Myocardial Enzyme Levels Research Articles

Experimental model of acute myocardial infarction for evaluation of prevention and rehabilitation strategies in cardiovascular diseases – a pilot study

Introduction: Acute myocardial infarction (AMI) is an important acute disease of myocardial tissue, that occurs as a result of an imbalance between coronary blood supply and myocardial demand. Isoproterenol (ISO) is a synthetic catecholamine, a beta-adrenergic agonist that produces extensive biochemical, functional, and histological alterations in the heart, characteristic for AMI. The present study has been designed to identify the best dose of ISO that induces electrocardiogram (ECG) alterations, enzymatic reaction, and histopathological changes characteristic of AMI. Material and method: AMI was induced to Wistar-Bratislava white male rats, using three different subcutaneous doses of ISO (85 mg/kg bw, 100 mg/kg bw, and 150 mg/kg bw). ISO was administrated twice, with the second dose at 24h after the initial one. The ECGs were recorded at 24 hours after the last dose of ISO. Blood samples were collected for measurement of creatine kinase (CK), and CK-MB serum levels, and the hearts were excised and prepared for histopathologic examination. Results and discussions: All doses of ISO induced alterations in the ECG patterns such as increased heart rate and prolongation of QT and QTc intervals. Depression of the ST segment coupled with marked T wave inversion were observed at the doses of 100 mg/kg bw and 150 mg/kg bw of ISO. All doses of ISO induced an elevation of CK and CK-MB with highest levels observed for the dose of 150 mg/kg bw. Histopathologic examination revealed subendocardial AMI lesions for all doses tested. Conclusions: ISO in doses of 100 mg/kg and 150 mg/kg is useful for induction of infarct-like lesion on ECG, increased levels of myocardial necrosis enzymes and morphological changes characteristic for AMI.

The efficacy observation of ulinastatin combined with creatine phosphate sodium in pediatric viral myocarditis.

This study aimed to compare the efficacy and safety of ulinastatin combined with creatine phosphate sodium and ribavirin combined with creatine phosphate sodium in the treatment of pediatric viral myocarditis. 155 children with viral myocarditis in the Xuzhou Children's Hospital, were retrospectively analyzed. 80 of them received ulinastatin combined with creatine phosphate sodium, and were regarded as observation group; other 75 patients received ribavirin combined with creatine phosphate sodium and were regarded as the control group. The therapeutic efficacy of the two groups was observed, the improved condition of myocardial enzyme indicator and myocardial troponin I (cTn I) in the two groups were compared before and after the treatment. The total effective rates of the patients in the observation group and the control group were 93.75% and 76.00%, respectively. The clinical efficacy of the observation group was better than that of the control group (p<0.05). The electrocardiogram improvement condition of the observation group was better than that of the control group (p<0.05); after the treatment, the expression levels of lactate dehydrogenase (LDH), aspartate aminotransferase (AST), Creatine Kinase (CK-MB), and cTn I in the observation group were (313.37±9.42) U/L, (29.38±4.97) U/L, (23.67±2.89) U/L, (0.12±0.02) μg/L, respectively. The expression levels of LDH, AST, CK-MB, and cTn I in the control group were (322.43±12.32) U/L, (33.43±5.14) U/L, (26.22±3.37) U/L, (0.24±0.04) μg/L. The levels of myocardial enzyme and cTn I in the observation group and the control group after the treatment were lower than that before the treatment (p<0.05), while the level of myocardial enzyme and cTn I in the observation group after the treatment was significantly lower than that in the control group (p<0.05). The results indicated that, compared with ribavirin combined with creatine phosphate sodium, ulinastatin combined with creatine phosphate sodium had better clinical efficacy in the treatment of pediatric viral myocarditis. It could significantly improve the level of myocardial enzyme indicator and cTn I, and had certain clinical and promotional values and application values.

