Effects of ullnastatin on cerebral injury in patients undergoing cardiac valve replacement

Objective To investigate the effects of ulinastatin on cerebral injury during cardiac valve replacement and the possible mechanisms involved. Methods Twenty-four NYHA Ⅱ or Ⅲ patients of both sexes (13 male, 11 female) aged 23-45 yr undergoing cardiac valve replacement with hypothermic cardiopulmonary bypass (CPB) were randomly divided into two groups: control group (group C, n = 12) and ulinastatin group (group U, n = 12) . In group U ulinastatin 12 000 U·kg-1 was given i.v. after induction of anesthesia, 6 000 U· kg-1 was added to the priming solution and another 6 000 U·kg-1 was given at 5 min before aortic unclamping. In group C normal saline was given instead of ulinastatin. Internal jugular vein was cannulated and the catheter was advanced in a cephalad direction till jugular bulb. Blood samples were taken from jugular bulb after induction of anesthesia(T1) , when rewarming to 36℃(T2), 30 min (T3 ) and 6 h (T4 ) after discontinuation of CPB for determination of plasma S100β protein, neuron specific evolase (NSE) , MDA concentrations and SOD activity. Plasma TNF-α, IL-6, IL-8 and IL-10 levels were also determined at T1, T3 and T4.Results Plasma levels of S100β protein, NSE and MDA were significantly increased during and after CPB (T2-4) compared to the baseline values before CPB (T1), but were significantly lower in group U than in group C (P0.05 or 0.01). SOD activity was significantly decreased during and after CPB as compared to the baseline valve (T1) in group C, while there was no significant change in SOD activity in group U. Plasma TNF-α, IL-6, IL-8 and IL-10 levels were significantly increased as compared to the baseline values at T1 in both groups but plasma TNF-α, IL-6 and IL-8 levels were significantly lower at T3 and T4 whereas IL-10 level was significantly higher at T4 in group U than in group C (P 0.05 or 0.01) . Conclusion Ulinastatin can attenuate cerebral injury during cardiac valve replacement with CPB. The decrease in proinflammatory cytokines and increase in anti-inflammatory cytokines and antioxidation produced by ulinastatin may explain the mechanisms involved.