Objective Damage to the nervous system remains an inevitable complication for the clinical application of cardiopulmonary bypass(CPB)technique.Experiment studies in animals with cerebral ischemia-reperfusion injury have revealed the association between inflammation and the impaired endothelium-dependent vasodilation in the brain vessels.Few studies have described theeffects of CPB on the vascular endothelial cells of the brain.This study is to investigate functional changes,which occurred in the different CPB modes,of the cerebrovascular endothelial cells and the associations between CPB and inflammatory factors.Methods Twenty-four S.D.rats were equally divided into four groups and underwent normothennic CPB for 120 min(group A),deep hypothermic low flow(DHLF) for 60 min(Group B),deep hypothermic circulatory arrest(DHCA) for 60 min(Group C) and sham group (Group D) respectively via right carotid and jugular cannulation.Blood samples from the internal jugular vein were collected before and after bypass to test the serum levels of nitrogen monoxide (NO) and 1L-6.The middle cerebral artery (MCA) in the right side was harvested for the evaluation of the endothelial cell response to acetylcholine at different concentrations.The protein expression of endothelial NO synthase (eNOS) was determined by Western immunoblotting.The ICAM-1 expression in the cerebral vessels was tested with immunohistochernistry staining.Results Bypass in all of the rats were established and removed successfully.Plasma concentrations of NO were reduced in CPB groups as compared with that in the sham group.Plasma NO levels were lower in group B and C than that in group A[(3.94±0.15) mg/L in group B and (2.93±0.33) mg/L in group C vs.(4.33±0.17) mg/L in group A,P=0.002].Acetylcholine induced a dose-dependent MCA vasodilation in sham group [(24.26 ± 1.90)% increase in diameter],that was attenuated in all CPB groups [(9.60± 1.09)% in group A,(5.97±0.68)% in group B and (5.72±0.67)% in group C,P＜0.01].The hypothermic bypass was associated with significantly reduced eNOS expression as compared with that in group A(P＜0.01),and the eNOS expression was even lower in group C than in group B (P=0.002).The IL-6 level increased in all of the bypass groups (P＜0.05).ICAM-1 was overexpressed in all of the bypass groups and the amount of ICAM-1 expression increased significantly in these groups as compared with that in the control group.Conclusion CPB may induce injury to the cerebrovascular endothelial cells,particularly in the DHCA/DHLF bypass modes.The damage to the endothelial cells may be represented mainly as impaired vasodilatation and loss of endothelium-dependent regulatory factors.Endothelial cell injury may be mainly accounted for by the systemic inflammatory response syndrome.Severe damage to the vasodilation function of the endothelial cells in the middle cerebral artery observed in the DHLF and DHCA groups,as compared with that in the normothennic CPB group,may be associated with damage to the endothelial cells induced by hypothermia,more severe hypoperfusion status and ischemia-reperfusion injury.