Naringin mitigates myocardial strain and the inflammatory response in sepsis-induced myocardial dysfunction through regulation of PI3K/AKT/NF-κB pathway

Sepsis-induced myocardial dysfunction (SIMD) is a manifestation of severe sepsis and is the main cause of increased mortality in sepsis patients. Naringin (Nar) has been reported to possess various biological activities and pharmacological properties. Therefore, the present study was undertaken to evaluate whether Nar can protect rats from the effects of LPS-induced SIMD. SD Rats were pre-treated with Nar (50 and 100 mg/kg) for 7 days before administration of a single dose of LPS (10 mg/kg, i.p.) on the seventh day. We found that Nar treatment markedly improved the global strain and strain rate of longitudinal, circumference, and radial direction (GLS/GLSr, GCS/GCSr, GRS/GRSr) compared to the LPS group. The layer-specific strain decreased gradually from the endocardial layer to epicardial layer, and the most serious damage occurred in the endocardial layer. Moreover, Nar significantly decreased the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and myocardial enzymes (CK, LDH, and AST) induced by LPS and attenuated the inflammation response. Finally, Nar also inhibited NF-κB nuclear translocation and the activity of iNOS in H9c2 cardiomyocytes by activating PI3K/AKT signaling pathway. These results suggest that naringin may possess novel therapeutic potential for protection against LPS-induced myocardial dysfunction.

MicroRNA-325-3p protects the heart after myocardial infarction by inhibiting RIPK3 and programmed necrosis in mice

BackgroundReceptor-interacting serine-threonine kinase 3 (RIPK3)-mediated necroptosis has been implicated in the progression of myocardial infarction (MI), but the underlying mechanisms, particularly whether microRNAs (miRNAs) are involved, remain largely unknown.ResultsA microarray analysis was used to screen for miR-325-3p expression in myocardial tissues from MI mice, and the expression was confirmed with qRT-PCR. The levels of myocardial enzymes were measured using commercial kits, and an echocardiography system was utilized for the detection of cardiac function parameters. The pathological features and infarction sizes of cardiac tissues were examined using H&E, TCC and Masson’s trichrome staining, and the amount of cell apoptosis was determined using an in situ TUNEL assay. Cardiomyocytes were isolated and then subjected to hypoxia induction in vitro. The expression of the RIPK1, RIPK3 and phosphorylated MLKL (p-MLKL) proteins was measured using a Western blot. The mouse cardiomyocyte cell viability was analyzed by an MTT assay. The mRNA target of miR-325-3p was predicted using TargetScan v7.2 and then validated using a dual-luciferase reporter assay. The overexpression of miR-325-3p evidently decreased the expression levels of lactate dehydrogenase (LDH), phosphocreatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA), inhibited left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD), and promoted left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVES). In addition, miR-325-3p overexpression attenuated the degree of injury to the cardiac tissue, decreased the infarct sizes and downregulated the expression of the necrosis-related proteins RIPK1, RIPK3 and p-MLKL.ConclusionsThe RIPK1/RIPK3/p-MLKL axis-induced necroptosis that occurred during MI was mediated by a miRNA module, miR-325-3p, which can effectively ameliorate the symptoms of MI by suppressing the expression of RIPK3.

H2S attenuates sepsis-induced cardiac dysfunction via a PI3K/Akt-dependent mechanism.

The heart is the most vulnerable target organ in sepsis, and it has been previously reported that hydrogen sulfide (H2S) has a protective role in heart dysfunction caused by sepsis. Additionally, studies have demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway has a protective function during sepsis. However, the potential association between H2S and PI3K/Akt in sepsis-induced cardiac dysfunction is unclear. Therefore, the PI3K inhibitor LY294002 was used to investigate the role of PI3K/Akt signaling in the protective effects of H2S during sepsis-induced myocardial injury. A rat sepsis model was established using cecal ligation and puncture (CLP) surgery. Sodium hydrosulfide, a H2S donor, was administered intraperitoneally (8.9 µmol/kg), and serum myocardial enzyme levels, inflammatory cytokine levels, cardiac histology and cardiomyocyte apoptosis were assessed to determine the extent of myocardial damage. The results demonstrated that exogenous H2S reduced serum myocardial enzyme levels, decreased the levels of the inflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-6, and increased the level of anti-inflammatory IL-10 following CLP. Staining of histological sections demonstrated that myocardial damage and cardiomyocyte apoptosis were alleviated by the administration of exogenous H2S. Western blot analysis was used to detect phosphorylated and total PI3K and Akt levels, as well as NF-κB, B-cell lymphoma-2, Bcl-2-associated X protein (Bax) and caspase levels, and the results demonstrated that H2S significantly increased PI3K and Akt phosphorylation. This indicated that the PI3K/Akt signaling pathway was activated by H2S. Additionally, H2S reduced Bax and caspase expression, indicating that apoptosis was inhibited, and decreased NF-κB levels, indicating that inflammation was reduced. Furthermore, the PI3K inhibitor LY294002 eliminated the protective effects of H2S. In conclusion, the results of the current study suggest that exogenous H2S activates PI3K/Akt signaling to attenuate myocardial damage in sepsis.

