我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

洛伐他汀预处理的延迟性心肌保护作用及其机制(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第1期
页码:
50-53
栏目:
基础研究
出版日期:
2006-01-01

文章信息/Info

Title:
Delayed myocardial protection and its mechanisms of Lovastatin preconditioning in the ischemic and reperfused rat hearts
作者:
张晓捷;  孙宗全;  杜心灵
华中科技大学同济医学院附属协和医院心外科, 湖北 武汉 430022
Author(s):
ZHANG Xiao-jie;  SUN Zong-quan;  DU Xin-ling
Department of Cardiovascular Surgery, Union Hospital,Wuhan,Hubei 430022,China
关键词:
洛伐他汀;  血流动力学; 延迟性心肌保护;  缺血/再灌注
Keywords:
Lovastatin;  hemodynamics;  delayed myocardial protection;  ischemia/reperfusion
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
目的 探究洛伐他汀在大鼠心脏急性缺血/再灌注中的延迟性心肌保护作用及其机制。方法 SD大鼠24只随机分为3组（每组8只）：模型对照组（C）; Lovastatin组（L）,洛伐他汀直接灌胃两周15 mg/(kg·d)； Lovastatin 复合LNAME组（N）,洛伐他汀15 mg/(kg·d)直接灌胃2周同时腹腔注射LNAME 30 mg/(kg·d);2周后建立在体急性缺血/再灌注心脏模型，监测缺血/再灌注前后血流动力学各项指标，同时观察各组血脂水平及其血浆中MDA 、SOD、LDH以及CK的变化情况。结果 L组和N组较C组心率显著减慢(P<0.01)，缺血/再灌注心律失常消失和再灌注时-dp/dtmax下降显著改善 (P<0.05)；各项血脂指标不变的情况下,洛伐他汀显著减少再灌注时血浆中MDA生成和LDH及CK的释放（P<0.01）, 并且提高心肌组织SOD活性(P<0.05)。结论 Lovastatin对在体大鼠心脏急性缺血/再灌注时具有非降脂外的延迟性心肌保护作用。NO合酶途径是其心脏保护作用的诸多途径之一。
Abstract:
AIM To investigate the delayed protective effects of Lovastatin on ischemic and reperfused (I/R) rat myocardium and its underlying mechanism. METHODS Twentyfour SpragueDawley male rats were randomly divided into three groups: the model control group, L group treated with Lovastatin (15 mg/kg per day), and N group receiving combination of Lovastatin (15 mg/kg per day) and LNAME (30 mg/kg per day). Two weeks after the preconditioning, I/R model was set up in all rats via 30 min coronary occlusion followed by 30 min reperfusion of the left anterior descending artery. Hemodynamic measurement and measurement of superoxide dismutase (SOD), malondialdehyde (MDA), LDH and CK were done. RESULTS In both L and N group, heart rate reduced obviously, arrhythmia caused by reperfusion was not observed and the descent of dp/dtmax was improved. Pretreatment with Lovastatin decreased the yield of MDA, LDH and CK in the serum and enhanced the activity of SOD during I/R, while the level of blood lipid was found unchanged. CONCLUSION Lovastatin may have a delayed protective effect on I/R myocardium not through reduction of blood lipid.

参考文献/References

［1］Lazar HL,Bao Y, Zhang Y, et al. Pretreatment with statins enhances myocardial protection during coronary revascularizartion［J］. J Thorac cardiovasc surg,2003,125:1037-1042.

［2］ Di NP, Antonio TA, Grilli A,et al. Simvastatin reduces reperfusion injury by modulating nitric oxide synthase expression: an ex vivo study in isolated working rat hearts［J］. Cardiovas Res 2001,51: 283-293.

［3］ Yilmaz MI, Baykal Y, Kilic M,et al. Effects of statins on oxidative stress［J］. Biol Trace Elem Res, 2004,98(2):119-127.

［4］ Wassmann S, Laufs U, Muller K, et al. Cellular antioxidant effects of atorvastatin in vitro and in vivo［J］. Arterioscler Thromb Vasc Biol， 2002，22(2):300-305.

［5］ 李小鹰,郑华光,刘玲玲,等. 腺苷Ａ1受体激动剂对兔心肌缺血/再灌注一氧化氮及其合酶基因表达的影响［J］. 中华心血管病杂志,1996,24(2):139-142.

［6］ De Jonge R, De Jong JW. Ischemic preconditioning and glucose metabolism during low flow ischemia:role of the adenosine A1 receptor［J］. Cardiovasc res,1999,43:909-918.

［7］ Liu GS,Thomton J,Winkle DMV. Protection against infarction afforded by preconditioning is mediatd by A1 adenosine receptors in rabbit heart［J］. Circulation,1991,84:350.

［8］ Light PE. Cardiac KATP channels and ischemic preconditioning: current perspectives［J］. Can J Cardiol,1999,15(10):1123-1130.

备注/Memo

备注/Memo:
收稿日期：2004-12-12.作者简介：张晓捷，博士 Tel：（027）85726086 Email：zxxjjj@sina.com
更新日期/Last Update: