Prostaglandin e biosynthesis during cardiopulmonary bypass

Initiation of cardiopulmonary bypass (CPB) causes immediate drop in blood pressure and peripheral vascular resistance (PVR) with activation of complex neurohumoral reflex mechanisms and redistribution of systemic blood flow. Prostaglandin E (PGE) is a potent vasodilator released during ischemia and low flow states. This study was designed to determine if CPB provided stimulus for PGE biosynthesis and its effect on PVR.Fourteen dogs were placed on CPB for 60 min at 80 ml/kg/min. Plasma PGE concentration and PVR were determined prior to and immediately after the start of CPB and at 15-min intervals. There were eight control animals (Group I) and six (Group II) had PGE inhibited by indomethacin (2.5 mg/kg). With the initiation of CPB, PVR decreased to 18 ± 1 U in both groups. In Group I, PGE increased from 404 ± 88 to 619 ± 256 pg/ml. In Group II, PGE levels dropped from 363 ± 94 to 218 ± 96 pg/ml after indomethacin block and did not change in response to CPB. At 15 min, Group I PVR rose to 30 ± 3 U while Group II PVR was higher at 42 ± 2 U (P < 0.001). PGE concentrations at this time were 652 ± 106 in Group I and 260 ± 92 pg/ml in Group II (P < 0.01). After 15 min, PGE returned to control in Group I but remained significantly elevated over Group II at 30 and 45 min. PVR continued to increase in both groups for the duration of CPB and Group II PVR remained significantly elevated (P < 0.05) compared to Group I.These data show that PGE is released in response to the initiation of CPB and is one of several factors affecting PVR during CPB.