Differences of clinical manifestations and organ damage between patients with severe fever with thrombocytopenia syndrome and patients with tsutsugamushi disease

Objective To analyze the differences of clinical manifestations and organ damage between patients with severe fever with thrombocytopenia syndrome(SFTS) and patients with tsutsugamushi disease, and to investigate the prognostic factors of SFTS. Methods The research was performed on 49 patients with SFTS and 16 patients with tsutsugamushi disease who visited the First Affiliated Hospital of Anhui Medical University from October 2014 to June 2017. The general information of patients including region, age, gender and clinical manifestations were evaluated. Blood routine, liver and kidney function, myocardial enzyme levels, lipase, amylase, electrolytes, C-reactive protein, procalcitonin, prothrombin time(PT) and activated partial thromboplastin time(APTT) were continuously monitored during the course of disease. T test was used for continuous variables of normal distribution, and non-parametric test was used for variables of non-normal distribution. Chi-square test was used for categorical variables. Results The mean age of SFTS patients was 62.1±15.5(ranging from 17 to 87 years) and the mean age of tsutsugamushi patients was 56.1±9.2 (ranging from 47 to 73 years). There was no significant difference between the two groups (t=1.47, P=0.147). There were 25 males(51%) in SFTS patients and 8 males (50%) in tsutsugamushi disease patients. There was no significant difference between the two groups (χ2=0.005, P=0.943). The incidences of headache, vomiting, superficial lymphadenectasis, disturbance of consciousness, proteinuria, hematuria, pulmonary infection, multiple organ dysfunction and acute pancreatitis in SFTS patients were all significantly higher than those in tsutsugamushi disease patients (χ2=8.82, 4.38, 8.71, 11.17, 7.88, 5.56, 4.35, 9.43, and 8.13, respectively, P<0.05 or 0.01). The counts of leukocytes (Z=2.73), neutrophils (Z=2.46), lymphocytes (Z=3.15), platelets (Z=4.25), albumin (Z=2.65) and sodium ion (t=2.10) in SFTS patients were all significantly lower than those in patients with tsutsugamushi disease (P<0.05 or 0.01). The levels of aspartate aminotransferase (Z=2.94), lactate dehydrogenase (Z=3.42), creatine kinase(CK)(Z=2.88), amylase (Z=2.77), lipase (Z=2.82), creatinine (Z=2.07) and urea nitrogen (Z=2.50) in fatal SFTS patients were all significantly higher than those in patients with tsutsugamushi disease (P<0.05 or 0.01). Among 49 SFTS patients, 16 patients died and 33 patients recovered finally. The age(t=3.33), platelet count (Z=2.55), alanine aminotransferase (ALT)(Z=2.10), aspartate aminotransferase (AST)(Z=2.22), lactate dehydrogenase (Z=2.26), CK(Z=3.50), CK-MB (Z=3.10), creatinine (Z=2.17), urea nitrogen (Z=2.36), and sodium (t=2.65) between the two subgroups had significant differences (P<0.05 or 0.01). Conclusions SFTS is more severe and has high mortality, while tsutsugamushi disease has a better prognosis. Early differential diagnosis and early rational treatment are important to reduce the mortality of patients with SFTS. Key words: Scrub typhus; Severe fever with thrombocytopenia syndrome; New bunyavirus; Organ damage

Immediate Proximal Coronary Graft Anastomosis after Completion of Related Distal Anastomosis, During Off Pump Cabg; Is It Efficient?

Objective: Evaluation of early outcome and safety of proximal coronary graft anastomosis immediately after finishing its related distal anastomosis, during beating heart CABG. It presents rapid reperfusion of ischemic myocardium. So, it could reduce intraoperative hemodynamic instability. Methods: The results in 27 patients underwent off pump CABG with simultaneous proximal coronary graft anastomosis after the end of its related distal anastomosis (group A), were compared with the results in 28 patients had conventional late all proximal anastomoses after completion of all distal anastomoses (group B). Effectiveness of simultaneous proximal coronary graft anastomosis was evaluated during and after the operation by clinical, hemodynamic, electrocardiographic and echo-cardio graphic assessment. Results: Conversion to cardio-pulmonary bypass (CPB) was significantly lower in immediate proximal anastomosis (group A). The ischemic time for each coronary territory (the sum of the time without distal perfusion for each coronary artery after finish of distal anastomosis) was lower significantly in group A than group B (17.6 vs. 24.0 minutes). The patients requiring high dose inotropic support were lower in (group A). Laboratory results showed significant lower myocardial enzyme levels at 1st and 2nd days after operation in group (A). During 6 months follow up, ejection fraction (E.F) in group A was better than in group B. Conclusions: Immediate proximal coronary graft anastomosis resulted in superior myocardial protection when compared to late all proximal coronary anastomosis during off-pump coronary artery grafting.

