Enhanced adverse electrophysiologic effects of histamine after myocardial infarction in guinea pigs.

To evaluate the electrophysiological sensitivity of infarcted myocardium to histamine, we used microelectrodes to study its effects in isolated guinea-pig left ventricles 1 hr (acute), 24 hr (subacute) and 4 to 6 weeks (chronic) after multiple (6-8) ligations of the left coronary artery system. In both control and infarcted preparations, histamine (10(-8) to 10(-5) M) caused marked concentration-dependent increases in automaticity. Histamine also induced rhythm disturbances, including premature depolarizations, irregular patterns of spontaneous depolarization and spontaneous bursts of rapid ventricular activity. In each case, threshold concentrations for these effects were lowest in the preparations with infarcts. Cimetidine (10(-5) M) abolished the arrhythmogenic effects of histamine, whereas chlorpheniramine (10(-5) M) did not; beta adrenergic blockade induced by propranolol also had no effect. The effects of histamine were mimicked in normal hearts by the H2-agonist dimaprit. These data indicate that threshold concentrations of histamine induce rhythm disturbances in the setting of experimental myocardial infarction. We suggest histamine plays some role in arrhythmias associated with myocardial infarction in humans.