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Milhoan, Kirk A., Thomas A. Lane, and Colin M. Bloor. Hypoxia induces endothelial to increasetheir adherencefor s: role of PAF. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H956-H962, 1992.-We investigated the interactions of polymorphonuclear s (PMN) and endothelial in myocardial ischemiausing a hypoxia model. We exposed porcine aortic (PAEC) and porcine coronary microvesse1(PCMEC) endothelial to 2% O2 for 2 h (Po2 = 53 mmHg) and measuredthe adherenceof unstimulated s (PMN) to both control and hypoxia-conditioned endothelial cell monolayers. Hypoxia conditioning increasedPMN adherence to PAEC and PCMEC by 51 and lOl%, respectively, above control levels. The increasein PMN to PAEC was associatedwith a threefold increase in endothelial cellassociated platelet-activating factor (PAF) comparedwith control PAEC. The conditioned media from PAEC exposedto hypoxia alsocontained sixfold more PAF than control conditioned media, and it activated PMN to becomeadherent to untreated PAEC. The PAEC response was inhibited by preincubating PMN with the specific PAF receptor antagonist, L-659,989. We conclude that PAF is produced by cultured endothelial in response hypoxia and that PAF to generation is chiefly responsiblefor the increased adherence properties of hypoxia-conditioned endothelial . This responsemay play a major role in regulating PMN margination during myocardial ischemia. ;porcine aortic coronary microvessels
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Sep 1, 1992
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