A hospital-based exercise training program increased endurance capacity but did not improve recovery of cardiovascular antonomic function after uncomplicated acute myocardial infarction.

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1. The positive inotropic and chronotropic responses to adrenoceptor agonists (noradrenaline, phenylephrine), to compounds which increase cAMP by post-adrenoceptor mechanisms (forskolin, theophylline and dibutyryl cAMP) and to calcium chloride were measured in isolated rat atria and papillary muscles from both ventricles. 2. Noradrenaline produced similar maximal inotropic responses to calcium chloride in all tissues. Forskolin gave similar responses to calcium chloride in atrial but not ventricular tissues; the reverse was observed with dibutyryl cAMP. Phenylephrine and theophylline produced significantly smaller inotropic responses than calcium chloride in all tissues, especially in ventricular tissues. 3. Maximal chronotropic responses to noradrenaline, theophylline and dibutyryl cAMP were similar. Forskolin produced significantly greater responses while calcium chloride and phenylephrine produced significantly smaller responses than noradrenaline. 4. These results show that the maximal positive inotropic response of some agonists is markedly dependent on the tissue chosen. Further, chronotropic responses in right atria do not mimic inotropic responses in left atria.

Using an isolated working heart model, we studied the effects of dopamine, adrenaline, or noradrenaline pretreatment on ischemia/reperfusion injury. Hearts from Wistar rats were perfused in the first 20-minute working mode, 15 minutes in Langendorff mode, and in the second 20-minute working mode. Hearts were treated with dopamine (0.52 and 2.60 mmol/L), adrenaline (16 and 80 nmol/L), or noradrenaline (16 and 80 nmol/L) during the second working perfusion, then arrested with St. Thomas' Hospital cardioplegic solution and subjected to global ischemia (37 degrees C or 20 degrees C). During reperfusion, recoveries of cardiac function and creatine kinase leakage were measured. At 37 degrees C, dopamine and adrenaline had a harmful effect at both doses; noradrenaline was harmful at a high dose but beneficial at a low dose. At 20 degrees C, adrenaline, dopamine, and noradrenaline had a harmful effect at high doses but no harmful effect at low doses. To determine the role of beta adrenergic stimulation before ischemia, a dose-response study was undertaken with isoprotelenol and milrinone at 37 degrees C. Combined pretreatment with isoprotelenol and milrinone accelerated ischemia/reperfusion injury dose-dependently. Preischemic beta adrenergic stimulation thus plays a significant role in the deleterious effect of catecholamine pretreatment at high doses. At low doses, however, the effect of the inotropic agent could be changed depending on ischemic temperature. Our results suggest that catecholamine should not be given at high doses before ischemia, regardless of temperature during ischemia.