Abstract

Recently, it has been demonstrated that polymorphonuclear neutrophils (PMNs) affect coronary vascular tone. We have reported that unstimulated PMNs constrict the porcine proximal coronary artery. However, the mechanism(s) of interaction between PMNs and coronary artery and the regional differences in susceptibility of the coronary arterial tree have not been fully explored. We examined changes in the isometric tension of porcine distal coronary arterial rings caused by unstimulated PMNs, in which the levels of superoxide anion detected by the cytochrome C method were slight when unstimulated and significant when stimulated with A23187. Unstimulated PMNs relaxed the distal coronary artery and the effect was suppressed by endothelial denudation, indomethacin and the prostacyclin synthetase inhibitor, tranylcypromine. During vasorelaxation, prostacyclin was produced (n=8, with without relaxation; 596 +/- 76/247 +/- 26 pg/ml, p < 0.01) and was considered, therefore, to be the vasodilatory substance responsible for the action. These results suggest that PMNs modulate coronary arterial tone via an interaction between PMNs and endothelium and the release of vasodilating prostaglandins, of which prostacyclin is considered to be one of the substances responsible. Further, the effect differed markedly depending on the site of the coronary artery. In vivo, coronary artery tone is complexly regulated, therefore, the relative contribution of the present PMN-endothelial cell interaction observed in vitro is unclear.

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