The possible involvement of PGI2 in the PEEP-induced changes in cardiac output and blood pressure.
Ventilation with positive end-expiratory pressure (PEEP) is employed in clinical and aviation medicine. The widespread application of PEEP, however, is limited principally because of its adverse effect on cardiac output (CO) and systemic arterial blood pressure (BP). Recently, it has been suggested that this PEEP-induced cardiovascular depression may be mediated by vasoactive agents, possibly prostaglandin in nature. This study examined the possible involvement of PGI2 in the PEEP-induced decreases in CO and BP. Chloralose-anesthetized mechanically ventilated dogs were subjected to brief intervals (75 s) of PEEP 10 or 20 mm Hg. Arterial levels of 6-keto-PGF1 alpha (stable metabolite of PGI2) were monitored by radioimmunoassay. These parameters were compared before and during PEEP application. During PEEP, tracheal pressure-related decreases in both CO and BP were noted. Application of either PEEP 10 or 20 mm Hg resulted in an increase in circulating 6-keto-PGF1 alpha levels in three animals while a decrease was noted in two others. Overall, application of PEEP did not result in a significant change from baseline levels. Furthermore, there was no correlation between changes in either CO or BP with changes in arterial 6-keto-PGF1 alpha levels. These results do not support the hypothesis that the short term PEEP-induced changes in CO or BP are mediated by endogenously released PGI2.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D011464:Epoprostenol / Q000502:physiology*; D005260:Female; D006339:Heart Rate; D008297:Male; D011175:Positive-Pressure Respiration / Q000009:adverse effects*; D011863:Radioimmunoassay
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol