大鼠肺血管反应性种系差异的机制  

Mechanisms of Strain Difference in Pulmonary Vascular Responsiveness in Rats

作　　者：金咸瑢[1] 范明[1] 王志强[1] 苏远超 杨光田[1] 胡汉波[1] 张业平[1] 冯长建[1] 车东媛[2] 王迪浔[1] 

机构地区：[1]同济医科大学基础医学部病理生理学教研室 [2]同济医科大学基础医学部病理学教研室

出　　处：《同济医科大学学报》1990年第1期1-5,71,共5页Acta Universitatis Medicinae Tongji

基　　金：国家自然科学基金

摘　　要：本文综合报道了对Hilltop(HT)大鼠和Wistar (W)大鼠缺氧性肺血管收缩反应(HPV)的研究。观察抑制白三烯(LTs)或前列腺素(PGs)合成对HPV和慢性缺氧性肺动脉高压产生的影响,以及测定急性缺氧时血浆TXB_2和6-酮-PGF1α的变化,均表明LTs是两种大鼠HPV的主要介质,HT鼠还有缩管性PGs参与介导,而W鼠则受扩管性PGs调节;加之肺小动脉结构的差别,构成了两种大鼠肺血管反应性差异的主要原因。Studies on the hypoxic pulmonary vasoconstriction(HPV) in Hilltop (HT) rats and Wistar (W) rats are reported.Effects of inhibition of leukotriene (LT) synthesis or prostaglandin (PG) synthesis on HPV and chronic hypoxic pulmonary hypertension were observed,and variations in plasma TXB2 and 6-keto-PGF1α during hypoxia were determined.The results show that LTs are the main mediators of HPV in rats of both strains.HPV is also mediated by vasoconstric-tive PGs in HT rats,but modulated by vasodilative PGs in W rats.This might be an important factor contributing to the stronger vasoresponsiveness in HT rats.In addition,the structural features of pulmonary arteriole might be another contributing factor.

关 键 词：缺氧症 肺血管反应性 白三烯 PGS 

分 类 号：R594.302[医药卫生—内科学]