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机构地区:[1]浙江大学医学院生理学教研室
出 处:《中国病理生理杂志》2007年第8期1484-1487,共4页Chinese Journal of Pathophysiology
基 金:浙江省科技厅基金资助项目(No.2005C30026);浙江医学高等专科学校自然科学基金资助项目(No.2005XZ02)
摘 要:目的:探讨缺氧后处理在全心停灌缺氧模型中是否具有对抗心肌缺氧/复氧(A/R)损伤的作用,以及钙激活钾通道(KCa)和线粒体透性转换孔道(mPTP)是否参与缺氧后处理的抗心肌缺氧/复氧损伤。方法:采用离体大鼠心脏Langendorff灌流模型,全心缺氧30 min、复氧120 min复制A/R模型。测定心室力学指标和复灌各时点冠脉流出液中乳酸脱氢酶(LDH)含量。实验结束测定心肌组织甲臜(formazan)含量。分离心肌线粒体,测定高钙诱导下mPTP的开放情况。结果:缺氧后处理心肌细胞的formazan含量明显高于、而复灌期间冠脉流出液中LDH含量低于单纯A/R组,明显改善心室力学指标,缓解冠脉流量的减少。KCa通道阻断剂paxilline能明显阻断缺氧后处理的心肌保护作用。缺氧后处理心肌细胞的mPTP开放程度显著低于A/R组。结论:缺氧后处理具有抗心脏缺氧/复氧损伤的作用,这种保护作用可能与其抑制KCa通道的开放和降低mPTP的开放有关。AIM : To investigate whether calcium activated potassium channel ( KCa ) and mitochondrial permeability transition pore (mPTP) contribute to cardioprotective effect elicited by anoxic postconditioning. METHODS: The isolated perfused hearts of male Sprague - Dawley rats were subjected to 30 min global anoxic followed by 120 min reoxygenation. Formazan content of myocardium was measured at 490 nm spectrophotometrically, and the level of lactate dehydrogenase (LDH) in the coronary effluent was detected. The absorbance of isolated heart mitochondria at 520 nm was determined. RESULTS: Anoxic postconditioning increased formazan content, reduced LDH release, improved the hemodynamic parameters of the left ventricular developed pressure, maximal rise/fall rate of left ventricular pressure, left ventricular end - diastolic pressure and rate pressure product and attenuated the decrease of coronary flow during reperfusion. Pretreatment with paxilline ( 1 μmol/L) inhibited the effect of anoxic postconditioning. The opening of mPTP was suppressed in the mitochondria isolated from A/R hearts treated with anoxic postconditioning. CONCLUSION: The findings indicate that in the isolated rat heart, anoxic postconditioning protects myocardium against anoxic/reoxygenation injury via inhibiting KCa and the mPTP opening.
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