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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。
Twenty rabbits were divided into two groups: one group was normal rabbits and the other group was rabbits with acute poisoning of sodium tartrate (SAT). Respectively remove the sinoatrial node - atrial muscle specimens. Using floating microelectrode to guide the action potential, we observed the effect of SAT on two groups of specimens. SAT in both groups can lead to the following changes: the amplitude of action potential of pacemaker cells, the average depolarization rate of 0-phase and the depolarization rate of diastole increased, the duration of action potential (APD_ (25), APD_ (50), APD_ (90)); the amplitude of action potential of atrial myocytes increased, the duration of action potential (APD_ (25), APD_ (50) and APD_ (90)) increased; the amplitude of atrial contraction increased, increase. Various types of arrhythmia were also observed: premature beat, esophageal stroke, paroxysmal tachycardia and bradycardia, post-early post-depolarization and late post-depolarization. The above effects of SAT may be related to the increase of intracellular Ca2 +. We also observed that the above-mentioned changes of rabbits in the acute toxicity group of antimony agent are less than that of the normal rabbits, and we speculate that this may be related to the inhibitory effect of antimony agent intravenous injection in the myocardium.