摘要
目的 :确定电刺激兔缺血腓肠肌的预适应是否对缺血心肌有保护作用 ,并初步探讨其保护机制。方法 :建立预适应的动物模型 ,分为 4组 :1对照组 (I/R,n=8) ,开胸旷置 30 m in;2电刺激组 :电刺激右侧腓肠肌 30 min(E+ I/R,n=8) ;3股动脉狭窄组 (S+ I/R,n=8) ,右侧股动脉局部狭窄 30 min;4股动脉狭窄 +电刺激组 (ES+ I/R,n=8) ,右侧股动脉局部狭窄的同时电刺激右侧腓肠肌 ,持续 30 min。然后各组均阻断冠脉 30 m in,再灌注 4h。用左室功能、心肌梗死范围、血清一氧化氮 (NO)及一氧化氮合酶 (NOS)和凋亡细胞百分率为观察指标。结果 :与其他组相比 ,ES+ I/R组能显著缩小缺血 /再灌 (I/R)后的心肌梗死范围 (P<0 .0 5 ) ;显著改善 I/R后的左室收缩功能 (P<0 .0 5 ) ;减少心肌细胞凋亡的发生 (P<0 .0 5 ) ,同时血清 NO及 NOS水平下降 (P<0 .0 5 )。而 E+ I/R,S+ I/R组各观察指标与 I/R组无显著性差异 (P<0 .0 5 )。结论 :ES+ I/R组预适应模式能减轻 I/R后的心肌损伤 ,可能通过NO/c GMP途径产生其保护作用。
AIM:To determine whether partial reduction of blood supply combined stimulation of the gastrocnemius muscle in the rabbit has protective effects on myocardium,and to study its mechanism. METHODS:Rabbits were randomly divided into four groups:control group(I/R, n =8);Muscle stimulation preconditioning group (E+I/R, n =8);femoral artery stenosis precondtioning group (S+I/R, n =8);muscle stimulation with femoral artery stenosis preconditioning group (ES+I/R, n =8). Changes in left ventricular functions,myocardial infarct size,nitric oxide (NO) and nitric oxide synthase (NOS) in serum,and the ratio of apoptotic cells were investigated. RESULTS:Compared with other three groups,muscle stimulation with femoral stenosis preconditioning would increase the functions of the left ventricular of the injuryed heart (all P <0 05);reduce the myocardial infarct size (all P <0 05) and the ratio of apoptotic cells (all P <0.05),and would also decrease NO and NOS in serum (all P <0.05). CONCLUSION:The preconditioning model which reduce blood supply combined with rapid stimulation of the gastrocnemius muscle has protective effects on ischemic myocardium and that the mechanism may be correlated to the changes of NO/cGMP.
出处
《心脏杂志》
CAS
2000年第6期437-439,共3页
Chinese Heart Journal
关键词
心肌
腓肠肌
再灌注损伤
一氧化氮
一氧化氮合酶
细胞凋亡
myocardium
gastrocnemius muscle
reperfusion injury
nitric oxide:nitric oxide synthase
cell apoptosis
