Lack of Circulating Prostacyclin (PGI2) In Guinea Pig And Rat

Abstract

Under light ether anesthesia, blood of male guinea pigs (Hartley strain, 330-410 g, Simonsen, Gilroy, CA) or rats (Sprague-Dawley, 230-575 g, Simonsen) was withdrawn into sodiun citrate (0.38% w/v). Platelet rich plasm (PRP) was then prepared by a rapid centrifugation procedure. Aggregation induced by ADP (1.6 μg/ml) was then examined in 0.15 or 0.25 ml aliquots of PRP at various time intervals from 5-60 min after blood withdrawal. A spontaneous time-dependent rise in aggregation response occurred that was similar to that observed when PGI2 (0.5-3ng) was added to PRP in vitro. In both species, intraperitoneal ackninistration of indanethacin (100 mg/kg, 1h previously) failed to interfere with the spontaneous rise in aggregation although vascular PGI2 formation was shown to be virtually abolished. Similar results were seen in essential fatty acid (EFA) deficient rats that had been chronically maintained on a fat free diet. In these animals, vascular PGI2 product ion was less than 15% that of controls. These results clearly indicate that any basal levels of PGI2 present in the arterial circulation are less than those (0.3-1ng/ml) necessary to appreciably inhibit aggregation. This conclusion coincides with that of Steer, et al. (Nature, 283, 194, 1980) who failed to detect biologically active amounts of PGI2 in hiimn venous blood and of several other groups who have failed to detect significant blood levels of the PGI2 breakdown product, 6-keto-PGF1α.