum cTnI and CK-MB concentrations were significantly increased, the expression of Beclin-1, LC3Ⅱ and cathepsin B was up-regulated, and the activity of cathepsin B was enhanced in I/R and SP groups(P<0.05). Compared with group I/R, the serum cTnI and CK-MB concentrations were significantly decreased, the expression of Beclin-1 and LC3Ⅱ was down-regulated, the expression of cathepsin B was up-regulated, and the activity of cathepsin B was enhanced(P<0.05), the pathological changes of myocardial tissues were significantly attenuated, and autophagosomes were reduced in group SP. Conclusion The mechanism by which sufentanil postconditioning inhibits cardiomyocyte autophagy during myocardial I/R is probably related to increased expression and activity of cathepsin B in rats. Key words: Sufentanil; Cathepsin B; Myocardial reperfusion injury; Ischemic postconditioning

Evaluation of cardiac troponin I (cTnI), electrocardiography, creatine kinase (CK) and aspartate aminotransferase (AST) in diagnosis of selenium deficiency in Markhoz goat kids breed

BACKGROUND: Cardiac Troponin I (cTnI) is known as a cardiac biomarker in determining the myocardial damage of diseases which affect the heart muscle. OBJECTIVES: This study aims to evaluate the serum cTnI concentration in Markhoz Breed goats suffering selenium (Se) deficiency and its correlation with electrocardiographic parameters, and activity of creatine kinase (CK) and aspartate aminotransferase (AST) enzymes, as well as to determine the diagnostic value of troponin in that disease. METHODS: Blood samples of 94 goat kids of Markhoz breed with the age less than one month were taken, serum analyzed for the assessment of cTnI, CK and AST, 2 ml blood was used for determination of selenium concentration. Electrocardiography was recorded from all kids by using base-apex lead. Kids were divided into two groups based on serum selenium concentration. RESULTS: The concentration of cTnI was significantly higher in deficient kids compared with the control group. Results indicated significant negative correlation between cTnI and selenium concentration. There was no significant correlation between cTnI and AST, CK in deficient kids. Results show no significant difference in concentration of AST, and CK enzymes for two group of deficient kids and control group. The presence of arrhythmia is significantly higher in deficient kids than control group. CONCLUSIONS: The results of this study showed that the measurement of serum cTnI concentration can be useful in diagnosis of kids suffering from Se deficiency. Also ECG can be used aiming at the diagnosis of arrhythmia in kids with Se deficiency.

Effect of dexmedetomidine on myocardial injury in pediatric patients undergoing living-related liver transplantation

Objective To evaluate the effect of dexmedetomidine on myocardial injury in pediatric patients undergoing living-related liver transplantation. Methods Fifty-eight pediatric patients of both sexes, aged 5-20 months, weighing 4.5-15.0 kg, of American Society of Anesthesiologists physical status Ⅲ or Ⅳ, scheduled for elective living-related liver transplantation, were divided into 2 groups(n=29 each)using a random number table: control group(group C)and dexmedetomidine group(group D). In group D, dexmedetomidine was intravenously infused at a dose of 0.5 μg/kg over 10 min starting from the time point immediately before skin incision, followed by an infusion of 0.8 μg·kg-1·h-1 until the end of surgery. The equal volume of normal saline was given instead in group C. Immediately before skin incision(baseline, T0), at 10 min of anhepatic phase(T1), at 30 min of neohepatic phase(T2)and at the end of surgery(T3), blood samples were obtained from the central vein for determination of serum cardiac troponin I(cTnI), lactate dehydrogenase(LDH), alpha-hydroxybutyrate dehydrogenase(α-HBDH), interleukin-6(IL-6)and IL-10 concentrations. The changing rate of serum cTnI concentrations were calculated at T2. The occurrence of myocardial ischemia and ventricular premature beat and requirement for dopamine were recorded during surgery. Results Compared with the baseline at T0, the serum concentrations of cTnI, LDH and α-HBDH were significantly increased at T2, 3, and the serum concentrations of IL-6 and IL-10 were increased at T1-3 in both groups(P 0.05). Conclusion Dexmedetomidine can attenuate the myocardial injury to some extent in pediatric patients undergoing living-related liver transplantation. Key words: Dexmedetomidine; Liver transplantation; Child; Myocardium; Prognosis

