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电刺激兔缺血腓肠肌预适应对心肌的保护作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2000年第6期
页码:
437-439
栏目:
论著
出版日期:
2000-12-01

文章信息/Info

Title:
Protective effects on myocardium by partial reduction of blood supply combined with rapid stimulation of the gastrocnemius muscle in the rabbit
作者:
王智泉 任江华 周 毅 匡永东 李 军
湖北医科大学附属二医院心内科, 湖北武汉430071
Author(s):
WANG Zhi-quan REN Jiang-hua ZHOU Yi KUANG Rong-dong LI Jun
Department of Cardiology, Second Affiliated of Hubei Medical University, Wuhan Hubei 430071, China
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
Keywords:
myocardium gastrocnemius muscle reperfusion injury nitric oxide:nitric oxide synthase cell apoptos
分类号:
R542.22
DOI:
-
文献标识码:
A
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/cGMP 途径产生其保护作用。
Abstract:
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 functionss, 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 gast rocnemius muscle has protective effects on ischem icmyocardium and that the mechanism may be correlated to the changes of NO/cGMP.

参考文献/References

[1] Ballligand JL , Cannon PJ. Nitric oxide sythases and cardiac muscle[J]. Arterioscler Thromb Vasc Biol, 1997, 17 (10) : 1846.

[2] Brady AJB, Warren JB, Poole-Wilson PA, et al. Nitric oxide attenuates cardiac myocyte contraction [J]. Am J Physiol, 1993, 265 (1) : H176.

[3] Crystal GL, Gurevicius J. Nitric oxide does not modulate myocardial conctractility acutely in situ canine hearts[J]. Am J Physiol, 1996, 270 (5) : H1568.

[4] Beck KF, Eberhardt W, Frank S. Inducible NO synthase: role in cellular signaling[J]. J Exp Biol, 1999, 202 (6) : 645.

[5] Shimojo T, Hiroe M, Ishiyama S. Nitric oxide induces apoptotic death of cardiomyocyte via a cyclic-GMP-dependent pathway[J]. Exp Cell Res, 1999, 247 (1) : 38.

备注/Memo

备注/Memo:
收稿日期:1999-11-01.
更新日期/Last Update: 2000-12-01