Serum Creatine kinase-MB Activity Research Articles

Influence of Gender on Total Serum Creatine Kinase and Creatine Kinase-Mb Levels of Nigerian Hypertensives

Introduction: Hypertension is a long-term medical condition which when not detected and managed properly and on time often results to complications leading to disabilities and mortality. Gender has been known to affect the interpretation of some variables necessitating the need for gender-specific ranges.
 Objectives:This study evaluated total creatine kinase (CK) and creatine kinase-MB (CK-MB) isoenzyme activities of hypertensive subjects in Calabar, Nigeria and to assess if gender has influence on the activities of these enzymes.
 Methodology:One hundred and two participants were consecutively enrolled in this case control study. Serum total serum CK and CK-MB activity were evaluated in fifty one hypertensive and 51 normotensive subjects. The total CK levels were assessed using a spectrophotometric method while immunoinhibition method was used to determine the activity of CK-MB. Data was analyzed using Student’s t-test and Pearson’s correlation. Statistical significance was set at p<0.05.
 Results:The total creatine kinase activities of the hypertensives did not differ significantly from those of the normotensive controls (p = 0.428) while the serum CK-MB activities of the hypertensive subjects were significantly higher than those of the normotensive controls (p=0.000). The body mass index of the hypertensives was significantly higher than those of the normotensive subjects (p=0.030). Gender had no effect on the blood pressure, body mass index and levels of CK and CK-MB (p>0.05). There was also no significant correlation (p>0.05) between blood pressure, body mass index and the levels of CK and CK-MB.
 Conclusion:CK-MB activities were significantly higher in hypertensive subjects compared to normotensive controls. There were no gender specific differences in the CK-MB levels of male and female hypertensives. This cardiac marker should be included in the routine assessment of hypertensives and gender-specific considerations may not be necessary in the interpretation of the data.

Systemic implications of metallic foreign body syndrome in dairy cattle

This study aimed to evaluate the systemic implications of 37 cattle with traumatic reticulitis, evaluating clinical, laboratory, ultrasonographic and necroscopic changes. A clinical, laboratory and ultrasonographic examination was performed, and the animals were distributed in reticuloperitonitis (GI; n=21) and reticulopericarditis (GII; n=16) traumatic, based on necropsy findings. Blood samples were taken for haematological tests, serum total protein, albumin, globulin, gamma glutamyltransferase (GGT), aspartate aminotransferase (AST), glutamate dehydrogenase (GLDH), creatinine, urea, cortisol, creatine kinase (CK), creatine kinase-MB (CK-MB), cardiac troponin-I (cTn-I), plasma glucose and L-lactate. The abdominocentesis was productive in eight GI (n=8) and seven GII (n=7) animals, allowing the evaluation of physical, cytological and biochemical characteristics of the peritoneal fluid as a total protein, albumin, GLDH, AST, GGT, glucose and L-lactate. Changes in behavior, appetite, dehydration and temperature were observed, most expressive in GII. Hematology showed neutrophilic leukocytosis with regenerative left shift and hyperfibrinogenemia in both groups. Increased globulin, L-lactate concentration and serum GGT, GLDH, CK and CK-MB activity were observed, as well as significant elevation of cTnI (p=0.0190) in GII. In the peritoneal fluid exudate was observed in both groups and a higher concentration of L-lactate in relation to plasma. Ultrasound revealed retocular, cardiac, hepatic and splenic abnormalities. The anatomopathological lesions confirmed the ultrasound findings of both groups. The understanding of the syndrome helps in the diagnosis, as well as the adoption of preventive measures, minimizing the economic impact caused to the dairy cattle breeding.

Puerarin protects against myocardial ischemia/reperfusion injury by inhibiting inflammation and the NLRP3 inflammasome: The role of the SIRT1/NF-κB pathway

