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AIM:To study the relationship between myocardial HSP70 and PKC during myocardial ischemic preconditioning(IPC). METHODS: PKC inhibitor, polymyxin B(PMB) and PKC activator, phorbol 12-myristate 13-acetate(PMA) were applied to the models of myocardial ischemia/reperfusion in vivo and in vitro in rabbits, respectively, and the ventricular functions, PLA2 in the serum, and the expression of mycardial HSP70 mRNA were examined. RESULTS:IPC decreased PLA2 activity, improved the left ventricular function and increased the expression of myocardial HSP70 mRNA. Howerer, all these effects of IPC could be blocked by PMB. Interestingly, PMA mimicked IPC with attenuating the injuries of cardial myocytes and increasing myocardial HSP70 mRNA expression. CONCLUSION:PKC is involved in the myocardial HSP70 expression in case of ischemic preconditioning. 相似文献
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AIM:To examine the effect of external counterpulsation(ECP) on renin-angiotensin system(RAS) and hemodynamics in dogs with myocardial ischemia and their relationship. METHODS:Acute myocardial ischemia was induced by occluding the left anterior descending of the dogs. The local renin activity, angiotensin Ⅱ(AngⅡ) level, angiotension-converting enzyme(ACE) activity were tested by biochemical methods and hemodynamics was recorded by a 8-channel physiological recorder.RESULTS:Ischemia could actiivate renin,ACE and AngⅡ in cardiovasculature and ECP reduced them except for renin in ischemic myocardium. Ischemia also could activate RAS in lung and kidney, which play an important role on circulating RAS, and ECP reduced them. Furthermore, ECP could improve hemodynamics and there existed a close relationship between local AngⅡlevel and hemodynamics. CONCLUSION:ECP can reduce local RAS and improve hemodynamics in dogs with myocardial ischemia, which might be one of mechanisms underlying the protective effect of ECP on ischemic myocardium. 相似文献
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AIM:To investigate the mechanism responsible for albumin microbubbles adherence to activated leukocytes. METHODS: In vitro studies were performed in which activated or nonactivated leukocytes were incubated with albumin microbubbles and observed under microscopy. The suspensions of leukocytes and microbubbles which contained or absented of integrins were analyzed with flow cytometry.RESULTS: A minimum of 50cells were identified under transillumination. 5 min after microbubbles were incubated with leukocytes, the number of cells interacting with microbubbles was greater for activated cells than for nonactivated cells(20.30±2.67 vs 4.50±1.43, P <0.01).Microbubbles attached to the surface of activated leukocytes were phagocytosed and remained intact for up to 30min. Microbubble attachment was inhibited notably by blocking the leukocyte β2-integrin Mac-1(P <0.01) and by VLA-4mAb slightly(P <0.05) CONCLUSION: The mechanism of albumin microbubbles attaching to and phagocytosed by leukocytes was due to β2-integrin and VLA-4 mediation. Phagocytosed microbubbles can remain at the regions of inflammation for15 min, also responsible to ultrasound. 相似文献
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应用Kromasil-C18色谱柱(250 mm×4.6 mm,5 μm),WatersTM480型可调波长紫外检测器,0.01M磷酸钾(pH=7):乙腈(3:1)为流动相,检测波长265 nm,含量测定采用标准曲线法,建立了RP-HPLC法检测绵羊尿中克洛素隆含量的方法.方法有效性评价结果表明,尿药含量在0.01~5.0μg/ml及5.0~30.0μg/ml范围呈良好线形关系(r=0.9993、0.9995),方法平均回收率99.32%,日内、日间变异系数分别为3.91%、6.28%.尿药最低检测限0.005μg/ml.试验绵羊以7 mg/kg单剂量经静脉、肌肉及口服三种途径给药后,尿中药物浓度分析表明,克洛素隆经体内处理后主要经肾脏排泄,给药96 h内,静注经尿排泄原药为81.76%,肌注为64.03%,口服为48.50%. 相似文献
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