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目的 研究抑肽酶对缺血再灌注心肌的保护作用。方法 30只SD大鼠随机分成三组 :对照组、小剂量组 (抑肽酶 10 5U/L)和大剂量组 (抑肽酶 10 6U/L)。采用Langendorff离体鼠心动物模型 ,以充 95 %O2 +5 %CO2 气体的K H液进行逆灌 ,以晶体停搏液、抑肽酶 10 5U/L、10 6U/L的晶体停搏液低温停搏 6 0min ,复灌30min ,检测停搏前和复灌 5min、15min、30min的左室均压及最大收缩及舒张速率 ,记录冠脉流量 ,收集灌流液测定乳酸脱氢酶 (LDH)、肌酸磷酸激酶 (CPK) ,计算恢复率。复灌 30min心肌匀浆测定丙二醛 (MDA) ,并行电镜检查。结果 大剂量组心脏收缩及舒张功能恢复较好 ,与对照组及小剂量组相比差异有显著性 (P <0 .0 5 ) ;LDH和CPK漏出较少 ,与对照组及小剂量组相比差异有显著性 (P <0 .0 5 ) ;心肌MDA含量较低 ,与对照组及小剂量组相比差异有非常显著性 (P <0 .0 0 1)。超微结构提示大剂量组的心肌肌丝溶解少 ,线粒体损害轻。结论大剂量抑肽酶具有心肌保护作用。
Objective To study the protective effects of aprotinin on myocardial ischemia-reperfusion. Methods Thirty SD rats were randomly divided into three groups: control group, low dose group (aprotinin 105U / L) and high dose group (aprotinin 106U / L). The Langendorff isolated rat heart model was used to reverse-fill with KH solution filled with 95% O2 +5% CO2 gas. The crystalloid cardioplegia, aprotinin 10 5U / L, and 10 6U / L crystalloid cardioplegia The left ventricular pressure and maximal systolic and diastolic velocities were measured before cardioplegia and reperfusion for 5min, 15min and 30min respectively. The coronary flow rate was recorded and the concentration of lactate dehydrogenase (LDH) Creatine phosphokinase (CPK), calculate the recovery rate. Reperfusion 30min myocardial homogenate was measured malondialdehyde (MDA), parallel electron microscopy. Results Compared with the control group and the low-dose group, the cardiac contractile and diastolic function recovery of the high-dose group was better than that of the control group and the low-dose group (P <0.05), and the leakage of LDH and CPK was less. Compared with the control group and the low-dose group (P <0.05). The content of MDA in myocardium was lower than that in control group and low-dose group (P <0.01). Ultrastructural remodeling of high-dose group of myocardial fibroids less mitochondrial damage. Conclusion High-dose aprotinin has myocardial protective effect.