Selective Activation of Cannabinoid Receptor 2 Attenuates Myocardial Infarction via Suppressing NLRP3 Inflammasome

The administration of cannabinoid receptor 2 (CB2R) agonist has been reported to produce a cardioprotective effect against the pathogenesis and progression of myocardial infarction (MI). Here in this study, we investigated the specific mechanism related to inflammatory suppression. JWH-133 was used for the activation of CB2R. MI mice models and cardiomyocytes under oxygen-glucose deprivation (OGD) challenge were used for the in vivo and in vitro studies, respectively. Detection of cardiac infarct size and levels of myocardial enzymes as well as echocardiographic examination were applied to assess MI severity and cardiac function. Cell viability and lactate dehydrogenase (LDH) release were detected in vitro. Real-time-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect the levels of proinflammatory cytokines. Western blot was used for the analysis of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation. We found that the administration of CB2R agonist attenuated the severity of MI through reducing infarct size ratio and levels of myocardial enzymes and improved cardiac function in ejection fraction (EF), fractional shortening (FS), left ventricular end-systolic diameter (LVESD), and left ventricular end-diastolic diameter (LVEDD) in MI mice. JWH-133 also produced a cardioprotective effect in murine primary cardiomyocytes by improving cell viability and LDH release. JWH-133 largely reduced the production and secretion of proinflammatory cytokines, which was significantly attenuated by AM630. HU308 showed the same effects as JWH-133. Taken together, we demonstrated for the first time the cardioprotective effect of CB2R agonist and its NLRP3 inflammasome-related mechanism in MI.

Cardiotoxicity of Consolida rugulosa, a poisonous weed in Western China

Poisonous weeds are a global problem since they not only hinder local economic development, but also cause ecological harm. Consolida rugulosa (family Ranunculaceae) is a weed that is widespread in Northwestern China and causes severe poisoning when ingested by livestock. In the present study, we purified the toxins in this plant and investigated their mechanism of action. Five natural diterpene alkaloids (compounds 1–5)—including two new compounds (1 and 2)—were isolated, and five semi-synthetic derivatives (6–10) were synthesised based on 4 or 5 for structure-activity analysis. The toxicity of the compounds was evaluated in vitro with lactate dehydrogenase (LDH) assay. All of the compounds—especially 1—stimulated LDH release in primary cultured rat myocardial cells, an effect that was blocked by the Na+ channel blocker lidocaine. Electrocardiography revealed that rats treated with 1 had severe arrhythmia, while heart Doppler echocardiography and analysis of serum biomarkers levels revealed that administration of 1 for 15 days induced changes in cardiac structure and myocardial enzyme levels. These effects were antagonised by lidocaine treatment. Thus, diterpene alkaloids are the main compounds responsible for the cardiotoxicity of C. rugulosa, which can be mitigated by co-administration of lidocaine.

Clinical significance of serum myocardial enzyme detection in infants with rotavirus enteritis

Objective To explore the clinical significance of serum myocardial enzyme detection in infants with rotavirus (RV) enteritis. Methods One hundred and two infants with enteritis were selected as study objects.52 cases diagnosed as RV enteritis were selected as observation group, while the other 50 cases with negative RV were selected as control groups.The fasting serum myocardial enzyme levels of the two groups were detected. Results The serum myocardial enzyme levels including AST, ALT, LDH, CK, CK-MB, α-HBD in the observation group were (46.54±3.27)U/L, (28.32±12.90)U/L, (395.61±38.75)U/L, (148.43±18.22)U/L, (62.98±4.17)U/L, (271.28±22.64)U/L, respectively, which were significantly higher than those in the control group[(34.02±8.93)U/L, (22.27±11.42)U/L, (295.84±56.36)U/L, (119.74±20.06)U/L, (42.85±9.73)U/L, (235.30±19.18)U/L] (t=26.765, 24.572, 38.337, 31.329, 25.453, 56.832, all P<0.05). Conclusion Infants with RV enteritis are more likely to have myocardial injury than simple RV negative enteritis, it is important to monitor ECG and serum myocardial enzyme levels, which can help to diagnose and improve prognosis. Key words: Enteritis; Rotavirus infections; Creatine kinase; Lactate dehydrogenases

