Effect of Isoprenaline or Stress on Adrenaline-Induced Arrhythmias in Albino Rats
Rona et al. (1) described for the first time that isoprenaline (ISP) produces infarct-like myocardial lesions in experimental animals. Since then the ISP model has been widely used to understand the pathophysiology of myocardial ischemia. During the subsequent years it has been reported that rat-myocardium develops relative insensitivity to the necrosis-inducing effects of ISP after a prior exposure to myocardial insults (2,3,4,5). Selye et al. (2) showed that ligation of the left coronary artery provided resistance against ISP-induced myocardial necrosis in rat. This resistance was reported to be maximal after 48 hr after coronary ligation and then gradually declined, the myocardium regaining sensitivity 3 wk after coronary ligation (3). Balazs et al. (4) found that myocardial resistance to ISP challenge occurred in rats pretreated with ISP for 2 consecutive days, and that the sensitivity had returned 11 wk after the initial treatment. The development of resistance was found to be dependent on the initial production of myocardial lesions, and not on the size of the necrosis (5). In a subsequent study, it was reported that it took at least 5 days for the myocardial resistance to develop after a single dose of ISP, and the normal myocardial sensitivity after multiple doses of ISP did not return even after 19–20 wk of the initial insult (6). In another study it has been reported that rats which were pretreated with ISP have more hypoxic tolerance 14 days after pretreatment with ISP than after 48 hr (7).
KeywordsCholinergic System Atropine Sulphate Coronary Ligation Arrhythmogenic Effect Atropine Treatment
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