AimsThe purpose of this study was to investigate the protective effects of puerarin and elucidate the underlying mechanisms of puerarin in myocardial ischemia/reperfusion (MI/R) injury. Main methodsC57BL/6 mice were exposed to puerarin (100 mg/kg) with or without the SIRT1 inhibitor nicotinamide (500 mg/kg) and then subjected to MI/R operation. Myocardial infarct size, serum creatine kinase-MB (CK-MB) activity, apoptotic cell death, and cardiac structure and function were examined to evaluate MI/R injury. RT-PCR and western blotting were used to determine the inflammatory response and inflammasome activation, as well as activation of SIRT1/NF-κB pathway. ResultsPuerarin significantly reduced myocardial infarct size, serum CK-MB activity, and apoptotic cell death, and improved cardiac structural damage and dysfunction. Moreover, puerarin notably decreased the mRNA and protein levels of TNF-α, IL-6, and IL-1β, indicating that puerarin attenuated MI/R-induced inflammation. Furthermore, puerarin markedly decreased the protein levels of Ac-NF-κB, NLRP3, cleaved caspase-1, cleaved IL-1β, and cleaved IL-18 and increased the protein level of SIRT1. More importantly, the SIRT1 inhibitor nicotinamide prevented these puerarin-induced cardioprotective effects and regulation of the SIRT1/NF-κB pathway, as well as the NLRP3 inflammasome activation. ConclusionPuerarin protected against MI/R injury by inhibiting inflammatory responses probably via the SIRT1/NF-κB pathway, and inhibition of the NLRP3 inflammasome was also involved in puerarin-induced cardioprotective effects. These results suggest that puerarin may be a novel candidate for the treatment of ischemic heart disease.

Intravenous cannula can increase serum creatine kinase MB activity

Intravenous cannula can increase serum creatine kinase MB activity

Ameliorative effect of gallic acid on sodium arsenite-induced spleno-, cardio- and hemato-toxicity in rats

AimArsenic is an important toxic chemical affecting millions of people around the world. Exposure to inorganic arsenic results in various health problems including skin lesions, hypertension, hematological disturbance, cardiovascular disease, spleen enlargement and cancer. Gallic acid (GA) is an important phenolic compound possessing various pharmacological properties including anti-inflammatory, antioxidant and free radical scavenging activities. The present study investigated effects of GA against sodium arsenite (SA)-induced spleno-, cardio- and hemato-toxicity. Main methodsThirty-five adult male Wistar rats were randomly divided into five groups; group I received normal saline (2 ml/kg/day, p.o.) for 21 days, group II received SA (10 mg/kg/day, p.o.) for 14 days, group III and IV were treated with GA (10 and 30 mg/kg/day, respectively) for 7 days prior to receive SA and treatment was continued up to 21 days in parallel with SA administration, group V received GA (30 mg/kg/day, p.o.) for 21 days. The level of MDA, NO and glutathione (GSH) and the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase were measured in heart and spleen tissues. Creatine kinase-MB (CK-MB) activity and hematological and histopathological parameters were also assessed. Key findingsGA significantly decreased SA-induced elevation of MDA and NO levels and reduction of GSH level and GPx and SOD activity in heart and spleen tissues. Furthermore, GA improved SA-induced alteration in hematological and histopathological parameters and reduced SA-induced elevation of serum CK-MB activity. SignificanceOur results suggest that GA inhibits SA-induced spleno-, cardio- and hemato-toxicity through reducing oxidative stress.

Preoperative oral thyroid hormones to prevent euthyroid sick syndrome and attenuate myocardial ischemia-reperfusion injury after cardiac surgery with cardiopulmonary bypass in children: A randomized, double-blind, placebo-controlled trial.