Cardioprotective role of azafrin in against myocardial injury in rats via activation of the Nrf2-ARE pathway

BackgroundThe root of Centranthera grandiflora Benth. is a Chinese ethnodrug known as Ye-Can-Dou-Gen (YCDG) and has been widely used to treat cardiovascular diseases in Hmong, Yunnan Province, China; however, its mechanisms of action were largely unknown. Azafrin, a natural carotenoid, is one of the most abundant active ingredients in YCDG. PurposeWe aimed to explore the cardioprotective effects of azafrin on myocardial infarction (MI) and myocardial ischaemia-reperfusion (MIR) injury and to clarify its underlying myocardial protective mechanisms. MethodsThe in vitro cardioprotective effects of azafrin against oxidative stress injury in H9c2 cells were assessed by the ferric reducing antioxidant power (FRAP) assay and a viability assay in the presence of H2O2-induced oxidative insults, whereas the in vivo effects were assessed with the echocardiographic and histopathological evaluation together with 2,3,5-triphenyltetrazolium chloride (TTC) and serum biochemical analyses in vivo. Then, we used the luciferase reporter gene assay to measure Nrf2 transcriptional activity in HEK 293 cells and analysed the expression levels of enzymes downstream of Nrf2-ARE signalling by q-PCR and western blotting. ResultsAzafrin showed higher FRAP values than FeSO4 and exhibited prophylactic and therapeutic potency against H2O2-induced cell injury. Additionally, azafrin treatment dramatically improved cardiac function; ameliorated the infarct size and pathological changes in rats; decreased the levels of MDA, cTnI, and myocardial enzymes and elevated SOD activity in vivo. In addition, azafrin significantly elevated the transcriptional activity of Nrf2 in HEK 293 cells and up-regulated the mRNA expression levels of genes downstream of Nrf2-ARE pathway activation in H9c2 cells. Furthermore, the protein expression levels of HO-1 and NQO1 in the cytoplasm and Nrf2 in the nucleus were also up-regulated in both the in vivo and in vitro experiments. ConclusionAzafrin exhibited cardioprotective effects against myocardial injury via activation of the Nrf2-ARE pathway. As a natural carotenoid antioxidant, this molecule represents a promising cardioprotective adjuvant for the prophylaxis and treatment of ischaemic heart diseases.

Effects of microRNA-292-5p on myocardial ischemia-reperfusion injury through the peroxisome proliferator-activated receptor-α/-γ signaling pathway.

Ischemia-reperfusion injury (IRI) is a major cause of cardiac damage following various pathological processes, such as free radical damage and cell apoptosis. This study aims to investigate whether microRNA-292-5p (miR-292-5p) protects against myocardial ischemia-reperfusion injury (IRI) via the peroxisome proliferator-activated receptor (PPAR)-α/-γ signaling pathway in myocardial IRI mice models. Mouse models of myocardial IRI were established. Adult male C57BL/6 mice were divided into different groups. The hemodynamic indexes, levels of related inflammatory factors and serum myocardial enzymes, and malondialdehyde (MDA) content and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected. The 2,3,5-triphenyltetrazolium chloride (TTC) staining was applied to determine infarct size. TUNEL staining was used to detect cardiomyocyte apoptosis. RT-qPCR and western blotting were performed to measure the related gene expressions. Compared with the model group and the T0070907 + miR-292-5p inhibitor, the miR-292-5p inhibitor group exhibited decreased incidence and duration time of ventricular tachycardia and ventricular fibrillation, serum myocardial enzymes, TNF-α, IL-6, IL-1β, MDA, cardiomyocyte apoptosis, expressions of Bax and p53 in addition to increased SOD and GSH-Px activity, and increased expressions of Bcl-2, PPARα, PPARγ, PLIN5, AQP7, and PCK1. The T0070907 group exhibited opposite results compared to the miR-292-5p inhibitor group. The results indicate that miR-292-5p downregulation protects against myocardial IRI through activation of the PPAR-α/PPAR-γ signaling pathway.