Short-term prognostic value of serum cardiac troponin I levels in neonates with perinatal asphyxia

Background Neonatal hypoxic–ischemic encephalopathy (HIE) is a neonatal brain injury caused by perinatal asphyxia and is a major cause of neonatal morbidity and mortality. Cardiac dysfunction forms a part of the clinical spectrum of multiorgan dysfunction in asphyxiated newborns. The more cardiac dysfunction the patients have, the more severe encephalopathy they would suffer. Cardiac troponin I (cTnI) is one of neonatal HIE-related biomarkers that can aid the diagnosis of perinatal asphyxia and anticipate the severity of associated myocardial dysfunction. Aim The current study was designed to assess the serum cTnI concentration and to evaluate its short-term prognostic value in newborns with HIE. Patients and methods The present study is a prospective observational study conducted on 100 full-term newborn infants in the period from May 2016 to May 2017. Enrolled newborns were divided into two groups: the case group (50 full-term newborn infants with evidence of perinatal asphyxia) and the control group (50 full-term newborn infants without evidence of perinatal asphyxia). Quantitative estimation of serum cTnI concentrations was done in all enrolled newborns within 12 h of birth using direct chemiluminometric technology performed on ADVIA Centaur Immunoassay System (TnI-Ultra). Serum levels of creatine kinase-MB (CK-MB) were also measured to assess its sensitivity and specificity as a marker of perinatal asphyxia. Additionally, echocardiography was done to exclude structural heart diseases. Left ventricular fractional shortening (LVFS) was also measured to assess cardiac involvement. Results Serum concentrations of cTnI were statistically significantly higher among the case group when compared with the control group. Additionally, serum levels of cTnI were found to increase with increasing severity of HIE. Serum levels of CK-MB were also statistically higher among the case group. However, pairwise statistical comparison of serum CK-MB concentrations in different stages of HIE revealed no statistical significant difference. No statistical significant difference was found between the two studied groups regarding LVFS. Moreover, LVFS did not differ significantly between the different stages of HIE. Among the different markers of myocardial dysfunction assessed in the current study, cTnI was found to be the most sensitive and specific predictor of poor short-term outcome in newborns with perinatal asphyxia. When comparing serum concentrations of cTnI and CK-MB in both surviving and nonsurviving newborns in the asphyxia group, it was found that serum concentrations of cTnI were statistically significantly lower in the group of survivors. In contrast, there was no statistical significant difference regarding serum concentrations of CK-MB between surviving and nonsurviving asphyxiated newborns. Conclusion Serum concentrations of cTnI were elevated in asphyxiated newborns with respect to healthy infants and increase with increasing severity of HIE. cTnI can also be used as an excellent early predictor of mortality in newborns with perinatal asphyxia.

Usefulness of serum cardiac troponin I concentration as a marker of survival of harbor seal (Phoca vitulina) pups during rehabilitation.

OBJECTIVE To measure serum cardiac troponin I (cTnI) concentrations in orphaned harbor seal (Phoca vitulina) pups at various points during rehabilitation in a seal rescue center and determine whether cTnI concentration was associated with survival during rehabilitation and duration of rehabilitation. DESIGN Serial cross-sectional study. ANIMALS Fifty-five 2- to 9-day-old harbor seal pups. PROCEDURES Blood samples for serum cTnI concentration measurement, CBC, and serum biochemical analysis were obtained from seal pups at admission into a seal rescue center, after 2 weeks of rehabilitation at the center, and prior to release. Serum cTnI concentrations were compared between seals that did or did not survive rehabilitation. RESULTS Median serum cTnI concentration was highest at admission (0.03 ng/mL). After 2 weeks, the median value was 0.01 ng/mL; prior to release, it was 0.01 ng/mL. Seal pups that were found to have died during or after rehabilitation (n = 7) had a significantly higher median serum cTnI concentration at admission (0.06 ng/mL) than did seal pups that survived rehabilitation (and for which the postrelease fate was unknown; 48; 0.03 ng/mL). No correlation was identified between serum cTnI concentration and duration of rehabilitation. CONCLUSIONS AND CLINICAL RELEVANCE The results of this study suggested some degree of myocardial injury was present in most of the orphaned seal pups admitted for rehabilitation. Measurement of serum cTnI concentration in seal pups at admission might provide prognostic information about their likelihood of survival during or after rehabilitation.

