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作 者:向继洲[1] 吴基良[2] 胡清华[1] 胡本容[1] 罗启发[1] 卢中举
机构地区:[1]同济医科大学基础医学院药理学教研室,武汉430030 [2]咸宁医学院药理学教研室,咸宁437100
出 处:《华中科技大学学报(医学版)》1997年第4期258-262,共5页Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基 金:国家自然科学基金!39170840
摘 要:采用两组猪肺动脉内皮细胞培养液(甲组:内皮细胞缺氧再给氧前tritonX-100处理;乙组:内皮细胞缺氧再给氧的模拟缺血再灌注)灌注离体大鼠Langendorff心脏,分别观测冠脉灌注压(CPP)、心率(HR)、心律、左室内收缩压(LVSP)[并计算其微分(±dp/dtmax)]以及冠脉流出液中乳酸脱氨酶(LDH)、磷酸肌酸激酶(CPK)和心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)和ATPase的变化。结果显示:经缺氧再给氧处理的内皮细胞培养液可使大鼠心功能发生异常并加重心肌损伤,进一步证实冠脉内皮细胞在心脏病理生理中起重要作用。For perfusing Langendorff rat hearts, we used culture fluid of endothelial cells in swine pul-monary artery (in two groups, group one: hypoxiaendothelial cells treated with triton X-100 before being oxygenated: group two: ischemia-reperfused model of hypoxia-oxygenated endothelial cells ). The indices ob-served were: coronary perfusion pressure (CPP), heart rate(HR), rhythm of the heart, left ventricular sys-tolic pressure (LVSP) and its differentiat ion (±dp/dt max ), lactate dehydrogenase (LDH) and creatinphos-phokinase(CPK) in coronary flowing fluid, superoxide dismutase (SOD), molonaldehyde (MDA) and Na+-K+ ATPase in myocardial tissue. The results suggest that culture fluid of hypoxia-oxygenated endothelial cells can cause the abnormality of rat cardiac function and aggravate myocardial damage. This further proves that endothelial cell of coronary artery plays an important role in the pathophysiology of heart.
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