摘要
为探讨缺血预处理延迟保护作用的非缺血诱导方式，我们在离体大鼠心脏等容收缩灌流模型上观察到：24小时前腹腔注射ZnS4诱导心肌金属硫蛋白（MT）含量增高1．6倍；与单纯缺血再灌注组比较，诱导MT组显著减少了肌红蛋白漏出和MDA增加，减轻了心肌ATP耗竭，增强了左室做功能力，但不影响冠脉流量。因此我们认为，ZnSO4注射诱导MT合成，能代替缺血预处理，模拟出缺血预处理的延迟保护作用。
In order to search for the non-ischaemic induced methed of ischarmic preconditioning (IPC),we observed on the Langedorff model in rat heart that: (1) the metallothionein (MT) contents whi-ch were indued by infusion of ZnSO4 ip 24 hours ago are increased by 160% (P<0.01); (2) both the lea-kage of Mb and the increase of MDA content are decreased, the exhauslion of myocardial ATP is att-enuated and the doing work of left ventricle is increased in induced MT group,significanlly in comparison with single ischemia/reperfusion group. We conclude that the increasement of MT content induced by ZnSO4,in place of IPC,can mimic the delayed protection of IPC.
出处
《中国介入心脏病学杂志》
1997年第4期177-179,共3页
Chinese Journal of Interventional Cardiology
关键词
金属硫蛋白
缺血预处理
心肌
Preconditioning Metallothionein Myocardioprotection
