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A study of the roles of endothelium-derived relaxing factor and endothelin in the regulation of coronary blood flow.In vivo experiments.

内皮源性舒张因子和内皮素在冠状动脉血流调节中的作用研究。体内实验。

基本信息

批准号：
04670543
负责人：
OKUMURA Ken
金额：
$ 1.34万
依托单位：
Kumamoto University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04670543/
关键词：
Coronary circulation Endothelium-derived relaxing factor Nitric oxide L-arginine Endothelin Acetylcoline

项目摘要

We investigated the effect of cumulative doses of N^G-nitro-L-arginine methyl ester (LNAME), an inhibitor of nitric oxide (NO) synthesis, on coronary blood flow of anesthetized and conscious dogs. It was also examined whether the inhibition of EDNO synthesis enhances the effects of exogenous vasoconstrictor agents, neuropeptide Y (NPY), clonidine (CL) and ergonovine (EM), on the coronary vasculature. (1)Four doses of LNAME(10^<-5>M, 10^<-4>M, 10^<-3>M, and 10^<-2>M in the LCX blodd) were infused into the left circumflex artery (LCX). All dogs were pretreated with 8-phenyltheophylline and aspirin to inhibit endogenous adenosine and vasodilator prostaglandin, respectively. In 10 anesthetized dogs, systolic blood pressure was increased with 10^<-2>M of LNAME and heart rate was decreased with (〕SY.gtoreq.〔)10^<-3>M of LNAME.All doses of LNAME significantly decreased the LCX blood flow in a dose-dependent manner without affecting rate-pressure product. In 7 conscious dogs, LNAME showed similar effects to those seen in anesthetized dogs. Thus, there is a basal NO release from the endothelium in the coronary resistance vessels of anesthetized and conscious dogs. (2)Of the 15 anesthetized dogs, 9 were pretreated with intracoronary LNAME (300muM in the LCX blood) and the other 6 with normal saline. Three doses of NPY (4.3, 43, 430 ng/kg), 2 doses of CL (30 and 300 ng/kg) and one dose of EM (20 mug/kg)were infused into the LCX.NPY increased the coronary vascular resistance (CVR) in a dose-dependent manner in both groups and there was no significant difference in the dose-response relation between LNAME- and saline-treated groups. CL increased CVR in both groups and there was no difference between two groups. In contrast, EM increased CVR to a greater degree in LNAME-treated group than in saline-treated group. Thus, the inhibition of EDNO synthesis by LNAME did not result in the enhancement of the vasoconstrictor effects of NPY and CL, whi

我们研究了累积剂量的一氧化氮（NO）合成抑制剂N^G-硝基-L-精氨酸甲酯（LNAME）对麻醉和清醒犬冠状动脉血流量的影响。还检查了EDNO合成的抑制是否增强了外源性血管收缩剂神经肽Y（NPY）、可乐定（CL）和麦角新碱（EM）对冠状血管的作用。（1）将LNAME（10 μ <-5>M、10 μ M、10 <-4>μ <-3>M、10 μ <-2>M）注入左回旋支（LCX）。所有犬分别用8-苯基茶碱和阿司匹林预处理以抑制内源性腺苷和血管扩张剂前列腺素。在10只麻醉的狗中，10 μ M的LNAME使收缩压升高<-2>，SY. gt.使心率降低。()10所有<-3>剂量的LNAME均以剂量依赖性方式显著降低LCX血流量，而不影响心率-血压乘积。在7只清醒犬中，LNAME显示出与麻醉犬相似的作用。因此，在麻醉和清醒的狗的冠状动脉阻力血管中，存在从内皮释放的基础NO。(2)Of 15只麻醉犬中，9只用冠状动脉内LNAME（LCX血液中300 μ M）预处理，另外6只用生理盐水预处理。在LCX内注入3个剂量的NPY（4.3，43，430 ng/kg），2个剂量的CL（30和300 ng/kg）和1个剂量的EM（20 μ g/kg），NPY以剂量依赖的方式增加两组的冠状动脉血管阻力（CVR），LNAME组和生理盐水组之间的剂量-反应关系无显著差异。CL使两组CVR均增加，但两组间无差异。与此相反，EM在LNAME治疗组中增加CVR的程度大于盐水治疗组。因此，LNAME抑制EDNO的合成并不导致NPY和CL的血管收缩作用增强，