Cardioprotection of tilianin ameliorates myocardial ischemia-reperfusion injury: Role of the apoptotic signaling pathway.

Our previous research demonstrated that tilianin protects the myocardium in a myocardial ischemia reperfusion injury (MIRI) rat model and has prominent pharmacological potential as a cardiovascular drug. Our study aimed to investigate the molecular signaling implicated in the improvement of myocardial survival induced by tilianin, a flavonoid antioxidant. Tilianin (2.5, 5, and 10 mg/kg/d) or saline was orally administered to rats for 14 days. On the 15th day, ischemia was induced by ligating the left anterior descending artery for 45 min, followed by 4 h of reperfusion. The levels of MIRI-induced serum myocardial enzymes and cardiomyocyte apoptosis as well as infarct size were examined to assess the cardioprotective effects. Cardiac tissues were collected for western blot analyses to determine the protein expression of anti-apoptotic signaling molecules. In MIRI-treated rats, our results revealed that pre-administration of high dose-tilianin the reduced release of LDH, MDA, and CK-MB and increased the plasma SOD level, and significantly attenuated the infarct size. Western blot analysis showed that a remarkable rise in expression of Bcl-2 and XIAP, and decline in expression of Bax, Smac/Diablo, HtrA2/Omi, cleaved caspase-3, caspase-7 and caspase-9 was observed in the myocardium. The apoptosis index of cardiomyocytes further supports the cardioprotective effect of tilianin. Additionally, compared with the MIRI model group, pretreatment with high dose-tilianin group upregulated phosphorylated Akt and PI3K. In contrast, using the PI3K inhibitor LY294002 to block Akt activation effectively inhibited the protective effects of tilianin against MIRI. Tilianin pretreatment was beneficial for activating the PI3K/Akt signaling pathway and inhibiting myocardial apoptosis.

Celastrol pretreatment attenuates rat myocardial ischemia/ reperfusion injury by inhibiting high mobility group box 1 protein expression via the PI3K/Akt pathway

Background/AimsCelastrol pretreatment has been shown to protect against myocardial ischemia/reperfusion (I/R) injury, but the underlying mechanism is poorly understood. This study aimed to investigate the cardioprotective effects of celastrol pretreatment on I/R injury and to further explore whether its mechanism of action was associated with the inhibition of high mobility group box 1 protein (HMGB1) expression via the phosphoinositide 3-kinase (PI3K)/Akt pathway. MethodsIn a fixed-dose study, hematoxylin and eosin staining and myocardial enzyme measurements were used to determine the optimal dose of celastrol that elicited the best cardioprotective effects against I/R injury. Furthermore, rats were pretreated with 4 mg/kg celastrol, and infarct size and the levels of myocardial enzymes, apoptosis, inflammatory and oxidative indices, and HMGB1 and p-Akt expression were measured. ResultsOur results indicated that celastrol dose-dependently attenuated histopathological changes and the elevation in myocardial enzymes induced by I/R. Moreover, the celastrol pretreatment (4 mg/kg) not only significantly decreased infarct size as well as myocardial enzyme levels but also inhibited myocardial apoptosis, inflammatory response and oxidative stress. Additionally, celastrol downregulated HMGB1 expression and upregulated p-Akt expression in the myocardium. LY294002, a specific pI3k inhibitor, partially reversed the decreased HMGB1 expression, increased p-Akt expression induced by celastrol, and abolished the anti-apoptotic, anti-inflammatory and anti-oxidative effects of celastrol. ConclusionThese findings suggest that short-term pretreatment with celastrol protects against myocardial I/R injury by suppressing myocardial apoptosis, inflammatory response and oxidative stress via pI3k/Akt pathway activation and HMGB1 inhibition.

Analysis of liver function and myocardial enzyme level of 395 cases with infantile rotavirus enteritis

