Effects of ulinastatin on pulmonary artery pressure during abdominal aortic aneurysmectomy

Abstract

Study Objective Abdominal aortic aneurysmectomy (AAAectomy) results in a general ischemia-reperfusion syndrome accompanied by an acute rise in pulmonary artery pressure (PAP). We examined whether ulinastatin, a urinary trypsin inhibitor, prevents ischemia-reperfusion injury and increase in PAP after aortic unclamping (XU) during AAAectomy. Design Prospective study. Setting Public, university-affiliated hospital. Patients Sixteen patients (11 males and 5 females) scheduled for AAAectomy. Interventions and Measurements The patients received 300 000 IU of ulinastatin intravenously before XU (n = 8) or no additional treatment (n = 8) (control). Heart rate, central venous pressure, PAP, pulmonary arterial wedge pressure, arterial pressure, mixed venous oxygen saturation (S vo 2), and cardiac output were monitored. Arterial and mixed venous blood samples were analyzed for pH, Pa co 2, Pa o 2, hemoglobin, and oxygen saturation, and the physiological shunt function (Qs / Qt) were calculated. Plasma concentrations of malondialdehyde, myeloperoxidase, granulocyte elastase, α1-antitrypsine, and thromboxane B2 and the stable hydrolysis products of thromboxane A2 were measured. Measurements were conducted before aortic crossclamping (XC) (baseline) and at 10, 30, and 60 minutes after XU. Main Results A significant increase in PAP was observed 10 minutes after XU in the control group but not in the ulinastatin group. At 60 minutes after XU, Qs / Qt values had increased in the control group but had decreased in the ulinastatin group. There were no significant changes in malondialdehyde, thromboxane B2, granulocyte elastase, and α1-antitrypsine levels after XU in either group. A significant decrease in the plasma level of myeloperoxidase after XU was found in both groups. Conclusions The present study demonstrated that ulinastatin prevents increase in PAP and shunting after XU during AAAectomy.