Serum cardiac troponin I in canine syncope and seizures

ObjectiveTo determine if serum cardiac troponin I (cTnI) concentration distinguishes between cardiogenic syncope and collapsing dogs presenting with either generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope. AnimalsSeventy-nine prospectively recruited dogs, grouped according to aetiology of collapse: generalized epileptic seizures (group E), cardiogenic syncope (group C), dogs with both epileptic seizures and cardiac disease (group B), vasovagal syncope (group V) or unclassified (group U). MethodsMost patients had ECG (n = 78), echocardiography (n = 78) and BP measurement (n = 74) performed. Dogs with a history of intoxications, trauma, evidence of metabolic disorders or renal insufficiency (based on serum creatinine concentrations >150 μmol/L and urine specific gravity <1.030) were excluded. Serum cTnI concentrations were measured and compared between groups using non-parametric statistical methods. Multivariable regression analysis investigated factors associated with cTnI. Receiver operator characteristic curve analysis examined whether cTnI could identify cardiogenic syncope. ResultsMedian cTnI concentrations were higher in group C than E (cTnI: 0.165 [0.02–27.41] vs. 0.03 [0.01–1.92] ng/mL; p<0.05). Regression analysis found that serum cTnI concentrations decreased with increasing time from collapse (p=0.015) and increased with increasing creatinine concentration (p=0.028). Serum cTnI diagnosed cardiogenic syncope with a sensitivity of 75% and specificity of 80%. ConclusionsSerum cTnI concentrations were significantly different between groups C and E. However, due to the overlap in cTnI concentrations between groups cTnI, measurement in an individual is not optimally discriminatory to differentiate cardiogenic syncope from collapse with generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope.

Cardiac troponin I concentrations, electrocardiographic and echocardiographic variables remained unchanged in dogs experimentally infected with Ehrlichia canis

Canine monocytic ehrlichiosis (CME, Ehrlichia canis) has occasionally been associated with myocardial injury. The aim of the present study was to serially measure and evaluate cardiac troponin I (cTnI) concentrations in dogs with experimentally induced acute and subclinical CME and to evaluate potential associations between cTnI concentration and an array of echocardiographic and electrocardiographic parameters. Serum cTnI concentration and simultaneous echocardiographic and electrocardiographic recordings were evaluated in 12 healthy Beagle dogs prior to experimental infection and on days 20 and 90 post-inoculation with E. canis. Almost all serum cTnI concentrations were below the limit of detection and selected electrocardiographic and echocardiographic parameters remained unchanged throughout the study.

Effect of inhibition of GSK-3β activity on sevoflurane postconditioning-induced cardioprotection in diabetic rats

