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BackgroundIschemia reperfusion (I/R) play an imperative role in the expansion of cardiovascular disease. Sinomenine (SM) has been exhibited to possess antioxidant, anticancer, anti-inflammatory, antiviral and anticarcinogenic properties. The aim of the study was scrutinized the cardioprotective effect of SM against I/R injury in rat.MethodsRat were randomly divided into normal control (NC), I/R control and I/R + SM (5, 10 and 20 mg/kg), respectively. Ventricular arrhythmias, body weight and heart weight were estimated. Antioxidant, inflammatory cytokines, inflammatory mediators and plasmin system indicator were accessed.ResultsPre-treated SM group rats exhibited the reduction in the duration and incidence of ventricular fibrillation, ventricular ectopic beat (VEB) and ventricular tachycardia along with suppression of arrhythmia score during the ischemia (30 and 120 min). SM treated rats significantly (P < 0.001) altered the level of antioxidant parameters. SM treatment significantly (P < 0.001) repressed the level of creatine kinase MB (CK-MB), creatine kinase (CK) and troponin I (Tnl). SM treated rats significantly (P < 0.001) repressed the tissue factor (TF), thromboxane B2 (TXB2), plasminogen activator inhibitor 1 (PAI-1) and plasma fibrinogen (Fbg) and inflammatory cytokines and inflammatory mediators.ConclusionOur result clearly indicated that SM plays anti-arrhythmia effect in I/R injury in the rats via alteration of oxidative stress and inflammatory reaction.  相似文献   
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von Willebrand factor (VWF) plays a crucial role in hemostasis and thrombosis. VWF is involved in platelet attachment to the subendothelium, serving as a carrier protein for coagulation factor VIII. In this study, myocardial tissues from deceased patients with ischemic heart disease and a mouse model of acute myocardial infarction were subjected to immunohistochemistry to determine VWF expression. We examined 28 neutral formalin-fixed, paraffin-embedded myocardial tissue samples obtained from the autopsies of patients who were diagnosed with ischemic heart disease within 48 h postmortem. Most myocardial cells were negative for VWF, although some cells showed nonspecific positivity. Elevated VWF expression was observed around myocardial cells undergoing remodeling, suggesting that endothelial proliferation occurred at these sites. In contrast, completely fibrotic myocardial foci did not show upregulated VWF expression. Positivity in fibrin deposition and hemorrhagic sites was observed. The same VWF expression characteristics as those observed in the human samples were observed in the mouse model. VWF immunostaining as an endothelial marker may be a useful supplementation to conventional staining techniques that are currently used in the diagnosis of ischemic heart disease in terms of examining the timing of myocardial remodeling in detail and highlighting the remodeling process.  相似文献   
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目的 研究蒙药安神补心六味丸对大鼠心肌缺血损伤的保护作用和氧化应激机制。方法 将60只大鼠随机分为空白组、模型组、阳性对照组(丹参滴丸)及蒙药安神补心六味丸低、中、高剂量组,使用腹腔注射异丙肾上腺素方法制备大鼠急性心肌缺血模型,记录并观察大鼠心电图活动变化,然后进行腹主动脉取血,分离血清,测定乳酸脱氢酶(Lactic dehydrogenase,LDH)、肌酸激酶(Creatine kinase,CK)、磷酸肌酸激酶(Creatine kinase isoenzyme,CK-MB)、谷草转氨酶(Aspartate aminotransferase,AST)、超氧化物歧化酶(Superoxide dismutase,SOD)、丙二醛(Malondialdehyde,MDA)和谷胱甘肽过氧化物酶(Glutathione peroxidase,GSH-PX)含量变化。取心肌组织固定,对大鼠心肌组织进行HE染色,通过对心肌酶学和和心肌组织形态学两个方面来考察蒙药安神补心六味丸对大鼠心肌缺血模型的保护作用。结果 与空白组比较,模型组大鼠血清中LDH活性极显著升高(P<0.01),CK、CK-MB、AST、MDA活性均显著升高(P<0.05),SOD活性显著降低(P<0.05),GSH-PX活性高度显著降低(P<0.001),且差异均具有统计学意义;与模型组比较,蒙药安神补心六味丸组高剂量组大鼠血清中LDH、CK、CK-MB、MDA活性显著降低(P<0.05),SOD活性显著升高(P<0.05),GSH-PX活性极显著升高(P<0.01),且差异均具有统计学意义。从HE染色分析,蒙药安神补心六味丸能够改善因缺血而造成的心肌组织损伤。结论 蒙药安神补心六味丸能有效改善心肌组织病理状态,减轻大鼠心肌缺血损伤,以达到保护心肌作用,机制可能与氧化应激机制相关。  相似文献   
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Elevated serum uric acid (SUA) levels have been associated with several cardiovascular risk factors and the progression of coronary artery disease. In the setting of acute myocardial infarction, increasing evidence suggests that high SUA levels could be related to adverse outcomes. Interestingly elevated SUA levels have been linked to endothelial dysfunction, inflammation and oxidative stress. The aim of this review is to discuss the potential negative effects of SUA in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention, analyzing the possible underlying pathophysiological mechanisms.  相似文献   
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AimsMyocardial strain analysis enables more precise assessment of cardiac performance but is relatively load dependent. New tools have been developed with afterload adjustment. Our objective was to assess myocardial work (MW) in patients with repaired aortic coarctation (rACo).MethodsProspective study of consecutive patients with rACo who underwent a routine transthoracic echocardiogram in 2018 and 2019 at our center. Patients with significant aortic valve disease, pacemaker, or other congenital heart diseases (except for mild bicuspid aortic valve disease) were excluded. Global longitudinal strain with two dimensional speckle tracking analysis and MW were obtained (GWI:Global Work Index; GCW: Global Constructive Work; GWW: Global Wasted Work; GWE: Global Work Efficiency). Blood pressure was measured in the patient's right arm.ResultsWe included 42 patients in the analysis, mean age of 37±10 years, 38% males. In this group, 52% had hypertension and 64% had a concomitant bicuspid aortic valve. In comparison to previously published reference values, patients with rACo had significantly lower GWI (1807 vs. 1896 mmHg%) and GCW (2173 vs. 2232 mmHg%) (p<0.001), particularly in males. Systolic blood pressure is an independent predictor for GWI (β=0.432) and for GCW (β=0.534) and GLS an independent predictor of all MW parameters (β>0.594). Neither age nor gender were independent predictors.ConclusionsIn patients with rACo, there are some signs of left ventricular dysfunction with a reduction in GCW and GWI and with preserved GWE, despite normal ejection fraction and strain.  相似文献   
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