摘要
作者观察了保心Ⅱ号对砷所致家兔在体急性心肌损害时心肌浆网功能的影响,旨在从分子生物学水平来探讨保心Ⅱ号保护心肌功能的机理。将25只家兔随机分为三组。分别观察各组动物心肌肌浆网Ca^(2+)吸收率和ATPase活性变化。结果为:(1)中毒组心肌肌浆网Ca^(2+)吸收率明显被抑制(P<0.05),用药后被抑制现象虽有部份改善,但与正常组比较仍有差异(P<0.05);(2)中毒组与正常组比较ATPase活性显著受到抑制(P<0.01),尽管用药后有改善的趋势,但与正常组比较仍有显著差异(P<0.01)。
We investigated the effects of cardiac sarcoplasmic reticulum (SR) when 'Bao Xin Ⅱ' was administered against arsenic-induced acute myocardial damage of rabbits, and attempted to inquire into its molecular biological mechanism in protecting the myocardial function. Twenty-five healthy rabbits were randomly divided into three groups SR Ca^(2+) uptake rates and SR ATPase activity in myocardium were observed respectively. The results were: (1) SR Ca^(2+) uptake rates in myocardium of the arsenic poisoned group was remarkably depressed (P<0.05). Although SR Ca^(2+) uptake rates were partly improved in post-administering, it was still different as compared to the control (P<0.05); (2) SR ATPase activity of the arsenic poisoned group was clearly depressed (P<0..1) .There was also a tendency of improvement in post-administering, but again it was significantly different compared to the control (P<0.01).
关键词
保心Ⅱ号
砷
心肌浆网
ATPASE
Bao Xin Ⅱ
arsenic
cardiac SR
ATPase
Ca^(2+) uptake rate
