Journal of Applied Physiology, Vol 73, Issue 6 2530-2537, Copyright © 1992 by American Physiological Society
Histamine decreases left ventricular contractility in normal human subjects
D. J. Cooper, C. R. Thompson, K. R. Walley, R. P. Gillis, P. E. Wolinski-Walley and R. R. Schellenberg
University of British Columbia, Division of Cardiology, St. Paul's Hospital, Vancouver, Canada.
To determine whether histamine alters human left ventricular contractility
we measured heart rate, calibrated carotid arterial pressure, and left
ventricular dimensions (echocardiogram) in nine healthy volunteers. We
assessed baseline contractility using the end-systolic pressure-dimension
relationship and the end-systolic meridional wall stress-rate-corrected
velocity of circumferential fiber shortening relationship determined over a
wide range of afterloads using phenylephrine and nitroprusside infusions.
We then infused histamine for 3-5 min at a dose predetermined to decrease
mean arterial pressure by 20%, both before and after H1 receptor antagonist
pretreatment (diphenhydramine 50 mg i.v.). Histamine decreased end-systolic
pressure but, unlike an equally hypotensive infusion of nitroprusside, did
not decrease end-systolic dimension or increase fractional shortening.
Histamine also decreased velocity of circumferential fiber shortening at
the same end-systolic meridional wall stress as controls (P < 0.05).
These effects of histamine were inhibited by H1 antagonist pretreatment. We
conclude that the dominant effect of histamine on the human heart is to
decrease left ventricular contractility and that this decrease in
contractility is dependent, at least partially, on H1-receptor activation.
