Histamine modification of spontaneous rate and rhythm in infarcted canine ventricle.

Histamine (10(-3) M) increased the spontaneous rate similarly in isolated preparations of normal left ventricular tissue from control, i.e. normal and sham-operated, dogs (control preparations) and in preparations consisting of normal and contiguous infarcted left ventricular tissue from dogs with subacute, i.e. 24 hours after left coronary artery ligation, myocardial infarction (infarcted preparations). Histamine (10(-3) M) markedly enhanced the irregular rhythm of infarcted preparations. The H1-receptor antagonist, chlorpheniramine (10(-4) M), and the H2-receptor antagonist, cimetidine (10(-3) M), antagonized the effects of histamine (10(-3) M) on the spontaneous rate of both control and infarcted preparations. The H1-receptor agonist, 2-pyridyl ethylamine (PEA, 10(-4) M), increased the spontaneous rate of control and infarcted preparations; these effects were antagonized by chlorpheniramine (10(-4) M). The H2-receptor agonist, dimaprit, had no effect. Similar to histamine (10(-3) M), PEA (10(-4) M) enhanced the irregular rhythm of infarcted preparations; dimaprit had no effect. High local concentrations of histamine may occur in poorly perfused ischemic tissue. The enhancement of irregular rhythm produced by histamine, and the specific H1-receptor agonist, PEA, leads us to suggest its involvement in arrhythmias associated with subacute myocardial infarction.