Objective To investigate the effect of inhibition of glycogen synthase kinase-3 beta(GSK-3β)activity on sevoflurane postconditioning-induced cardioprotection in diabetic rats. Methods Healthy adult male Sprague-Dawley rats, weighing 250-300 g, in which diabetes mellitus was induced by intraperitoneal 1% streptozotocin 60 mg/kg combined with high-fat and high-sucrose diet and confirmed by blood glucose level >16.7 mmol/L.Forty rats with diabetes mellitus were divided into 5 groups(n=8 each)using a random number table: sham operation group(S group), ischemia-reperfusion(I/R)group, sevoflurane postconditioning group(SP group), GSK-3β inhibitor SB216763 group(SB group), and sevoflurane postconditioning plus SB216763 group(SS group). Myocardial ischemia was induced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 min reperfusion.The rats inhaled sevoflurane with the end-tidal concentration of 2.5% for 5 min starting from 1 min before reperfusion in group SP.SB216763 0.2 mg/kg was injected via the caudal vein at 1 min before reperfusion in group SB.In group SS, the rats inhaled sevoflurane with the end-tidal concentration of 2.5% for 5 min starting from 1 min before reperfusion, and SB216763 0.2 mg/kg was injected via the caudal vein at 1 min before reperfusion.At 120 min of reperfusion, blood samples were collected from the carotid artery for determination of serum creatine kinase-MB(CK-MB)activity and cardiac troponin I(cTnI) concentrations.Myocardial specimens were collected at 120 min of reperfusion for microscopic examination of the pathological changes and for determination of myocardial infarct size(by 2, 3, 5-triphenyltetrazolium chloride staining)and phosphorylated GSK-3β(p-GSK-3β)expression(by Western blot). Results Compared with group S, the myocardial infarct size and serum CK-MB activity and cTnI concentration were significantly increased, and the expression of p-GSK-3β was significantly down-regulated in I/R, SP, SB and SS groups(P 0.05). Compared with group SB, the myocardial infarct size and serum CK-MB activity and cTnI concentration were significantly decreased, and the expression of p-GSK-3β was significantly up-regulated in group SS(P<0.05). The pathological changes of myocardium were significantly attenuated in SB and SS groups as compared with group I/R and group SP. Conclusion Inhibition of GSK-3β activity can improve sevoflurane postconditioning-induced cardioprotection in diabetic rats. Key words: Anesthetics, inhalation; Diabetes mellitus; Glycogen synthase kinase 3; Myocardial reperfusion injury

Effect of pentazocine on the alteration of cardiac troponin I in leg ischemia/reperfusion induced by tourniquet

Objective To explore the effect of pentazocine on the changes in cardiac troponin I(cTnI) and its association with calcitonin gene-related peptide(CGRP) in tourniquet-induced leg ischemia/reperfusion(I/R). Methods Sixty patients, undergoing elective unilateral leg surgery using tourniquet, under spinal anesthesia, were enrolled and randomly assigned to control group (group C) and pentazocine group(group P)(n=30), in accordance with a random number table. Patients in group P pretreated with pentazocine 0.5 mg/kg before surgery, while only the same volume of saline was infused intravenously in group C at the same schedule. 5 ml of blood samples were collected from cubital vein in a not transfusion arm immediately before inflating tourniquet (T0), 0.5 h(T1) and 24 h(T2) after tourniquet deflation. Serum concentration of cTnI and CGRP were measured by ELISA. Results There was no statistical difference detected in the general information in two groups(P>0.05). Compared with the cTnI at the time of T0 [(0.21±0.06) μg/L] the concentration of cTnI in group C at the time of T1 was not obvious changed(P>0.05), while significantly increased at the time of T2 [(0.28±0.10) μg/L] (P 0.05). No significant change in the concentration of CGRP of group C was detected at the time of T1 and T2(P>0.05), while CGRP in group P was increased significantly at the time of T1[(17.9±2.7) ng/L] and T2[(18.8±2.8) ng/L](P 0.05), cTnI in group P was decreased significantly at the time of T2[(0.22±0.06) μg/L vs (0.28±0.10) μg/L] (P<0.05), CGRP in group P was increased obviously at T1 and at T2(P<0.05). Conclusions The results of this study indicates that pentazocine may attenuate myocardial injury induced by leg I/R tourniquet, in which endogenous CGRP may be associated. Key words: Pentazocine; Tourniquets; Ischemia/reperfusion, Leg; Cardiac troponin I; Calcitonin gene-related peptide

Role of Akt/GSK-3β signaling pathway in isoflurane preconditioning-induced inhibition of mPTP opening during myocardial ischemia-reperfusion in rats

