To evaluate whether histamine exerts a direct effect on coronary hemodynamics in humans, and to investigate the role played by H1 and H2 receptors in this response, intracoronary saline solution or histamine (4 μg) was administered in 10 patients with normal coronary arteries during diagnostic cardiac catheterization. Histamine injection was repeated after intravenous cimetidine (400 mg) and diphenhydramine (10 mg). The electrocardiogram, arterial pressure and thermodilution coronary blood flow were continuously monitored during and for 40 seconds after each injection. Immediately after histamine injection there was a significant increase in coronary blood flow (65 ± 6%) and a decrease in coronary vascular resistance (-40 ± 3%) (both p <0.001), with minor changes in the RR interval and the mean arterial pressure. H2 receptor blockade with cimetidine did not affect these changes, while H1 receptor blockade with diphenhydramine significantly reduced the histamine-induced increase in coronary blood flow and the decrease in coronary vascular resistance (26 ± 6%, p <0.005 and -18 ± 5%, p <0.001, respectively). Twenty to 30 seconds after histamine injection, a significant decrease in mean arterial pressure (-17 ± 2%, p <0.001) and in the RR interval (-4 ± 1%, p <0.01) was observed. These changes persisted after H2 receptor blockade with cimetidine, but were completely abolished after H1 receptor blockade with diphenhydramine. In each case coronary and systemic hemodynamics returned to normal within 40 seconds of the injection. Therefore, in patients with normal coronary arteries, histamine induces a direct dilation of the small resistance coronary arteries, regardless of myocardial metabolic requirement, that is predominantly, but not completely, mediated by H1 receptors.
|Number of pages||7|
|Journal||Journal of the American College of Cardiology|
|Publication status||Published - 1987|
ASJC Scopus subject areas