The arrhythmogenic actions of histamine on human atrial fibers.

We used standard microelectrode techniques to study the effects of histamine on right atrial tissues from patients undergoing corrective cardiac surgery. In the 10(-6) to 10(-4) M range, histamine increased maximum diastolic potential, action potential amplitude, and automaticity. In some preparations, histamine also induced delayed afterdepolarizations and triggered activity. The potency of histamine in increasing automaticity was about 10 times less than that of epinephrine. Propranolol (2 x 10(-7)M), which abolished the chronotropic effect of epinephrine, did not alter the effect of histamine. Conversely, the effect of histamine but not that of epinephrine was antagonized by cimetidine (3 x 10(-6) to 1 x 10(-5) M). This suggests that H2 receptors mediate the chronotropic effects of histamine on the human heart. The slow channel blocker verapamil (2 x 10(-8) to 2 x 10(-6) M) counteracted the effects of histamine on automaticity, delayed afterdepolarizations, and triggered activity, suggesting that in human atrium histamine may act by increasing slow inward (presumably Ca2+) current. If one considers these arrhythmogenic effects of histamine and the fact that human cardiac tissue contains large amounts of histamine, our experiments lend further support to the concept that histamine release can induce arrhythmias.