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It was hypothesized that endurance exercise training would attenuate isoproterenol-induced myocardial necrosis in the rat by increasing the concentration of prostacyclin in the myocardial vasculature. Rats were randomly assigned to exercise and control groups. Exercisers ran on a motorized treadmill 1 h.d-1, 5 d.week-1 for 14 weeks. Immediately following the training program subgroups of rats were injected with 4 mg.kg-1 indomethacin or saline. One day later, all rats were given a subcutaneous injection of isoproterenol (20 mg.kg-1); after another 24 h they were sacrificed. A decrease of myocardial creatine kinase (CK) activity was used as a marker for myocardial necrosis. Endurance exercise training attenuated the isoproterenol-induced decrease in myocardial CK relative to control by approximately 37% (exercise: 16.4 +/- 0.6 U.mg-1 protein; control: 10.5 +/- 0.6 U.mg-1 protein; p less than 0.05). Pretreatment with indomethacin decreased myocardial CK in the exercise-trained rats (indomethacin: 15.4 +/- 0.8 U.mg-1 protein; saline: 17.7 +/- 0.7 U.mg-1 protein; p less than 0.05), but not in the controls (indomethacin: 10.3 +/- 1.0 U.mg-1 protein; saline: 10.8 +/- 0.6 U.mg-1 protein; p greater than 0.05). The concentration of myocardial 6-keto-PGF1 alpha, a marker for prostacyclin, was not altered by exercise but, as expected, was reduced by indomethacin pretreatment (p less than 0.05). Thus, exercise training reduces myocardial damage caused by isoproterenol, but the evidence does not support the hypothesis that prostacyclin mediated this effect of training. Further research is needed to determine the extent to which exercise training-induced alterations in sensitivity to PGI2 or TXA2 affect myocardial damage from isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

Study Objective: The aim was to determine if prostaglandin like activity might be involved in changes due to exercise training in the coronary flow responses to hypoxia., Design: The coronary flow response to hypoxia was measured under constant perfusion pressure in isolated perfused hearts from 12 endurance exercise trained rats and 12 control rats. Eight hearts were perfused with a solution containing indomethacin, a cyclo-oxygenase inhibitor, to determine its effect on any training induced changes in the coronary flow response to hypoxic stress., Experimental Material: 24 male Sprague-Dawley rats, 517 (SD 51) g, were used for this study. The animals were anesthetised and the hearts rapidly excised and perfused with a modified Langendorff perfusion system., Measurements and Main Results: Under constant perfusion pressure, the hearts of endurance exercise trained rats had a greater increase in coronary flow during hypoxia relative to normoxia than did hearts of untrained rats, at 13.52(2.15) v 9.56(1.05) ml.min-1.g-1 dry heart weight. Indomethacin treatment abolished this difference and lowered coronary flow: exercise -3.81(3.75) ml.min-1.g-1; control 0.38(2.44) ml.min-1.g-1., Conclusions: The inhibition by indomethacin of the endurance exercise training induced potentiation of the coronary fluid flow response to hypoxia suggests that prostacyclin or a related compound may be involved in this adaptation to exercise.