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出 处:《中国应用生理学杂志》1992年第1期56-59,共4页Chinese Journal of Applied Physiology
摘 要:家兔20只均分成两组:一组为正常家兔,另一组为酒石酸锑钠(SAT)急性中毒的家兔。分别取出窦房结-心房肌标本。用浮置式微电极引导动作电位,观察SAT对两组标本的影响。SAT在两组标本上均能导致如下改变:起搏细胞动作电位幅值、0相平均去极速率和舒张期去极速率增加,动作电位时程(APD_(25)、APD_(50)、APD_(90))缩短;心房肌细胞动作电位幅值增加,动作电位时程(APD_(25)、APD_(50)、APD_(90))延长;心房肌收缩幅值增加,收缩时程延长,心率增加。还观察到各种类型的心律失常:早搏、逸搏、阵发性心动过速和心动过缓、早发性后除极和迟发性后除极。SAT的上述作用可能与细胞内Ca^(2+)增高有关。我们也观察到:锑剂急性中毒组家兔的上述变化值均小于正常家兔的对应值,我们推测可能与锑剂静脉注射对在体心肌的抑制作用有关。The effects of sodium antimony tartrate (SAT) on electrophysiological properties and contractions of sinoatrial node-atrial preparation of rabbits were studied by means of floating glass microelectrode. The animals were divided into two groups: the group 1 consisted of 10 normal rabbits and the group 2 consisted of 10 SAT acutely intoxicated rabbits. In both groups, SAT perfusion caused increase in action potential amplitude (APA), phase 0 mean depolarization rate and diastolic depolarization rate, and shortening in action potential duration (APD25, APD50, APD90) of pacemaker cell; increase in APA and prolongation in APD25, APD50, APD90 of atrial cell; and increase in contraction amplitude (CA), contraction duration (CD) and heart rate (HR). In group 2, the alterations mentioned above were significantly smaller than those in group 1. The mechanism is not very clear. It is supposed that the SAT injection might depress the activity of heart. In both groups, various kinds of arrhythmia were observed, including premature beat, escape beat, bradycardia, tachycardia, early after -depolarization (EAD) and delayed after-depolarization (DAD). The results suggest that SAT perfusion may increase the intracellular calcium.
分 类 号:R331.38[医药卫生—人体生理学]
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