Background:Both euthyroid sick syndrome and myocardial ischemia-reperfusion injury are common and have been significantly associated with morbidity and mortality after pediatric cardiac surgery with cardiopulmonary bypass. This single-center, prospective, double-blind, randomized placebo-controlled clinical pilot trial was designed to assess if preoperative oral thyroid hormone therapy could prevent the occurrence of euthyroid sick syndrome (ESS) and attenuate myocardial ischemia-reperfusion injury (IRI) after cardiac surgery with cardiopulmonary bypass (CPB) in children.Methods:Forty children aged 3 to 12 year, scheduled for elective congenital heart disease repair surgery with CPB, were randomized into 2 groups of equal size to receive the following treatments in a double-blind manner: placebo (control group) and thyroid tablet 0.4 mg/kg (trial group) taken orally once a day for 4 days before surgery. The perioperative serum thyroid hormone levels and hemodynamic variables were determined. The extubation time, duration of intensive care unit (ICU) stay, and use of inotropic drugs in the ICU were recorded. The myocardial expressions of heat shock protein 70 (HSP70), myosin heavy chain (MHC) mRNA, and thyroid hormone receptor (TR) mRNA were detected. The serum creatine kinase-MB (CK-MB) activity and troponin I (TnI) positive ratio at 24 hour after surgery were assessed.Results:There were no significant differences in hemodynamic variables at all observed points, extubation time, and duration of ICU stay between groups. As compared with baselines on administration, serum triiodothyronine (T3) and free T3 (FT3) levels on the first, second, and fourth postoperative day, and serum thyrotropic-stimulating hormone (TSH), tetraiodothyronine (T4), and free T4 (FT4) levels on the first postoperative day were significantly decreased in the 2 groups. Serum T3, FT3, and T4 levels on the first and second postoperative day, and serum FT4 level on the first postoperative day were significantly higher in the trial group than in control group. As compared with the control group, the number of patients requiring inotropic drugs in the ICU, serum CK-MB activity, serum positive TnI ratio, and myocardial expression of MHCβ mRNA were significantly decreased, and myocardial expressions of both HSP70 and MHCα mRNA were significantly increased in the trial group.Conclusions:In children undergoing cardiac surgery with CPB, preoperative oral small-dose thyroid hormone therapy reduces severity of postoperative ESS and provides a protection against myocardial IRI by increasing HSP70 and MHCα expression.

Effects of excessive endoplasmic reticulum stress on lung ischemia/reperfusion induced myocardial injury in mice

To investigate the effects of excessive endoplasmic reticulum stress on lung ischemia/reperfusion (I/R) induced myocardial injury in mice. Forty healthy SPF male C57BL/6J mice were divided into 4 groups randomly (n=10):sham operation group (Sham group), lung I/R group (I/R group), endoplasmic reticulum stress (ERS) pathway agonist Tunicamycin group (TM) and ERS inhibitor 4-phenyl butyric acid group (4-PBA). The model of lung I/R injury was established by clamping the left hilum of lung for 30 min followed by 180 min of reperfusion. In sham group, only sternotomy was performed, the hilum of lung was not clamped, and the mice were mechanically ventilated for 210 min. In TM and 4-PBA groups, TM 1mg/kg and 4-PBA 400 mg/kg were injected intraperitoneally, respectively, at 30 min before establishment of the model. At 180 min of reperfusion, blood samples were collected from the orbit for determination of myocardial enzyme. The animals were then sacrificed, and hearts were removed for determination of light microscope, TUNEL, Caspase 3 enzymatic activity, real-time polymerase chain reaction and Western blot. Compared with sham group, the cardiomyocytes had obvious damage under light microscope, and the serum creatine kinase-MB (CK-MB) and lactic dehydrogenase (LDH) activities, apoptosis index and Caspase 3 enzymatic activity were increased significantly, the expressions of p-Jun N-terminalkinase(p-JNK), Caspase 12, CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose regulated protein 78(GRP78) protein and mRNA were up-regulated in I/R, TM and 4-PBA groups (P<0.01). Compared with I/R group, the cardiomyocytes damage was obvious under light microscope, and the serum CK-MB and LDH activities, apoptosis index and Caspase 3 enzymatic activity were increased significantly, the expressions of p-JNK, Caspase 12, CHOP and GRP78 protein and mRNA were up-regulated in group TM; while all above changes were relieved in group 4-PBA (P<0.01). Compared with TM group, the cardiomyocytes damage was relieved under light microscope, and the serum CK-MB and LDH activities, apoptosis index and Caspase 3 enzymatic activity were decreased significantly, the expressions of p-JNK, Caspase 12,CHOP and GRP78 protein and mRNA were down-regulated in group 4-PBA. The excessive endoplasmic reticulum stress participates in myocardial injury induced by lung ischemia/reperfusion (I/R) and inhibit excessive endoplasmic reticulum stress response can relieved myocardial injury.

Serum Creatine Kinase-MB Isoenzyme Activity among Subjects with Uncomplicated Essential Hypertension: Any Sex Differences.

