不同剂量吡那地尔后处理对兔心肌缺血再灌注损伤的保护作用-内科学专业论文.docxVIP

2012 2012 年研究生毕业论文 - - PAGE 10 - dose group: gave pinacidil 50μg/kg. Indicators for monitoring After modeling success, using Medlab bio-signal acquisition systems to record the changes of LVSP and LVEDP continuously, and detect plasma CK activity and MDA content before ischemia ,ischemia for 30 min, reperfusion for 60 min and 120 min separately. After the end of the experiment, acquired the myocardial samples, using Evans blue / chlorinated triphenyl tetrazolium double staining to detect myocardial ischemia and infarct area, using RT-PCR to detect Bcl-2 and Bax gene expression of ischemic myocardium. Results: Reperfusion for 120min, compared with ischemia-reperfusion group, middle dose and low-dose group, the LVSP level increased significantly (p 0.05); the LVEDP level decreased significantly (p 0.05); MDA level decreased significantly (p 0.05); Bcl-2 mRNA expression increased significantly (p 0.05); Bax mRNA expression decreased significantly (p 0.05). Compared with I / R group, the heart function parameters, the MDA level, the expression of Bcl-2 and Bax mRNA had no significant difference (P 0.05) in high dose group. Plasma CK activity of different concentrations of the pinacidil decreased significantly (P 0.05). Conclusion: middle dose and low dose of pinacidil had protective effect in ischemic reperfusion injury. The high dose pinacidil didn’t have obvious effect on ischemia and reperfusion myocardium. Keywords: Pinacidil, Ischemic postconditioning, reperfusion injury, cardioprotection, ATP-sensitive potassium channel 前 言 随着移植领域的拓展和心血管技术的蓬勃发展，缺血再灌注损伤(ischemia reperfusion injury，IRI)已成为当前研究的一大热点。IRI 是指器官组织在经历一定 时间缺血后恢复血液灌注，器官组织损伤程度进一步加重的病理生理现象。心肌(缺 血再灌注) I/R 损伤发生的机制主要涉及活性氧的大量形成、离子通道功能的异常、 中性粒细胞的激活、血管内皮功能的障碍[1]等。其损伤的主要表现为：心肌舒缩功 能的降低、梗死面积的扩大、再灌注心率失常、能量代谢障碍和心肌细胞超微结 构的变化等。 大量实验证明，缺血再灌注损伤可加重心、脑、肾、肝、肺、肠等器官的损 伤，不仅影响局部器官，同时还会引起远隔器官的功能障碍，成为影响治疗效果 的一十重要因素。1986 年 Murry 等[2]首先发现缺血预处理(ischemic preconditioning， IPC)能减轻心肌 I/R 损伤现象。随着 IPC 研究的深入，众多学者开始运用药物模拟 缺血预处理心肌保