Search

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.

Reflex vascular responses to local carotid chemoreceptor stimulation with hypoxic-hypercapnic, hypoxic, or hypercapnic blood were investigated in pentobarbitalized dogs. Bilaterally isolated carotid chemoreceptors were perfused via an extracorporeal lung circuit. Oxygen and carbon dioxide tensions of blood perfusing the carotid bodies were altered by ventilating the isolated lung with various O2-CO2 mixtures. Ventilation of the whole animal maintained normal systemic O2 and CO2 tensions. Perfusion pressures of the isolated kidney, ileum, forelimb, gracilis and hindpaw were measured during constant-flow perfusion. Carotid chemoreceptor stimulation with hypoxic-hypercapnic blood before vagotomy increased renal vascular resistance but caused no change in intestinal or forelimb resistance. Following vagotomy, hypoxic-hypercapnic, hypoxic, or hypercapnic carotid body stimulation increased renal, intestinal, and forelimb vascular resistance. Forelimb skin and muscle vascular beds contributed about equally to the increase in forelimb resistance. Gracilis muscle and hindpaw resistance also increased during hypoxic-hypercapnic stimulation after vagotomy.