Hypertension (high blood pressure) is a major health challenge and more women than men are affected by the condition. Complications as a result of this condition often lead to disabilities and premature death. The objective of this study was to evaluate creatine kinase-MB (CK-MB) activity in uncomplicated hypertension and to know whether sex differences exist in the activity of the enzyme. Serum creatine kinase-MB isoenzyme activity, troponin I, and lipid profile were evaluated in 140 male and 100 female Nigerians with hypertension. The control group was comprised of 100 (50 males and 50 females) normotensive subjects. Measured parameters were assayed using Selectra Pros chemistry analyzer. The means were compared between males and females using Students’t-test. The mean CK-MB activity of the female hypertensive subjects was significantly higher (p < 0.001) than the males. Similarly, the mean cardiac troponin I (cTnI) of the female hypertensive subjects was significantly higher (p < 0.001) than the males. Conversely, the mean CK-MB activity of the female normotensive subjects was significantly lower (p < 0.001) than the male counterparts. There was no difference in the levels of cTnI between male and female normotensive subjects. Serum CK-MB activity was higher in female than male hypertensive subjects. In the light of these results, cardiac markers should be routinely done in the evaluation of hypertensive subjects and sex-specific consideration may be recognized in the management of these patients.

Dexmedetomidine-induced cardioprotection in a mouse model of lung ischemia-reperfusion: the relationship with endoplasmic reticulum stress

Objective To evaluate dexmedetomidine-induced cardioprotection in a mouse model of lung ischemia-reperfusion(I/R)and the relationship with endoplasmic reticulum stress. Methods Forty healthy SPF male C57BL/6J mice, weighing 20-24 g, aged 8-10 weeks, were divided into 4 groups(n=10 each)using a random number table: sham operation group(Sham group), lung I/R group(I/R group), dexmedetomidine group(Dex group)and dexmedetomidine plus atipamezole(specific α2-adrenergic receptor antagonist)group(DA group). The model of lung I/R injury was established by clamping the left hilum of lung for 30 min followed by 180 min of reperfusion.In group Sham, only sternotomy was performed, the hilum of lung was not clamped, and the mice were mechanically ventilated for 210 min.In Dex and DA groups, dexmedetomidine 20 μg/kg and dexmedetomidine 20 μg/kg plus atipamezole 250 μg/kg were injected intraperitoneally, respectively, at 30 min before establishment of the model.At 180 min of reperfusion, blood samples were collected from the orbit for determination of creatine kinase-MB(CK-MB)and lactic dehydrogenase(LDH)activities in serum.The animals were then sacrificed, and hearts were removed for determination of apoptosis in cardiomyocytes(by TUNEL)and expression of phosphorylated c-Jun N-terminal kinase(p-JNK), caspase-12, CCAAT/enhancer-binding protein homologous protein(CHOP)and glucose-regulated protein 78(GRP78)in myocardial tissues(by Western blot), and expression of JNK, caspase-12, CHOP, GRP78 mRNA in myocardial tissues(by real-time polymerase chain reaction). Apoptosis index was calculated. Results Compared with Sham group, the serum CK-MB and LDH activities and apoptosis index were significantly increased, the expression of p-JNK, JNK mRNA, and caspase-12, CHOP and GRP78 protein and mRNA was up-regulated in I/R, Dex and DA groups(P 0.05). Compared with DEX group, the serum CK-MB and LDH activities and apoptosis index were significantly increased, the expression of p-JNK, JNK mRNA, and caspase-12 and CHOP protein and mRNA was up-regulated(P 0.05). Conclusion Dexmedetomidine can reduce myocardial injury induced by lung I/R, and the mechanism may be related to activation of α2-adrenergic receptors and inhibition of endoplasmic reticulum stress in myocardial cells of mice. Key words: Dexmedetomidine; Lung; Reperfusion injury; Myocardium; Endoplasmic reticulum; Stress

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

The Possible Cardio-Reno- Protective Effects of Vanillin on Isopretrenol- Induced Myocardial Infarction in Rats

