DIMINISHED BASAL NITRIC-OXIDE RELEASE AFTER MYOCARDIAL-ISCHEMIA AND REPERFUSION PROMOTES NEUTROPHIL ADHERENCE TO CORONARY ENDOTHELIUM
DIMINISHED BASAL NITRIC-OXIDE RELEASE AFTER MYOCARDIAL-ISCHEMIA AND REPERFUSION PROMOTES NEUTROPHIL ADHERENCE TO CORONARY ENDOTHELIUM
复制标题
DOI：
10.1161/01.res.72.2.403
复制
发表时间：
1993-02-01
影响因子：
20.1
通讯作者：
LEFER, AM
中科院分区：
文献类型：
--
作者：
MA, XL;WEYRICH, AS;LEFER, AM
在猫心肌缺血（90分钟）和再灌注模型中，我们测量了一氧化氮基础释放的变化及其对多形核白细胞（PMN）粘附内皮细胞（ECs）的影响。采用N(G)-硝基l -精氨酸甲酯（L-NAME）诱导血管收缩法测定心肌缺血/再灌注后左冠状动脉前降支（LAD）和对照组左旋冠状动脉（LCX）一氧化氮的基础释放量。L-NAME诱导对照LCX环明显的ec依赖性血管收缩（0.28+/-0.04 g）， l -精氨酸完全逆转了这种收缩，而d -精氨酸则没有。l - name诱导的LAD环血管收缩在心肌缺血无再灌注90分钟后无明显变化。然而，再灌注10分钟后，l - name诱导的血管收缩减少至0.13+/-0.04 g (p
We measured changes in basal release of nitric oxide and its effect on polymorphonuclear leukocyte (PMN) adherence to endothelial cells (ECs) in a feline model of myocardial ischemia (90 minutes) and reperfusion. Basal release of nitric oxide from the left anterior descending coronary artery (LAD) after myocardial ischemia/reperfusion and from the control left circumflex coronary artery (LCX) was assessed by N(G)-nitro L-arginine methyl ester (L-NAME)-induced vasocontraction. L-NAME induced a significant EC-dependent vasocontraction in control LCX rings (0.28+/-0.04 g), which was fully reversed by L-arginine but not D-arginine. L-NAME-induced vasocontraction of LAD rings was not significantly changed after 90 minutes of myocardial ischemia without reperfusion. However, 10 minutes of reperfusion reduced the L-NAME-induced vasocontraction to 0.13+/-0.04 g (p