Abstract
Isolated rat hearts were perfused with a O2--generating system consisting of purine plus xanthine oxidase for 15 or 20min. After the O2- pretreatment, washout (performed with normal Krebs solution) produced significant elevation of coronary perfusion pressure (CPP). After 20min O2- pretreatment, administration of 4μM nitroglycerin or 1μM sodium nitroprusside, which are nitric oxide (NO) donors, enhanced the elevation of CPP. Conversely, 100μM nitro-L-arginine or 10μM NG-monomethyl-L-arginine, which are NO synthase inhibitors, immediately induced vasorelaxation in O2--pretreated hearts. Thus, it was suggested that NO, a physiological vasodilator, paradoxically augments constriction of the coronary arteries, in O2--pretreated rat heart.
