摘要
缺硒是克山病发病的一种基本因素。硒缺乏是如何导致心肌坏死的?血管因素有何作用?争论很多。本工作以山东省克山病病区粮建立了低硒豚鼠模型,应用记录平滑肌张力及细胞膜电位的电生理方法,研究了其冠状动脉的反应性。发现:1、硒具有使冠脉平滑肌舒张及细胞膜电位降低的作用,而在模型动物上此种作用明显减弱。2、模型动物冠脉平滑肌对去极化溶液 KCl 的反应性增高,细胞膜电位去极化作用增强。3、模型动物冠脉平滑肌对 ACh 的反应性增高,细胞膜电位超极化作用增强。这些事实表明模型动物冠状血管的反应性增强,易受激惹产生兴奋等收缩。可以认为在低硒条件下,各种神经及体液因素极易引发反应性增高的冠状血管发生功能不全,导致心肌坏死,即血管因素在克山病发病中占有重要地位。
The Keshen disease characterixes perivascular necrosis of cardiac muscle fibre.This work re-ported the vascular role in the pathogenesis of mecrosis.Guinea pig fed with grains from the Ke-shan disease area used as the animal model.the coronary artery reactivity were examined by mea-surement of active isometric force development of vascular segment (mg/mm^2),and by intracellu-lar recording of membrane potential(Em).The results were as follows:1.In animal model the re-laxation of coronary artery smooth muscle to Se reduced significantly as indicated by rightwardshift in the dose response curve.The Se induced VSMC depolarixation revealed a dose—responsedependent manner in the animal model.The degree of the depolarization was smaller than those inthe normal guinea pig.2.In animal model the active tension of coronary artery smooth muscle in-duced by conventional agonist KCl and ACh increased obviously.ACh and KDl caused membranegyperpolarization and depolarization respectively in the model,but the changes of Em was higherthan those in the control.It is showed that the reactivity of coronary arterial smooth muscle aug-mented.Based on above findings wd hypothesized that increase of coronary artery responsivenessplay an important role in the pathogenesis of myocardial necrosis in animal model.
出处
《中国地方病学杂志》
CAS
CSCD
1993年第5期257-262,共6页
Chinese Jouranl of Endemiology
基金
国家自然科学基金
关键词
克山病
硒
冠状动脉
平滑肌
Keshan disease
Selenium
Guinea Pig
coronary artery
vascular smooth muscle
Membrane potential of vascular smooth muscle cell
ACh
KCl