Background Inflammation and coagulation are two intimately cross-linked defense mechanisms of most, if not all organisms to injuries. During cardiopulmonary bypass （CPB）, these two processes are activated and interact with each other through several common pathways, which may result in subsequent organ dysfunction. In the present study, we hypothesized that the addition of nitric oxide, prostaglandin E1 （PGE1）, and aprotinin to the systemic circulation, hereby referred to as blood hibernation, would attenuate the inflammation and coagulation induced by CPB. Methods Thirty adult mongrel dogs were equally divided into five groups, anesthetized and placed on hypothermic CPB （32℃）. Each group received respectively the following treatments： （1） inhalation of 40 ppm nitric oxide; （2） intravenous infusion of 20 ng.kgl.min1 of PGE1; （3） 80 000 kallikrein inhibitor units （KIU）/kg of aprotinin; （4） the combination of all three agents （blood hibernation group）; and （5） no treatment （control group） during CPB. Activation of leukocyte, platelet, endothelial cell, and formation of thrombin were assessed after CPB. Results As compared with the other four groups, leukocyte counts were higher, while plasma elastase, interleukin-8, CD11b mRNA expression, myeloperoxidase activities and lung tissue leukocyte counts were lower in the blood hibernation group （P 〈0.05 versus other four groups after CPB）. Plasma prothrombin fragment （PTF）1＋2, and platelet activation factors were lower, while platelet counts were higher in the blood hibernation group （P 〈0.05 versus other four groups at 6 and 12 hours after CPB）. Electron microscopy showed endothelial pseudopods protrusion, with cell adherence in all four groups except the blood hibernation group where endothelial cells remained intact. Conclusion Blood hibernation, effected by the addition of nitric oxide, PGE1 and aprotinin to the circulating blood during extra-corporeal circulation, was observed to attenuate the inflamm
ZHOU JingWU Xiao-dongLIN KeRaphael C. LuiAN QiTAO Kai-yuDU LeiLIU Jin
