Abstract

This study was designed to examine the effects of polymorphonuclear leukocytes (PMNs) on human internal mammary artery (IMA) and saphenous vein (SV) segments obtained from patients undergoing coronary bypass surgery. PMNs (107/mL) caused a modest (39% ± 4%) relaxation of precontracted IMA rings, but only minimal (5% ± 2%) relaxation of SV rings (P < 0.01, relaxation of IMA vs SV rings). Relaxation of SV rings in response to endothelium-dependent vasodilator acetylcholine was also less than that of IMA rings (P < 0.01). PMN-induced vasorelaxation was not modified by treatment of vascular rings with indomethacin, but the vasorelaxation was potentiated by superoxide dismutase and inhibited by both oxyhemoglobin and methylene blue, suggesting that PMNs release a material similar to the endothelium-derived relaxing factor (EDRF). PMN-induced vasorelaxation was associated with a 75% increase (P < 0.02) in the cyclic guanosine monophosphate (GMP) content of the IMA rings and a 20% increase in cyclic GMP in SV rings. To determine the role of the endothelium in PMN-vessel wall interactions, IMA and SV segments were exposed to superoxide anions generated by a combination of xanthine followed by xanthine oxidase (X + XO). In these X + XO-treated IMA and SV segments, PMNs caused a marked relaxation (55% ± 9% and 22% ± 8%, respectively) and a three- to fourfold increase in vascular cyclic GMP content. However, PMN-induced relaxation and the increase in cyclic GMP were less (P < 0.02) in the SV than the IMA rings. In manually deendothelialized vascular rings, PMNs caused a marked relaxation. These observations suggest that isolated PMNs, release an EDRF-like material that causes relaxation of IMA and SV rings by increasing tissue cyclic GMP. The reduced relaxation potential of the SV rings may explain the higher incidence of closure of SV grafts as compared to IMA grafts in patients undergoing coronary artery bypass surgery.

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