Time course of elastase alpha-1 protease inhibitor complex and white blood cell count in cardiac surgery with cardio-pulmonary bypass
Shimanuki, K.; Hamada, O.; Sakurabayashi, I.
Nihon Kyobu Geka Gakkai 36(1): 83-91
1988
ISSN/ISBN: 0369-4739 PMID: 3385249 Document Number: 325953
White blood cell count of 84 patients were measured at every 20 minutes undergoing cardiopulmonary bypass (CPB). In 43 (membrnae oxygeneator: 32. bubble oxygenator 11) of 84 patients, neutropenia occurred during bypass. Neutropenia was marked in case of respiratory dysfunction, with membrane oxygeneator. It has been suggested that neutropenia was caused by leukostasis in the lung with CPB. It has been known that hemolysis by destruction of red blood cell undergoing CPB. But it has not been known that destruction of white blood cell with CPB. In order to examine whether granulocyte elastase (GEL) would be discharged from destroyed granulocyte with cardiopulmonary bypass, we assayed GEL from 20 patients. Plasma level of GEL were measured with an enzyme-linked immunoassay for alpha-1 protease inhibitor complex. GEL level was 204.8 .+-. 158.5 .mu.g/l at preoperative state, and gradually increased during operation to 1021.5 .+-. 589.3 .mu.g/l. Level of GEL in inlet of CPB was higher than outlet of CPB. But this was not significant. Two cases of 20 patients, with neutropenia, felled in respiratory dysfunction. Alpha-1 antitrypsine (A-1 AT) that is one of protease inhibitors of GEL, was measured from 12 patients before and after operation. A-1 AT level was 255.7 .+-. 54.1 mg/dl before opertion and decreased to 164.6 .+-. 69.8 mg/dl after operation. One of 12 patients, level of A-1 AT prominentory decreased, felled in respiratory dysfunction. In operation using CPB a tremendous elevation of the GEL level was observed. Mechanism of triggering enzyme release may be very similar in hemodialysis. But it was supposed that GEL would be discharged from mechanical destroyed granulocyte with CPB, may produce endothermal cell damage in the lung. Decreased A-1 AT after operation with CPB may activate GEL in the lung. Elevation of GEL and decreased A-1 AT may play an important role in etiology of postperfusion lung syndrome.