Objective To evaluate the role of serine-threonine kinase(Akt)/glycogen synthase kinase-3 beta(GSK-3β)signaling pathway in isoflurane preconditioning-induced inhibition of mitochondrial permeability transition pore protein(mPTP)opening during myocardial ischemia-reperfusion(I/R)in rats. Methods Ninety-six male Sprague-Dawley rats, aged 3-4 months, weighing 200-250 g, were randomly divided into 4 groups(n=24 each)using a random number table: control group(group C); I/R group; isoflurane preconditioning group(group IPC); Akt inhibitor MK-2206 group(group MK). Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by 2 h of reperfusion.In group IPC, 1.5% isoflurane was inhaled for 30 min followed by 45 min washout, and then the model of myocardial I/R injury was established.In group MK, MK-2206 300 μg/kg(in dimethyl sulfoxide)was injected intraperitoneally at 30 min before isoflurane inhalation.At 2 h of reperfusion, 8 rats were selected and sacrificed, and the hearts were removed for determination of myocardial infarct size.At 2 h of reperfusion, 8 rats were selected, and blood samples were collected from the right internal jugular vein for determination of serum cardiac troponin I(cTnI) concentrations.The rats were then sacrificed, and myocardial specimens were obtained for determination of the expression of phosphorylated GSK-3β(p-GSK-3β)in cytoplasm and mitochondria(by Western blot)and co-expression of p-GSK-3β with adenine nucleotide translocator(ANT), voltage-dependent anion channel or cyclophilin D in myocardial tissues(using co-immunoprecipitation). At 2 h of reperfusion, 8 rats were selected and sacrificed, myocardial cells were obtained, and the opening time of mPTP was determined with a laser scanning confocal microscope. Results Compared with group C, the myocardial infarct size and serum cTnI concentrations were significantly increased, and the expression of p-GSK-3β in cytoplasm and mitochondria was up-regulated in I/R and IPC groups, the co-expression of p-GSK-3β with ANT was significantly down-regulated, and the opening time of mPTP was shortened in group I/R, and the co-expression of p-GSK-3β with ANT was significantly up-regulated, and the opening time of mPTP was prolonged in group IPC(P 0.05). Compared with group IPC, the myocardial infarct size and serum cTnI concentrations were significantly increased, the expression of p-GSK-3β in cytoplasm and mitochondria was up-regulated, the co-expression of p-GSK-3β with ANT was significantly down-regulated, and the opening time of mPTP was shortened in group MK(P<0.05). No co-expression of p-GSK-3β with voltage-dependent anion channel or cyclophilin D was found in myocardial tissues. Conclusion The mechanism by which isoflurane preconditioning inhibits mPTP opening during myocardial ischemia-reperfusion is partially related to activation of Akt/GSK-3β signaling pathway in rats. Key words: Isoflurane; Ischemic preconditioning; Myocardial reperfusion injury; Mitochondrial membrane transport proteins; Protein-serine-threonine kinases; Glycogen synthase kinase 3

Effect of creatine phosphate on myocardial injury induced by lung ischemia-reperfusion in rats

Objective To evaluate the effect of creatine phosphate on the myocardial injury induced by lung ischemia-reperfusion (I/R) in rats. Methods Twenty-four male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-350 g, were randomly divided into 3 groups (n=8 each) using a random number table: sham operation group (group S), I/R group, and I/R+ creatine phosphate group (group CP). Lung I/R was induced by clamping the left hilum of lung for 0.5 h with a non-invasive microvascular clip followed by mechanical ventilation and 2.0 h of reperfusion.Creatine phosphate 6.6 mg·kg-1·min-1 were infused intravenously at 30 min before ischemia in group CP, while the equal volume of normal saline was administered in group I/R.At 2.0 h of reperfusion, blood samples were obtained from the right ventricle for determination of the serum concentration of cardiac troponin I (cTnI). Myocardial specimens were obtained from the apex for microscopic examination and for determination of the levels of myocardial superoxide dismutase (SOD), malondialdehyde (MDA), and myeloperoxidase (MPO). Results Compared with group S, the serum cTnI concentrations, MDA content, and MPO activity were significantly increased, and the SOD activity was significantly decreased in I/R and CP groups (P<0.05). Compared with group I/R, the serum cTnI concentrations, MDA content, and MPO activity were significantly decreased, and the SOD activity was significantly increased in group CP (P<0.05). Myocardial injury was significantly attenuated in group CP as compared with group I/R. Conclusion Creatine phosphate can attenuate the myocardial injury induced by lung I/R in rats, and the mechanism is related to decrease in damage caused by lipid peroxidation. Key words: Phosphocreatine; Lung; Reperfusion injury

