摘要
本文旨在探讨缺血预适应（ＩＰ）心肌保护效应是否与其阻止中性粒细胞（ＰＭＮ）ＣＤ１１ｂ／ＣＤ１８分子的 表达有关。采用犬前降支动脉（ ＬＡＤ）建立ＩＰ模型，在长缺血前各予 ５ｍｉｎ缺血和再灌注，反复 ４次，于基 础、缺血前、缺血１ｈ、再灌注０．５和２ｈ分别采集冠状窦血作流式细胞仪分析ＰＭＮ ＣＤ１１ｂ／ＣＤ１８的表达，并 与单纯ＩＲ组比较。ＩＲ组在心肌缺血与再灌注各时点ＰＭＮ ＣＤ１１ｂ／ＣＤ１８表达均显著增加，而ＩＰ组除长缺血 前升高外，缺血与再灌注各叶点均无增加。ＩＰ阻止缺血再灌注激发的ＰＭＮ ＣＤ１１ｂ／ＣＤ１８分子的表达，提示 通过减轻而激注损伤可能是ＩＰ心肌保护效应的重要机制。
The myocardial protection of ischemic preconditioning (IP) may be involved in its inhibition to PMNs adhesion. We therefore examined the effects of lp on the expression of CD 11b/CD18. Anesthetized open-chest dogs (n=6) subjected to 5min ischemia and 5min reperfusion for 4 times before 1 hour of left descending coronary artery (LDA) occlusion followed by 2 hours of reperfusion. Coronary sinus blood samples were obtained for flow cytometric analysis then compared with IR group at different intervals: base, pre-occlusion, 1 hour after occlusion, 30min and 2 hours after reperfusion. PMN CD 11b/CD18 expression increased significantly in IR group while no differece in IP group except for that enhanced at the time of pre-occlusion. IP attenuates ischemia-reperfusion-stimulated PMNs adhesion which may be one of the mechanism of IP protection.
出处
《基础医学与临床》
CSCD
2000年第4期24-26,共3页
Basic and Clinical Medicine
