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Patients receiving metoprolol before cardiac revascularization surgery were randomly divided into those in whom metoprolol was discontinued before the operation (N = 10) and those in whom metoprolol was continued up to the time of operation (N = 10). Cardiovascular responses to neuroleptanesthesia and sternotomy were studied. Coronary sinus catheterization for blood-flow measurement and sampling was performed in 5 patients in each group. Two of 10 patients had a myocardial infarction after discontinuation of metoprolol and surgery was therefore postponed. Tachycardias were common during intubation after discontinuation of metoprolol, but otherwise hemodynamic responses and myocardial oxygen consumption were similar in both groups. Recurrent ST-T depression occurred in 7 of 8 patients and myocardial lactate release in 2 of 5 patients in whom metoprolol was withdrawn, whereas patients who continued to receive metoprolol showed few episodes of ST-T depression (2 of 10) and no lactate release. The latter had lower plasma norepinephrine (NE) levels, but myocardial release of NE was similar in both groups. Preoperative metoprolol withdrawal seemed to precipitate myocardial ischemia, whereas maintenance of therapy was well tolerated.

The effects of restraint stress on heart activity, blood catecholamines and the development of myocardial necrosis were studied in five unoperated and five unsuccessfully amygdalectomized (sham-operated) pigs and compared with six bilaterally amygdalectomized pigs. In the sham-operated and the nonoperated animals, restraint stress often provoked intense tachycardia, as well as considerable elevations of blood catecholamines, particularly noradrenaline, associated with more or less widespread foci of myocardial necrosis. In contrast, the same restraint produced only minor heart rate increase in the six completely amygdalectomized animals; their blood noradrenaline levels were significantly lower and no myocardial necrosis could be detected, either macro- or microscopically. The results indicate that the amygdaloid part of the limbic system and the sympathoadrenal system are of importance in the induction of myocardial necrosis often noted in pigs when exposed to situations of severe mental stress.

The aim of the study was to examine regional changes in sympathetic nerve activity (SNA) and baroreceptor function and arterial plasma catecholamines, arginine vasopressin (AVP) and plasma renin activity during morphine withdrawal in chloralose-anesthetized rats. Dependence was induced by s.c. morphine base pellets. Adrenal, renal and splanchnic SNA and SNA from the lumbar sympathetic chain were recorded before and after i.v. injections of naloxone. Baroreceptor function was examined with phenylephrine-induced increases in mean arterial pressure. In separate experiments, arterial plasma norepinephrine, epinephrine, dopamine, plasma renin activity and AVP were measured before and after naloxone-precipitated withdrawal. Naloxone administration elicited an increase in mean arterial pressure and heart rate. Although renal SNA was inhibited by approximately 50%, adrenal SNA and lumbar SNA increased by approximately 400 and 80%, respectively. Splanchnic SNA did not change significantly. The baroreceptor-mediated inhibition of adrenal SNA was facilitated while that for renal SNA was attenuated. The arterial plasma level of norepinephrine was doubled and epinephrine increased almost 20-fold. AVP increased about 15-fold, whereas plasma renin activity showed only a minor increase after naloxone. This study shows that a marked differentiation of the SNA response occurs during morphine withdrawal in rats, which suggests an interaction between opioid receptors and the control of regional sympathetic output. Furthermore, large amounts of AVP and epinephrine are released, which probably contribute to the cardiovascular changes seen in the withdrawal phase.