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|

左型精氨酸及左型精氨酸甲酯对心肌缺血-再灌注大鼠血压和心率的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
1999年第1期
页码:
8-10
栏目:
论著
出版日期:
1999-01-01

文章信息/Info

Title:
The effects of L-Arginine and L-NG-Arginine Methyl Ester on blood pressure and heart rate during myocardiac ischemic-reperfusion in rats
作者:
吴丹宁1　贾国良2　马颖艳2　李　飞2　李　伟2
1杭州解放军117医院心内科 310013　2第四军医大学西京医院心内科
Author(s):
Wu Danning1;  Jia Guoliang2;  Ma Yingyan2;  Li Fei2;  Li Wei2
1117th hospital of PLA , Hangzhou 310013 　2Xijing Hospital, Fourth Military Medical University
关键词:
再灌注损伤　左型精氨酸　左型精氨酸甲酯　心率　血压　血流动力学　一氧化氮　大鼠
Keywords:
reperfusion injury 　L-argine　L-NAME 　heart rate 　blood pressure 　hemodynamics　nitric oxide　rats
分类号:
-
DOI:
-
文献标识码:
-
摘要:
本研究利用SD大鼠心肌缺血2再灌注模型, 通过用左型精氨酸及左型精氨酸甲酯的干预, 探讨一氧化氮对SD大鼠血压和心率的影响。实验分缺血-再灌注模型组、左型精氨酸干预组及左型精氨酸甲酯干预组。结果显示: 左型精氨酸和左型精氨酸甲酯均减慢SD大鼠的心率; 左型精氨酸具有降低血压作用, 左型精氨酸甲酯具有升血压及抗低血压的作用。本文结果为临床应用一氧化氮制剂提供了实验依据。
Abstract:
The effects of L-Argine (L-Arg) and L-NG-Argine Methyl Ester (L-NAME) on blood pressure and heart rate in myocardiac ischemic-reperfusion (I/R) rats were studied. 75 rats were divided into three groups: myocardiac I/R group,L-Arg infusion group and L-NAME infusion group.The results showed that compared with the myocardiac I/R group,the heart rate decreased both in L-Arg infusion group and in L-NAME infustion group , and that the blood pressure was lower in L-Arg infusion group but higher in L-NAME infusion group. It is suggested that both L-Arg and L-NAME slow the heart rate, and that L-Arg may produce hypotension,however, L-NAME may be helpful to anti-hypotension.

参考文献/References

［1］刘耕陶. 一氧化氮的研究前景. 中华医学杂志, 1996; 76 (8) :563.

［2］Balligand JL , Kelly RA , Narden PA , et al. Control of cardiac muscle cell function by an endogenous nitric oxide signalling system. Proc Natl Acad Sci USA , 1993; 90: 347.

［3］Mery PF, Lohmann SM , Walter U , et al. Ca2+ current is regulated by cyclic GMP-dependent protein kinase in mammalian cardiac myocyte. Proc Natl Acad Sci USA , 1991; 88: 1197.

［4］Reid IA , Bhi H, Chou L. Role of nitric oxide in the renin and heart rate responses to β-adrenergic stimulation. Hypertension,1994; 23 ( suppl Ⅰ ) : I49.

［5］Pagliaro P, Gattullo D, MerlttiA , et al. Heart rate decrease after inhibition of nitric oxide release in the anethetized dog. J Gen Physiol, 1995; 106: 11.

[6]Nayler WG, Panagiotopouls S, Elz JS, et al. Fundamental mechanisms of calcium antagonists in myocardial ischemia. Am J Cardiol, 1987; 60: 700.

[7]Nery PF, Pavoine C, Belhasson L , et al. Nitric oxide regulates cardiac Ca2+ current . Invo lvement of cGMP inhibited and cGMP-stimulated phosphodiesterases through guanylyl cyclase activation. J Biol Chem , 1993; 268: 26286.

[8]Kourembanes S, Mcquillan LP, Leung GK, et al. Nitric oxide regulates the expression of vasoconstrictors and growth factors by vascular endothelium under both nomoxia and hypoxia. J Clin Invest, 1993; 92: 99.

[9]Finkel MS, Oddis CV , Jacob TD, et al. Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science,1992; 257: 387.

备注/Memo

备注/Memo:
(收稿1998-01-05)
更新日期/Last Update: 1999-01-01