摘要
离体大鼠心脏经10min左冠状动脉缺血加30min再灌注后,心肌中Na+,K+-ATP酶的活力显著降低,Ca2+,Mg2+-ATP酶的活力稍上升。离体心脏经3次3min全心缺血加5min再灌注的缺血预处理后,显著减轻随后缺血-再灌注引起的Na+,K+-ATP酶活力降低,并有进一步增高Ca2+,Mg2+-ATP酶活力的趋势。缺血预处理也显著减轻缺血-再灌注时的心肌收缩力下降和心律失常的发生。在体大鼠心脏缺血预处理对这些酶活力的影响与离体缺血预处理的结果相似,表明缺血预处理对这些酶活力的影响是作用于心脏本身所致。
o investigate whether ischemic preconditioning will influence Na^+,K^+ATPase andCa^2+,Mg^2+ATPase ,the enzyme activity was measured in rat hearts with or without ischemic preconditioning.Ischemic preconditioning was induced with 3 cycles of 3 min ischemia and 5 min reperfusion in rat hearts in vivo or in vitro.Severe ventricular tachycardia and ventricular fibrillation occured and myocardial contraction declined after 10 min ischemia and 30 min reperfusion in isolated buffer perfusing rat hearts. Na+,K+ATPase activity significantly decreased and Ca2+,Mg2+ATPase activity slightly increased after the ischemia and reperfusion. The ischmic preconditioning procedure either in vivo or in vitro significantly ameliorated the decline of Na+,K+ATPase and further increased Ca2+,Mg2+ATPase activity after the ischemia and reperfusion. Arrhythmias was greatly reduced and myocardial performance was improved with ischemic preconditioning compared with that of nonischemic preconditioning. There was no difference in the enzyme activity between in vivo and in vitro ischemic preconditioning. The results indecated that ischemic preconditioning could protect rat hearts of Na+,K+ATPase,Ca2+,Mg2+ATPase and myocardial performace from ischemia and reperfusion injury and reduce ischemia and reperfusion induced arrhythemias.
出处
《基础医学与临床》
CSCD
1997年第6期59-63,共5页
Basic and Clinical Medicine
基金
江苏省自然科学基金
关键词
心肌缺血
预处理
三磷酸腺苷酶
心律失常
钠
钾
Ischemic preconditioning Adenosine triphosphatase arrhythemias myocardium rat