Myocardial infarction (MI) continues to be a major public health problem in the world. Vanillin is a natural phenolic compound that possesses significant anti-oxidant and anti-inflammatory activities. The present study aimed to investigate the effects of pretreatment with vanillin (150 mg/kg, p.o.) and vanillin (300 mg/kg, p.o.) on isoprenaline-induced MI in rats. Markers chosen to assess cardiac damage included serum activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), in addition to serum level of cardiac troponin-I (cTn-I), as well as antioxidant activity of cardiac catalase (CAT) as well as cardiac contents of RGH, lipid peroxides, and nitrite. Furthermore Electrocardiograph (ECG) monitoring and histological examinations of cardiac tissues were done. In addition markers chosen to assess renal impairment included serum and urine levels of creatinin, blood urea nitrogen (BUN), also creatinine clearance (Ccr), urea clearance (Ucr) and glomerular filteration rate (GFR) were assessed. In addition, antioxidant activity of renal CAT and renal contents of RGH, lipid peroxides, and nitrite. Furthermore, histological examinations of renal tissues were done. Isoprenaline increased serum CK-MB and LDH activity and cTn-I level, cardiac and renal oxidative stress biomarkers. In addition, it produced ST-segment elevation and degenerative changes in heart and renal tissues. Pretreatment with vanillin in previous doses significantly suppressed isoprenaline-induced pathological changes, as the elevated levels of cTn-I, LDH and CK-MB in serum coupled with reduction in cardiac and renal oxidative stress markers. Moreover marked improvement in ECG and histopathologic alterations in both cardiac and renal tissues were produced. In conclusion, vanillin can be regarded as a promising cardio- and reno- protective natural agent in MI.

Exploring the protective role of apocynin, a specific NADPH oxidase inhibitor, in cisplatin-induced cardiotoxicity in rats

Despite the clinical reports, few studies have focused on reducing the cardiotoxicity of cisplatin. In the present study, cardiotoxicity was examined after a single ip injection of cisplatin (7mg/kg) in rats. Apocynin was given in drinking water (600mg/L) for five successive days before and after cisplatin injection. At the end of the experiment, hemodynamic parameters were recorded, animals were sacrificed and serum creatine kinase-MB activity was determined. The whole ventricle was isolated for estimation of tumor necrosis factor-alpha (TNF-α) content, NADPH oxidase, myeloperoxidase and caspase-3 activities in addition to nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and nuclear factor kappa B (NF-κB) gene expressions. Furthermore, oxidative stress markers and antioxidant enzymes were measured in postmitochondrial and mitochondrial fractions. Mitochondrial membrane potential, nuclear DNA fragmentation and cardiomyocyte cross-sectional area were also evaluated. Apocynin was effective against cisplatin-induced decrement in heart rate and blood pressure. Moreover, pretreatment with apocynin notably ameliorated the state of oxidative stress, mitigated inflammation and preserved mitochondrial membrane potential. Apocynin provided also a significant cardioprotection as revealed by alleviating the overexpression of Nrf2, HO-1 and NF-κB, the elevation of caspase-3 activity, the prominent nuclear DNA fragmentation and the decreased cardiomyocyte cross-sectional area. This study highlights the potential role of apocynin in inhibiting cisplatin-induced hemodynamic changes, postmitochondrial and mitochondrial damage as indicated by improvement in the state of oxidative stress, inflammation and apoptosis.

Protective effects of atorvastatin and quercetin on isoprenaline-induced myocardial infarction in rats

Myocardial infarction (MI) continues to be a major public health problem in the world. Statins exhibit cardio-protective effects by several mechanisms beyond their lipid lowering activity. Quercetin is a natural flavonoid that possesses significant anti-oxidant and antiinflammatory activities. The present study aimed to investigate the effects of pretreatment with atorvastatin (10mg/kg) and quercetin (50mg/kg), as well as their combination on isoprenaline-induced MI in rats. Markers chosen to assess cardiac damage included serum activity of creatine kinase-MB (CK-MB) and serum level of cardiac troponin-I (cTn-I), as well as oxidative stress and inflammatory biomarkers including serum levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interleukin-10 (IL-10) as well as cardiac contents of lipid peroxides, reduced glutathione (GSH), and nitrite. Furthermore, ECG monitoring and histological examinations of cardiac tissues were done. Isoprenaline increased serum CK-MB activity and cTn-I level as well as inflammatory and oxidative stress biomarkers. In addition, it produced ST-segment elevation and degenerative changes in heart tissues. Pretreatment with atorvastatin suppressed significantly the elevated levels of cTn-I, CRP, TNF-α, and IL-10 in serum coupled with reduction in cardiac lipid peroxides; however, it increased cardiac nitrite content. Quercetin decreased isoprenaline-induced changes in oxidative stress and inflammatory biomarkers with marked improvement in ECG and histopathologic alterations. Combination of quercetin with atorvastatin resulted in similar protective effects. In conclusion, quercetin can be regarded as a promising cardio-protective natural agent in MI alone or combined with atorvastatin.

