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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。
Se deficiency is a basic factor in the pathogenesis of Keshan disease. How does Selenium deficiency lead to myocardial necrosis? What is the role of vascular factors? A lot of controversy. In this study, a low-selenium guinea pig model was established in Keshan disease area of Shandong Province. The electrophysiological method of recording smooth muscle tension and cell membrane potential was used to study the reactivity of the coronary artery. It was found that: 1, selenium has the role of diastolic coronary artery smooth muscle cell membrane potential decreased, while in the model animals this effect was significantly weakened. The reactivity of model animal coronary smooth muscle to KCl in depolarizing solution was increased, and the depolarization of cell membrane potential was enhanced. The reactivity of coronary arterial smooth muscle cells to ACh increased and the hyperpolarization of membrane potential increased. These facts indicate that the reactivity of the model animals with coronary vessels is enhanced and irritability and contraction are easily induced. It can be considered under low selenium conditions, a variety of neurological and humoral factors can easily lead to increased reactivity coronary insufficiency, leading to myocardial necrosis, that is, vascular factors play an important role in the pathogenesis of Keshan disease.