AJP - Heart and Circulatory Physiology, Vol 249, Issue 3 698-H702, Copyright © 1985 by American Physiological Society
Unique coronary vasodilator induction by leukotriene D4
D. Ezra, G. Feuerstein, J. F. Czaja, F. R. Laurindo, C. K. Finton, G. C. Yeh and R. E. Goldstein
Coronary blood flow (CBF) and myocardial contractility decrease markedly in
response to intracoronary administration of leukotriene D4 (LTD4). With
steady infusion, however, both CBF and contractility escape, approaching
preinfusion values despite ongoing LTD4 administration. To clarify the
mechanism of this escape, we reinfused plasma from the coronary vein
draining the myocardial area receiving LTD4. Introducing this plasma into a
coronary artery caused a marked rise in coronary flow for the duration of
the plasma infusion. Coronary flow reduction with vasopressin or mechanical
occlusion matching that caused by LTD4 failed to elicit vasodilator
production. Thus a unique coronary vasodilator factor is induced by LTD4.
Whole blood or platelet-rich plasma incubated with LTD4 in vitro produced
the same pattern of coronary dilation on intracoronary infusion; LTD4
incubation with platelet-poor plasma failed to elicit a vasodilation. The
vasodilator factor is stable and is not potassium, a prostaglandin,
catecholamine, histamine, serotonin, adenosine, adenosine diphosphate, or
platelet-activating factor. Production of this leukotriene-induced
vasodilator factor may account for the escape from LTD4-induced coronary
constriction.
