摘要
目的观察超极化停搏(超极化停搏)对体外循环中缺血再灌注心肌组织磷酯酶A2(PLA2)和ATPase活性的影响,评价其对心肌的保护作用,并初步探讨其可能的作用机制。方法在猫体外循环模型的基础上,比较超极化停搏组和去极化停搏组体外循环中心肌组织PLA2及Na+-K+-ATPase、Ca2+-Mg2+-ATPase和Ca2+-ATPase活性。结果超极化停搏处理组可明显减轻体外循环中缺血再灌注导致的PLA2活性升高和ATPase活性下降。结论超极化停搏可能通过减轻缺血再灌注期间的Ca2+超载及抑制细胞膜磷脂水解而发挥其心肌保护作用。
[Objective] To elucidate the influences of hyperpolarized arrest on activity of phospholipase A2 and ATPase of ischemia/repeffusion myocardial cell during cardiopulmonary bypass(CPB). [Methods] Seventy-five felines were randomized into three groups: simply CPB group, depolarized arrest group and hyperpolarized arrest group. In simple CPB group, CPB was conducted without aortic cross-clamping (ACC). In depolarized arrest group and hyperpolarized arrest group, hearts underwent 60 minutes of global ischemia after ACC and infusion of cardioplegic solution (10 mL/kg), followed by 90 minutes of repeffusion. The cardioplegic solution consisted of St. Thomas solution with KCl (16 mmol/L) in depolarized arrest group or pinacidil (50 mmol/L) in hyperpolarized arrest group. Activities of PLA2 and Na^+-K-^+ATPase, Ca^2+-Mg^2+ ATPase and Ca^2+-ATPase of myocardial cells were simultaneously measured during ACC and reperfusion periods. [Results] Hyperpolarized arrest significantly alleviated the upregulated activity of PLA2 and the inhibited activities of Na+-K-^+ATPase, Ca^2+-Mg^2+-ATPase and Ca^2+-ATPase of myocardium during periods of ischemia and repeffusion. [Conlusion] Hyperpolarized arrest can protect myocardial cells from ischemia and reperfusion injury during CPB by regulating the activities of PLA2 and the ATPases of myocardium, which may duo to alleviation of Ca^2+ overload and hydrolysis of membrane phospholipid.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2007年第21期2589-2592,共4页
China Journal of Modern Medicine
基金
福建省自然科学基金资助项目(C0110026)
关键词
体外循环
心肌再灌注损伤
磷酯酶
ATP酶
超极化停搏
cardiopulmonary bypass
myocardial reperfusion injury
phospholipase
ATPase
hyperpolarized arrest