Objective To detect the damage incidence rate of liver and myocardium in infantile rotavirus(RV) enteritis. And to provide the basis for prevention and cure of liver and myocardium damage in infantile RV enteritis. Methods The liver function and myocardial enzyme detection results of 395 patients with infantile RV enteritis were collected. These results were compared with those of 40 healthy kids from health examinations. Results The levels of alanine aminotransferase(ALT), aspartate amino transferase(AST), serum creatine kinase(CK) and serum creatine kinase isozyme(CK-MB) from infantile patients were (34.49±29.13)U/L, (52.44±24.10)U/L, (141.75±132.22)U/L and (48.69±32.53)U/L, respectively, which were higher than those of the healthy control [(16.00±3.24)U/L, (29.90±3.76)U/L, (101.82±64.56)U/L and (22.32±8.98)U/L, t=4.008, 5.901, 3.982, 5.64, all P<0.05]. The abnormal occurrence rates of ALT, AST, CK and CK-MB in infantile patients were 19.49%, 73.16%, 12.15%, 73.16%, respectively, which were higher than those in healthy controls(2.50%, 20.00%, 0.00%, 0.00%), the differences were statistically significant(χ2=7.128, 47.397, 5.464, 300.239, all P<0.05). The incidence rates of liver and myocardium damage were 19.49% and 73.16%, respectively. Conclusion There are higher incidence rates of liver and myocardium damage in infantile RV enteritis. So for the infantile RV enteritis patients, it is necessary to detect the liver function and myocardial enzyme level. The treatment for infantile RV enteritis should be included liver and myocardial protection except antivirus and correcting dehydration. Key words: Enteritis; Rotavirus infections; Liver function tests; Cardiomyopathies; Child

Detection of myocardial enzymes, cardiac troponin T and hepatic and renal function in the diagnosis and treatment of severe pneumonia in children.

Objective:To analyze the significance of myocardial enzymes, cardiac troponin T (cTnT) and hepatic and renal function in the treatment of severe pneumonia in children.Methods:One hundred and twenty children with severe pneumonia who were admitted to the hospital between April 2015 and February 2017 were selected and included as a severe pneumonia group; 120 children with common pneumonia were included as a common pneumonia group; 100 healthy children were included as controls. The myocardial enzymes, cTnT and hepatic and renal function of patients in the three groups were detected and compared. The children with severe pneumonia were divided into a mild hypoxia group, a moderate hypoxia group and a severe hypoxia group according to arterial partial pressure of oxygen; the myocardial enzymes, hepatic and renal function and cTnT of the children in the three groups were compared. The correlations of partial pressure of blood oxygen with myocardial enzymes, hepatic and renal function and cTnT were analyzed.Results:The levels of myocardial enzymes, hepatic and renal function and cTnT of the severe pneumonia group, common pneumonia group and control group declined, and the differences had statistical significance (P<0.05). The levels of myocardial enzymes, hepatic and renal function and cTnT were higher in the children with severe hypoxia. The partial pressure of blood oxygen was in a negative correlation with myocardial enzymes, hepatic and renal function and cTnT in the severe pneumonia group.Conclusion:Timely monitoring of myocardial enzymes, hepatic and renal function and cTnT has an extremely important role in the evaluation of children with severe pneumonia.

Remote ischemic conditioning improves myocardial parameters and clinical outcomes during primary percutaneous coronary intervention: a meta-analysis of randomized controlled trials.

We conducted a systematic review and meta-analysis to evaluate the effects of remote ischemic conditioning on myocardial parameters and clinical outcomes in ST segment elevation acute myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention. Ten eligible randomized controlled trials with 1006 STEMI patients were identified. Compared with controls, remote ischemic conditioning reduced the myocardial enzyme levels (standardized mean difference =-0.86; 95% CI: -1.44 to -0.28; P = 0.004; I2 = 94.5%), and increased the incidence of complete ST-segment resolution [odds ratio (OR) = 1.74; 95% CI: 1.09 to 2.77; P = 0.02; I2 = 47.9%]. Remote ischemic conditioning patients had a lower risk of all-cause mortality (OR = 0.27; 95% CI: 0.12 to 0.62; P = 0.002; I2 = 0.0%) and lower major adverse cardiovascular and cerebrovascular events rate (OR=0.45; 95% CI: 0.27 to 0.75; P = 0.002; I2 = 0.0%). Meta-analysis suggested that remote ischemic conditioning conferred cardioprotection by reducing myocardial enzymes and increasing the incidence of complete ST-segment resolution in patients after STEMI. As a result, clinical outcomes were improved in terms of mortality and incidence of major adverse cardiovascular and cerebrovascular events.

