缺血预处理通过2肾上腺素受体保护心肌细胞收缩功能.pdfVIP

生理学报 Acta Physiologica Sinica, June 25, 2008, 60 (3): 327-332 327 研究论文 Received 2007-10-15 Accepted 2008-03-05 This work was supported by the Social Development Program of Xuzhou Municipality (No. 58). *Corresponding author. Tel: +86-516 Fax: +86-516 E-mail: sunh@ 缺血预处理通过 β 2- 肾上腺素受体保护心肌细胞收缩功能 吴 芹，赵 智，孙 红 *，郝艳玲 徐州医学院生理学教研室，徐州 221002 摘 要：本文旨在探讨缺血预处理(ischemic preconditioning, IP)对缺血 / 再灌注(ischemia/reperfusion, I/R)损伤心脏的保护机 制，从细胞和受体水平研究 β2-肾上腺素受体(β2-adrenoreceptor, β2-AR)是否参与了 IP 对 I/R 损伤心脏的保护作用。Sprague- Dawley 大鼠随机分为单纯 I/R 组(对照组)、IP 组、短暂异丙肾上腺素(isoproterenol, ISO)处理组、IP + ICI118551 组、ISO + ICI118551 组和 ICI118551 组。除对照组外，其它各组大鼠处理后均行缺血 30 min/ 复灌 30 min。记录心脏收缩期左心室 内压上升的最大变化速率(+dp/dtmax)、舒张期左心室内压下降的最大变化速率(-dp/dtmax )及左心室内压差(difference of left ven- tricular pressure，ΔLVP，左心室收缩压- 左心室舒张压)。测定冠状动脉流出液乳酸脱氢酶(lactate dehydrogenase, LDH)含 量。进一步酶解分离心脏，获得单个心室肌细胞，测定其存活率和收缩功能。结果显示，IP 和 ISO 组 ±dp /dtma x、ΔLVP 较对照组增高；心肌细胞存活率和收缩幅度也显著升高；收缩时间(time-to-peak contraction, TTP)缩短；冠状动脉流出液 LDH 含量减少。选择性 β2-AR 拮抗剂 ICI118551 阻断 IP 和 ISO 的作用。各组间心肌细胞舒张 50% 时间(time-to-50% relaxation, R50)和舒张 100% 时间(time-to-100% relaxation, R100)均无明显差异。结果提示，β 2-AR 可能在 IP 对 I/R 损伤心脏的保护作用 中发挥重要作用。 关键词：缺血预处理；心肌细胞收缩功能；肾上腺素能受体 中图分类号：R331 .3 +1 β2-adrenoreceptor mediates the cardioprotection of ischemic preconditioning on myocardial contraction in rats subjected to ischemia/reperfusion injury WU Qin, ZHAO Zhi, SUN Hong*, HAO Yan-Ling Department of Physiology, Xuzhou Medical College, Xuzhou 221002, China Abstract: The aim of the present study is to investigate the role of β2-adrenoreceptor (β2-AR) in ischemic preconditioning (IP) in isolated rat heart model of ischemia/reperfusion (I/R). Sprague-Dawley rat hearts were quickly removed, mounted on Langendorff apparatus, and perfused with Krebs-Henseleit (KH) solution. After the initial stabilization period, the rats were randomly divided into 6 groups including control group (perfused for an additional 20 min), IP group (4 cycles of 5 min of ischemia fol