Biocompatible Microemulsion Modifies the Pharmacokinetic Profile and Cardiotoxicity of Doxorubicin

Doxorubicin (DOX) is an anthracycline antibiotic with a broad antitumor spectrum. However, the clinical use of DOX is limited because of its cardiotoxicity, a dose-dependent effect. Colloidal drug delivery systems, such as microemulsions (MEs), allow the incorporation of drugs, modifying the pharmacokinetic (PK) profile and toxic effects. In this study, we evaluated the PK profile and cardiotoxicity of a new DOX ME (DOX-ME). The PK profile of DOX-ME was determined and compared with that of the conventional DOX after single-dose administration (6 mg/kg, intravenous) in male Wistar rats (n = 12 per group). The cardiotoxicity of DOX formulations was evaluated by serum creatine kinase MB (CKMB) activity in both animal groups before and after drug administration. The plasma DOX measurements were performed by high-performance liquid chromatography with fluorescence detection, and the CKMB levels were assayed using the CKMB Labtest® kit. The ME system showed a significant increase in plasma DOX concentrations and lower distribution volume when compared with conventional DOX. Serum CKMB activity increased after conventional DOX administration but was unchanged in the DOX-ME group. These results demonstrate modifications in drug access to susceptible sites using DOX-ME. DOX-ME displayed features that make it a promising system for future therapeutic application.

Effects of long-term oral administration of levothyroxine sodium on serum thyroid hormone concentrations, clinicopathologic variables, and echocardiographic measurements in healthy adult horses

To determine the effects of long-term oral levothyroxine sodium (L-T(4)) administration on serum thyroid hormone concentrations, thyroid gland function, clinicopathologic variables, and echocardiographic examination measurements in adult euthyroid horses. 6 healthy adult mares. Horses received L-T(4) (48 mg/d) orally for 48 weeks. Every 4 weeks, physical examinations were performed; blood samples were collected for CBC, plasma biochemical analyses, and assessments of serum total triiodothyronine (tT(3)) and thyroxine (tT(4)) concentrations. Plasma creatine kinase MB activity and cardiac troponin I concentration were also measured. Echocardiographic examinations were performed before and at 16, 32, and 48 weeks during the treatment period. During the treatment period, mean body weight decreased significantly; heart rate varied significantly, but the pattern of variation was not consistent. Significant time effects were detected for certain clinicopathologic variables, but mean values remained within reference ranges. Cardiac troponin I was only detectable in 8 of 24 plasma samples (concentration range, 0.01 to 0.03 ng/mL). Serum creatine kinase MB activity did not change significantly over time. Compared with the pretreatment value, 5.4-, 4.0-, and 3.7-fold increases in mean serum tT(4) concentrations were detected at 16, 32, and 48 weeks, respectively. Some cardiac measurements changed significantly over time, but mean values remained within published reference ranges. Mean fractional shortening was lower than the pretreatment mean value at 16 and 32 weeks. In horses, long-term oral administration of 48 mg of L-T(4)/d significantly increased serum tT(4) concentrations and did not appear to adversely affect health.

Protective effect of total flavones from Elsholtzia blanda (TFEB) on myocardial ischemia induced by coronary occlusion in canines

This study was undertaken to determine the effect of total flavones from Elsholtzia blanda (Benth.) Benth. (TFEB), a traditional Chinese medicine, on myocardial ischemia induced by coronary occlusion in Beagle dogs. Infarct size of left ventricle, serum activity of creatine kinase-MB (CK-MB) and malondialdehyde (MDA), hemorrheologic variables and homodynamic parameters including mean arterial pressure (MAP), coronary blood flow (CBF), coronary vascular resistance (CVR), end-diastolic pressure of left ventricle (LVEDP), rate of rise and decline of left ventricular pressure (±dp/dtmax) were measured in this study. Administration with TFEB produced a dose-dependent reduction in infarct size. TFEB 100 mg/kg exerted notable inhibition in the elevation of serum CK-MB and MDA activity. TFEB significantly reduced MAP and CVR. The decrease in CBF also tended to be smaller in treated dogs. TFEB improved the recovery of myocardial function by depressing the degree of reduction in ±dp/dtmax and LVEDP. TFEB also showed a capacity to resist ischemic damage through lowering blood viscosity. The results indicated that TFEB kept heart from ischemic damage due to coronary occlusion in Beagle dogs.