Hyperbaric oxygen protects against myocardial reperfusion injury via the inhibition of inflammation and the modulation of autophagy

Our previous study demonstrated that hyperbaric oxygen (HBO) preconditioning protected against myocardial ischemia reperfusion injury (MIRI) and improved myocardial infarction. However, HBO’s effect on MIRI-induced inflammation and autophagy remains unclear. In this study, we investigate the potential impact and underlying mechanism of HBO preconditioning on an MIRI-induced inflammatory response and autophagy using a ligation of the left anterior descending (LAD) coronary artery rat model. Our results showed that HBO restored myocardial enzyme levels and decreased the apoptosis of cardiomyocytes, which were induced by MIRI. Moreover, HBO significantly suppressed MIRI-induced inflammatory cytokines. This effect was associated with the inhibition of the TLR4-nuclear factor kappa-B (NF-κB) pathway. Interestingly, lower expression levels of microtubule-associated protein 1 light chain 3B (LC3B) and Beclin-1 were observed in the HBO-treatment group. Furthermore, we observed that HBO reduced excessive autophagy by activating the mammalian target of the rapamycin (mTOR) pathway, as evidenced by higher expression levels of threonine protein kinase (Akt) and phosphorylated-mTOR. In conclusion, HBO protected cardiomocytes during MIRI by attenuating inflammation and autophagy. Our results provide a new mechanistic insight into the cardioprotective role of HBO against MIRI.

Relationship between the change in pacing threshold and the myocardial injury.

To investigate the effects of general conditions and past medical history of patients on the short-term pacing threshold after the implantation of active electrodes of a cardiac pacemaker, and to understand whether the application of active electrodes will cause muscle injury and the severity of the injury. A total of 156 patients who were treated with a cardiac pacemaker and implanted with single or double active electrodes in Cardiovascular Department of Central Hospital of Jiangjin District were enrolled, including 96 patients treated with a single active electrode and 60 patients treated with double active electrodes. Their clinical data were collected. During operation, the short-term atrial and ventricular pacing thresholds were monitored and recorded after the implantation of the active fixed electrode lead. Multivariate Logistic regression analysis showed that female sex, age, smoking, drinking, coronary heart disease, diabetes mellitus and hyperlipidemia had effects on pacing thresholds in a short-term to some extent after the implantation of active fixed electrode lead of cardiac pacemaker. The levels of myocardial enzymes, myoglobin (MYO), creatine kinase (CK), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTNI), in patients were gradually increased after the implantation of active fixed electrode lead and reached the peak at 24 h, which were higher than those before operation (p < 0.05). The levels were decreased at 72 h with statistically significant differences. Female sex, age, smoking, drinking, coronary heart disease, diabetes mellitus and hyperlipidemia are independent influencing factors of pacing thresholds in a short term after the implantation of active fixed electrode lead of cardiac pacemaker. The implantation of active electrodes can raise the myocardial enzyme indexes compared with those before operation, but will fall to the preoperative levels or normal, near normal levels at 72 h after operation. The implantation of active electrodes is safe and feasible for myocardial tissues.

Effect of atomization inhalation of ambroxol hydrochloride combined with erythromycin on high sensitivity C reactive protein, myocardial enzyme level in neonatal pneumonia patients

Objective To investigate the effect of ambroxol atomization inhalation combined with erythromycin on neonatal pneumonia patients and its influence on high sensitivity C reactive protein(hs-CRP), myocardial enzyme level. Methods 100 cases of neonatal pneumonia were selected and they were randomly divided into observation group and control group according to the digital table, 50 cases in each group.The control group was treated with erythromycin 30mg/kg, 1 time/d.The observation group was given ambroxol ultrasonic nebulizer inhalation, 15 minutes per time, 3 times daily, on the basis of the treatment of the control group.The patients were treated for 4 consecutive weeks.The clinical symptoms disappeared time, hs-CRP level, CK-MB level and clinical efficacy were detected and compared. Results Compared with before treatment, the hs-CRP and CK-MB levels were decreased after treatment.Compared with the control group, the hs-CRP[(7.25±2.11)mg/L vs.(12.21±3.76)mg/L] and CK-MB[(21.31±4.42)U/L vs.(27.12±3.17)U/L] levels in the observation group were lower(t=8.134, 7.553, all P<0.05), the clinical symptoms disappeared in a relatively shorter time(t= 6.520, 11.824, 19.473, all P<0.05), the clinical curative effect was better. Conclusion Ambroxol aerosol inhalation combined with erythromycin can reduce hs-CRP, CK-MB levels in neonatal pneumonia patients, and the clinical symptoms of the patients disappeared in a relatively short time, the clinical curative effect is better, has guiding significance in clinic. Key words: Infant, newborn; Pneumonia; Ambroxol hydrochloride; Erythromycin; C-reactive protein; Creatine kinase, MB form