Influence of 4 different membrane oxygenators on inflammation-like processes during extracorporeal circulation with pulsatile and non-pulsatile flow

Abstract

The influence of four different membrane oxygenators (HF 4000, BOS-CM 50, CML 2, Maxima) on leucocyte count, concentrations of PMN-elastase, clotting factor XII, AT-III, C1-INH, alpha 2-antiplasmin and C3a was registered before, during and after CPB with pulsatile and nonpulsatile flow in 80 male patients aged between 36 and 67 years. With all systems tested, there was a drop in the concentrations of clotting factor XII, AT-III, C1-INH and alpha 2-antiplasmin in the early extracorporeal circulation (ECC) phase, exceeding the average hematocrit reduction accounted for by dilution. This drop was the least distinct with CML 2 systems, both with pulsatile and nonpulsatile perfusion, indicating system-inherent influences. Leucocyte cound and PMN-elastase concentration rose significantly during ECC irrespective of oxygenator tested of flow type applied. The rise in leucocyte count even continued for about 4 h after ECC. During the first 40 min of ECC, these changes were paralleled by a significant rise in C3a concentration, suggesting complement activation as a main cause for PMN activation. However, there is reason to suppose involvement of further mechanisms operating in PMN activation, since the elevated C3a-concentrations began to fall off while leucocyte count and PMN-elastase concentrations were still increasing.

Mechanisms of the systemic inflammatory response

“…Furthermore, kallikrein directly activates complement C5 and neutrophils and also stimulates the fibrinolytic system by facilitating conversion of plasminogen to plasmin. 41,44 Activity of factor XII gradually increases during CPB 45 while its plasma concentration decreases, 46 probably as a result of accelerated consumption.…”

Down-regulation of surface monocyte lipopolysaccharide-receptor cd14 in patients on cardiopulmonary bypass undergoing aorta-coronary bypass operation

“…Complement activation and neutropenia occur during CPB, and functional signs of leukocyte activation after cardiac operation, including the release of proteolytic enzymes, free radical production, and changes in leukocyte adhesiveness, have been reported. [4][5][6] Furthermore, measures of cell-mediated immunity, such as lymphocyte responsiveness to mitogens and antigen presentation, have been shown to be seriously impaired in patients after CPB. 7 The monocyte/macrophage cell system is believed to play a central role in regulating acute inflamma-tory responses.…”

Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion

“…Although we measured neither endotoxin nor any inflammatory markers, it is conceivable that a systemic inflammatory response syndrome or endotoxemia provoked by the extracorporeal circulation may have contributed to the impaired hepatic oxygen extraction (22,24,29,30).…”