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The contractile reactions of the caudal artery mediated by c~-adrenoceptors do not significantly differ during experimental myocardial infarction in nonadapted rats and rats adapted to graded physical exercise (swimming). In nonadapted rats, experimental myocardial infarction produces a drastic inhibition of the contractile responses in comparison with nonadapted intact rats, which is related to desensitization ofc~-adrenoceptors: In adapted rats the contractile reactions markedly increased during myocardial infarction due to high sensitivity and density of c~-adrenoceptors. Therefore, adaptation mobilizes the reserve capacities to normalize blood pressure during experimental myocardial infarction. Key Words: o~-adrenoceptors, experimental myocardial infarction; resistance artery; adaptation to physical exerciseAdaptation to physical exercise has been a long-standing and actual problem in physiology. Advantages of a trained organism and, in particular, enhanced resistance to damaging and adverse factors are well known. Adaptation to physical exercise can be preventive and therapeutic means, for example in myocardial infarction. There is evidence that the drop in blood pressure (BP) during myocardial infarction is determined by both decreased cardiac output and altered reactivity of resistance vessels [9]. Preadaptation to physical exercise greatly restricts acute hypotension provoked by myocardial infarction [7]. However, the mechanisms involved in this protective effect of adaptation at the vascular receptor level are not clear.In the present study we compare functional state of c~-adrenoceptor apparatus of a resistance artery during experimental myocardial infarction (EMI) in rats adapted and not adapted to graded physical exercise. MATERIALS AND METHODSExperiments were performed on male Wistar rats weighing 250-300 g. Adaptation consisted of 30 sessions of forced swimming at water temperature of 32~ The duration of the first session was 15 rain, and duration of each following session increased by 5 min up to the final duration of 60 min.EMI was produced according to Selye by ligating the left coronary artery [11]. The rats were decapitated 3 h postinfarction.BP on the tail artery was measured in alert rats by noninvasive method using a DMP-4F Physiograph (Narco Bio-Systems).Arterial segment (8 mm) was cut from the proximal part of the caudal artery, cannulated at both ends, and placed into a perfusion chamber. The vessel bathed in physiological saline (37~ was perfused with Krebs--Henseleit solution supplied by a peristaltic pump (LKB) at a rate of 2 ml/min. Vascular reaction was assessed by changes in the perfusion pressure measured with a pressure transducer (Statham).

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