dinoprost and Shock

Topics: Anti-Inflammatory Agents, Non-Steroidal; Dinoprost; Epoprostenol; Humans; Shock

The effects of platelet-activating factor (PAF) on prostanoid release during mesenteric ischemia-reperfusion-induced shock were investigated in anesthesized dogs 1) by measuring plasma levels of prostaglandin (PG)F2 alpha, 6-keto-PGF1 alpha and thromboxane (TX)B2 in the superior mesenteric vein during reperfusion following 2 hr occlusion of the superior mesenteric artery; 2) by monitoring the effects of BN 52021, a specific PAF receptor antagonist and indomethacin on hemodynamic parameters and prostanoid levels; and 3) by studying circulatory responses to PAF and PGF2 alpha injected into the superior mesenteric vein in the presence of BN 52021 or indomethacin. Restoration of the blood flow following 2 hr ischemia resulted in an immediate dramatic decrease in mean arterial blood pressure, with a concomitant increase in mean portal venous pressure, hematocrit values, and plasma prostanoid levels. Pretreatment of the animals either with BN 52021 (4 mg.kg-1) or indomethacin (2 mg.kg-1 plus 3 mg.kg-1hr-1) prevented the circulatory collapse and the increase in prostanoid levels during reperfusion. Administration of exogenous PAF (0.1 micrograms.kg-1) or PGF2 alpha (10 micrograms.kg-1) into the superior mesenteric vein evoked hypotension similar to that observed during reperfusion. Pretreatment of the animals with BN 52021 completely prevented the effects of PAF but failed to modify the responses to PGF2 alpha. Indomethacin at a dose that inhibited prostanoid formation was highly effective to attenuate the hypotensive response to exogenous PAF. These data suggest that prostanoid formation may be secondary to PAF release in circulatory collapse evoked by intestinal ischemia-reperfusion and give further support to the notion of the importance of PAF prostanoid interaction during ischemia-reperfusion-induced shock.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Dinoprost; Diterpenes; Dogs; Ginkgolides; Hemodynamics; Indomethacin; Lactones; Male; Mesenteric Arteries; Mesenteric Veins; Platelet Activating Factor; Prostaglandins; Reperfusion Injury; Shock; Thromboxane B2

The role of PGF2 alpha in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring PGF2 alpha levels in superior mesenteric vein, right ventricle, aorta, and femoral vein during superior mesenteric artery occlusion-induced shock by comparing the circulatory effects of exogenous PGF2 alpha injected into either the superior mesenteric or the femoral vein and by inhibiting of prostanoid synthesis with indomethacin. Release of the superior mesenteric artery occlusion caused a dramatic decrease in mean arterial blood pressure; an increase in mean portal venous pressure, and more than fivefold increases in plasma PGF2 alpha levels in superior mesenteric vein, right ventricle, and aorta. In spite of the decreased mean arterial blood pressure, postocclusion blood flow in the mesenteric artery did not fall below preocclusion values. Indomethacin in itself, significantly reduced plasma PGF2 alpha levels as well as intestinal blood flow and increased mean arterial blood pressure in animals without superior mesenteric artery occlusion. Furthermore, indomethacin attenuated the magnitude of postocclusion hypotension and completely prevented PGF2 alpha production during superior mesenteric artery occlusion shock. Exogenous PGF2 alpha 10 micrograms/kg injected into the superior mesenteric or femoral vein produced hypotension or hypertension, respectively. When PGF2 alpha was injected into the superior mesenteric vein, the plasma level of PGF2 alpha in the aorta was similar to that observed during superior mesenteric artery occlusion shock, whereas PGF2 alpha injected into the femoral vein gave a significantly higher concentration. Pulmonary metabolism of PGF2 alpha was significantly reduced in shock. The present results suggest that PGF2 alpha released by intestinal tissues might play an important role in shock caused by intestinal ischemia.

Topics: Animals; Blood Pressure; Dinoprost; Dogs; Hemodynamics; Indomethacin; Intestinal Mucosa; Intestines; Ischemia; Mesenteric Arteries; Mesenteric Vascular Occlusion; Shock

Among the mediators for development of endotoxic shock, plasma kallikrein and prostanoids have been suggested to play an important role. The role of kallikrein and PGF2 alfa in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring inactive and active kallikreins and PGF2 alpha in superior mesenteric vein, right ventricle and aorta during shock induced by occlusion of the superior mesenteric artery. After removal of the clamp in dogs subjected to occlusion for 1 hour, the mean arterial blood pressure fell rapidly within 5 min and gradually increased over the next 60 min, with return to the control values. The plasma concentrations of PGF2 alfa in superior mesenteric vein, right ventricle and aorta increased three- to fivefold within 5 min of reperfusion. Thereafter the PGF2 alfa levels fell, so that at 60 min after declamping they did not significantly differ from the control values. No significant changes were observed in the levels of inactive and active kallikreins. The results suggest that PGF2 alfa released by intestinal tissues may contribute to the development of shock caused by intestinal ischemia.

Topics: Animals; Aorta; Dinoprost; Dogs; Heart Ventricles; Intestinal Mucosa; Intestinal Secretions; Intestines; Kallikreins; Male; Mesenteric Arteries; Mesenteric Veins; Shock

Two groups of 5 bitches different in breed, age and size were given a single dose of PGF2 alpha at a dosage of 0.25 and 0.50 mg/kg of body weight respectively. Since the administration of PGF2 alpha is usually associated with a syntomatic shock in the bitch, four bitches per group were additionally treated with a single dose of atropine (0.050 mg/kg). Two of the four bitches were injected with atropina I.M. contemporaneously with the PGF2 alpha and the other two at the beginning of the symptomatology. Both the former and the latter show a marked reduction of symptomatic shock. The AA. discuss the possible use of PGF2 alpha associated to the administration of atropine in the current therapy of some reproductive disorders of the bitch.

Topics: Animals; Atropine; Dinoprost; Dogs; Female; Prostaglandins F; Shock