摘要
目的：观察猫心肌缺血再灌注过程中心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力、肌浆网钙摄取能力、线粒体丙二醛及心肌ＡＴＰ含量变化。方法：利用猫体外循环模型，心脏低温停搏６０ｍｉｎ后，恢复正常血液灌注６０ｍｉｎ。测定心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力、肌浆网钙摄取能力、心肌ＡＴＰ及线粒体丙二醛含量。结果：心脏缺血６０ｍｉｎ时，随着心肌ＡＴＰ含量的下降，Ｃａ２＋－ＡＴ－Ｐａｓｅ活力及肌浆网钙摄取能力下降，而丙二醛含量仅有轻微增加；恢复灌注６０ｍｉｎ后，Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力进一步下降，同时丙二醛含量明显增加。结论：缺血期间心肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力的下降主要与心肌能量储备降低有关，而复灌后Ｃａ２＋－ＡＴＰａｓｅ活力及肌浆网钙摄取能力进一步下降，可能与复灌过程中氧自由基大量产生。
Objective: To observe the changes of myocardial Ca^(2+)ATPase activity and Ca^(2+) uptake during myocardial ischemia/reperfusion in cats. Methods: Twenty-four cats were divided into three groups. Group Ⅰ was not subjected to ischemia or reperfusion injury. Group Ⅱ was subjected to 60 min hypothermic ischemia. Group Ⅲ was subjected to 60 min hypothermic ischemia and 60 min reperfusion. Results: Myocardial ATP content was markedly decreased after 60 min ischemia. Meanwhile myocardial Ca^(2+)ATPase activity and Ca^(2+)uptake were markedly decreased. But Ca^(2+)ATPase activity and Ca^(2+) uptake were further decreased on the basis of ischemia. Malondialdehyde (MDA) content elevated apparently after reperfusion. Conclusion: The decreased activity ofCa^(2+)ATPase and Ca^(2+) uptake during ischemia may have a relation to the low myocardial ATP content, and the further decreased activity of Ca^(2+)ATPase and Ca^(2+) uptake after reperfusion may be related to the reperfusion injury caused by free oxygen radicals.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1998年第4期347-349,共3页
Academic Journal of Second Military Medical University
关键词
心肌缺血
再灌注损伤
肌浆网
钙
ATPASE
myocardial ischemia
reperfusion injury
adenosine triphosphatase
sarcoplasmic reticulum
calcium uptake
malondialdehyde