Evaluation of cardioprotective activity of Lepidium sativum seed powder in albino rats treated with 5-fluorouracil

5-fluorouracil (5-FU) is a chemotherapeutic agent used for treatment of solid tumors. Cardiotoxicity is a major complication of 5-FU therapy. Therefore, the aim of the present study was to evaluate the possible cardioprotective potency of Lepidium sativum seed powder (LS) against 5-FU-induced cardiotoxicity and oxidative stress in albino rats. The rats were divided into three groups. Rats in the control group received saline daily for 8 days only. Rats in FU-treated group received saline orally for 8 days, then I.P. injected with 5-FU (150 mg\\kg B.W) on the 5th day. Rats in LS-treated group were orally dosed with LS (550 mg\\kg B.W\\day) for 8 days, and on the 5th day rats were administrated with the same previous dose of 5-FU. 5-FU induced cardiotoxicity was assessed by a significant increase in serum concentrations of cTnI, CK-MB, lipid profile and a moderate elevation of cardiac MDA. 5-FU significantly decreased serum HDL-c and GSH concentration in cardiac homogenate. Its administration also resulted in the release of some inflammatory markers such as myeloperoxidase and Interleukin-1β (IL-1β). All 5-FU altered parameters were markedly ameliorated by LS pre-co-post-treatment. Results of the present study suggest that LS has a significant effect on the protection of the heart against 5-FU-induced cardiotoxicity through maintaining the antioxidant and anti-inflammatory activities.

Efficacy of preoperative trimetazidine for preventing myocardial injury in patients undergoing off-pump coronary artery bypass grafting

Objective. Off-pump coronary artery bypass grafting (CABG) with median sternotomy have been shown to be beneficial and associated with reduced myocardial injury. However, there is still a risk for ischemic myocardial injury that results from the normothermic and metabolically active myocardium during the occlusion of the target coronary artery. We aimed to evaluate the efficacy of trimetazidine in prevention of myocardial tissue injury in patients undergoing off-pump CABG by measuring serum levels of cardiac troponin I (cTnI). Methods. Thirty patients undergoing first-time elective off-pump CABG were randomly assigned to two groups: 15 patients received trimetazidine 60 mg orally per day (trimetazidine group) for three weeks and 15 patients received placebo (control group). As a parameter of myocardial injury, we measured cTnI levels. Blood samples were taken sequentially from the patients before surgery (t1), 30 minutes after the last distal anastomosis (t2), at postoperative 12 th hour (t3) and at postoperative 24 th hour (t4). cTnI measurements were made by direct chemiluminometric technology. Results. Baseline and operative characteristics of patients are similar. All preoperative serum cTnI concentrations were within the normal range and rose with the beginning of the operation which reached to its peak value at t3 in the control group and t4 in trimetazidine group. When the increase in the serum cTnI concentrations of trimetazidine group and control group were compared there was a slight numerical increase in cTnI levels in all measurements after reperfusion but reached to statistical significance only at t3 (mean: 0.40 ng/ml; mean rank: 12.20; range: 0.05-1.66 vs. mean: 0.20 ng/ml; mean rank: 18.80; range: 0.11-0.30; p =0.041). Conclusion. Preoperative treatment with trimetazidine might reduce postoperative myocardial injury in patients undergoing first time isolated off-pump CABG, but larger randomized placebo controlled trials are still for recommendation of routine pretreatment with trimetazidine.