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作 者:张芸[1] 陈君柱[1] 张芙荣[1] 夏强[2] 胡晓晟[1]
机构地区:[1]浙江大学医学院附属第一医院,浙江杭州310003 [2]浙江大学医学院,浙江杭州310031
出 处:《浙江大学学报(医学版)》2002年第3期189-192,共4页Journal of Zhejiang University(Medical Sciences)
摘 要:目的 :探讨 HOE6 42对缺血再灌注心肌的保护作用。方法 :以离体灌注的 SD大鼠心脏为模型 ,4 0只大鼠随机分成 4组 :缺血再灌注对照组 (Control)、缺血前给药组 (HOE- Pr)、缺血期间给药组 (HOE- Is)、复灌期给药组 (HOE- Re) ,测定左室发展压、左室舒张末压、心律、心率、冠脉流量和心肌酶。结果 :与 Control组相比 ,HOE- Pr组在随后的缺血 /复灌期间左室发展压显著增加 ,左室舒张末压减少 ,心律失常评分减少 ,冠脉流出液中的心肌酶含量降低 ,复灌早期的冠脉流量增加 ,但心率无明显差异 ;HOE- Is组左室舒张末压减少 ,心律失常评分减少 ,冠脉流出液中的心肌酶含量降低 ,但左室发展压及心率较 Control组无明显差异 ;HOE- Re组心脏各项指标与 Control组相比无统计学差异。结论 :HOE6 42对缺血再灌注心肌有保护作用 ,缺血前给药能充分发挥其心肌保护作用。Objective: To investigate whether the specific sodium hydrogen antiporter HOE642 could modifies myocardial ischemia and reperfusion injury. Methods: The isolated working rat heart model was used. The rats were divided into four subgroups: Ischemiac reperfusion (Control group), HOE642 given before Ischemia (HOE Pr), HOE642 given during Ischemia (HOE Is), HOE642 given during reperfusion (HOE Re).LVDP,LVEDP, arrythmia ,coronary flow and myocardial enzymes were measured.Resluts: HOE642 given 15 minutes before ischemia increased coronary flow and significantly improved cardiac function,reduced the severity of ischemia,reperfusion arrhythmia and myocardial CK MB,LDH release,but had no effect on heart rate.HOE642 given during ischemia only reduced LVEDP,the ischemia severity,reperfusion arrhythmia and myocardial enzyme release.It had no effect on heart rate or LVDP.There were no effects when the drug was given during reperfusion. Conclusion: HOE642 demonstrates significant cardioprotective effects. These protective effects are most significant when the drug is given before ischemia is induced.
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