Age-Related Variations of Serum CK and CK MB Response in Females

The objective was to determine whether serum creatine kinase (CK) and serum CK MB activity following exercise-induced muscle damage activity differs among females of varying menarchial status and to determine whether there is a relationship between serum estradiol (E2) concentration, CK, and CK MB activity. Fifteen menarchial (M), 15 premenarchial (P), and 10 postmenopausal (PM) females participated in the study. Exercise consisted of eccentric hamstring contractions. Estradiol concentrations were significantly higher in M women (p =.0001; M, 125.0 +/- 20.8 pg/mL, P, 54.6 +/- 38.6 pg/mL, PM, 46.2 +/- 34.6 pg/mL). Menarchial women had lower resting CK and CK MB activity and responded with a higher efflux of CK and CK MB post exercise (p =.0001). An inverse relationship was found between E2 concentration and baseline CK (p =.02) and CK MB activity (p =. 006). No relationship existed between post exercise efflux of CK and CK MB and E2 concentration. At rest, E2 influenced CK and CK MB activity across menarchial levels. However, E2 did not significantly reduce the level of CK and CK MB activity following this intense bout of eccentric exercise.

Does lidocaine protect the heart during coronary revascularisation?

Lidocaine has been used as the primary antiarrhythmic agent for ventricular arrhythmias during acute myocardial infarction (MI) and open heart surgery. Its cardioprotective effects have been studied in experimental settings and also during angioplastic reperfusion and coronary revascularisation. The basic mechanism of action, probably also involved with cardioprotection, has been demonstrated to be blockade of cardiac sodium channels. In this open study we investigated the contribution of continuous lidocaine infusion to cardioprotection during coronary revascularisation with blood cardioplegia. During coronary revascularisation with cold blood cardioplegia, a study group of 50 patients received a prophylactic lidocaine infusion for 20 h started with a bolus dose before aortic clamping; another group of 50 patients without the infusion served as a control group. Serum troponin T concentration, serum creatine kinase MB activity and electrocardiography were the main parameters recorded. Serial measurement of Troponin T (P = 0.06) and CK-MB values: (P = 0.09) were slightly lower in the lidocaine group, but the differences were not statistically significant. Lacking statistically significant evidence of improved cardioprotection, lidocaine infusion cannot be recommended as a routine treatment during coronary revascularisation.

The prognostic value of serum troponin T in unstable angina

Background: Cardiac troponin T is a regulatory contractile protein not normally found in blood. Its detection in the circulation has been shown to be a sensitive and specific marker for myocardial cell damage. We used a newly developed enzyme immunoassay for troponin T to determine whether its presence in the serum of patients with unstable angina was a prognostic indicator. Methods: We screened 72 patients with unstable angina (Class III, acute unstable angina) for serum creatine kinase activity, creatine kinase myocardial band (isoenzyme M) activity, and troponin T, every 8 h for 2 days after admission to the hospital. The outcomes of interest during the hospitalization were death and myocardial infarction. Results: Troponin T was detected in the serum of 24 of the 72 patients (34%) with acute angina at rest. Only four of these patients had elevated creatine kinase M activity. Of the 24 patients who were positive for troponin T, 12 had myocardial infarction, and 6 of these died during hospitalization. In contrast, only 2 of the 48 patients with angina at rest who were negative for troponin T had an acute myocardial infarction, and these patients died. Thus, 12 of the 14 patients with myocardial infarctions had detectable levels of troponin T; only 2 had elevated creatine kinase M activity. Conclusions: Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial-cell injury than serum creatine kinase MB activity, and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina.

Effects of Physical Activity on Creatine Phosphokinase and the Isoenzyme Creatine Kinase–MB

Creatine phosphokinase (CPK) and creatine kinaseMB (CK-MB) have been used extensively as diagnostic markers for myocardial infarction and skeletal muscle injury. Many factors affect the variability of serum CPK and serum CK-MB activity, especially physical activity. We discuss the influence of physical activity on muscle and serum CPK and CK-MB. The effect of acute and chronic exercise on CPK and CK-MB activity emphasizes the need to use measurements of serum CPK and CK-MB with caution when evaluating and diagnosing acute myocardial infarctions and skeletal muscle injury.[Schneider CM, Dennehy CA, Rodearmel SJ, Hayward JR: Effects of physical activity on creatine phosphokinase and the isoenzyme creatine kinaseMB. Ann Emerg Med April 1995;25:520-524.]