Why the study?
Does indomethacin affect coronary reactive hyperemia and renal blood flow regulation in canine models?
Does indomethacin affect coronary reactive hyperemia and renal blood flow regulation in canine models?
Prostaglandins do not appear to participate significantly in the regulation of coronary blood flow, and have only minimal participation in renal blood flow regulation in canine models.
Answers are grounded in this paper and cite their sources.
Should not yet change NSAID use in cardiac or renal patients; leaves open prostaglandin roles in human vascular regulation.
In two series of experiments we studied the effects of indomethacin on (a) coronary reactive hyperemia and, (b) renal blood flow, autoregulation, and reactive dilation. Coronary blood flow was measured in closed-chest dogs. Reactive hyperemia was induced by coronary occlusion for 5 and 15 sec. Indomethacin, an inhibitor of prostaglandin synthesis, was infused intra-arterially in doses of 90-200 mg over periods ranging from 30-120 min. Coronary reactive hyperemia was not affected by indomethacin. The canine renal vascular bed was studied under conditions of natural flow, controlled flow, and controlled pressure. Intra-arterial infusion of 90 mg of indomethacin over a 30- to 60- min period caused increased renal vascular resistance and an attenuation of reactive dilation (induced by stopping renal blood flow for 90 sec). Indomethacin slightly attenuated the autoregulatory response to decreasing perfusion pressures, but did not affect the respone to increasing pressures. Thus the study fails to provide evidence for participation of the prostaglandins in regulation of coronary blood flow and suggests only minimal participation of prostaglandings in renal blood flow regulation.
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Owen et al. (1975) studied this question.
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