PROSTAGLANDIN SYNTHESIS INHIBITOR IMPROVES HYPOTENSION DURING CARDIOPULMONARY BYPASS

Abstract

Backgrounds: Cardiopulmonary bypass (CPB) is known to decline systemic blood pressure (SBP) and may contribute to renal dysfunction and cerebral ischemia. Vasoconstrictors are usually administered to elevate the SBP, whereas high-dose infusion of vasoconstrictors induces regional perfusion abnormalities. We previously reported that prostaglandin (PG) which was usually inactivated in the lung but increased during CPB, might play a substantial role in the hypotension. The purpose of this study is to investigate whether PG synthesis inhibitor (PGSI) can improve hypotension during CPB. Patients and Methods: A prospective controlled trial was performed in consecutive 30 patients undergoing elective cardiac surgery with CPB. Patients were divided into two groups. The control group (n=15) was performed conventional CPB, and the PGSI group (n=15) was administered 50 mg of flurbiprofen, a potent PGSI, before CPB and was occasionally added 50–100 mg of flurbiprofen according to CPB time. Both groups were maintained the total systemic flow in 2.5–3.0 L/min/m2 at all the CPB time and were controlled the mean SBP more than 45 mmHg by infusion of metaraminol, a vasoconstrictor. The mean SBP, the blood base excess (BE), the urine output and the dose of metaraminol were estimated. Results: The value of mean SBP throughout the CPB was significantly higher in the PGSI than the control group (59±5 vs. 49±6 mmHg, p < 0.01). The value of BE was not significantly different between the PGSI and the control group (0.8±1.7 vs. 0.2±2.0 mmol/L, p=0.40). The urine output was significantly higher in the PGSI than the control group (558±174 vs. 303±95 ml/hr, p < 0.01). The dose of metaraminol was significantly lower in the PGSI than the control group (14±6 vs. 22±8 mg, p < 0.01). Conclusion: Administration of PGSI during CPB can improve hypotension and increase urine output without impairing peripheral circulation.