| Background NO is an important vasoactive-substance. More and more researches showed that NO plays a vital role in the pathophysiological processe of shock,and NO is an important mediator for pathophysiological alterations associated with loss of vascular reactivity,multiple organ dysfunction and even lethality. By now almost all researches concentrate on the change,pathophysiological role and related therapies of NO during septic and hemorrhagic shock. NOS inhibitor,L-arginine,PARS inhibitor etc were proved to have therapeutic benefits,and applied in the clinical studies of septic shock. But traumatic shock differs from the "pure" hemorrhagic shock and septic shock. There is still some controversy over the changes and role of NO during traumatic shock.Objective To measure the levels of nitrate/nitrite (NOaY N02~,stable products of NO) in serum and tissue and investigate the mechnism of the NO synthase during traumatic shock. NOS inhibitor and L-arginine were infused during resuscitation in order to identify the effect on traumatic shock,which would provide experimental foundation for the clinical study.Methods and Results1 .Dynamic changes of serum levels of NO during traumatic shockA rat traumatic shock model was made by fracturing bilateral thighbone. Serum levels of nitrate/nitrite were measured by the method of Griess.The results showed that there were no significant changes of serum NO level during traumatic shock. But serum NO level (16.57 + 5.13 u mol L-1) of 1 hour after resuscitation decreased significantly(p<0.01)compared with the control group(31.66+3.56 u mol L-1 ),and then increased to the peak level at 6 hours after resuscitation (72.29+24.39 u mol L-1),and still maintained at a high level 24 hours after resuscitation. No apparent changes of serum NO levels were observed in those rats without resuscitation .Z.Changes of NO levels in organs during traumatic shock6 hours after resuscitation,heart,lung,liver,spleen,kidney and small intestine were dissected,homogenated,and then NO in homogenate was measured. The results showed that NO levels were significantly increased (p<0.05) in liver(201.83 + 52.44 u mol kg-1),spleen(142.90 + 20.27 u mol kg'1),and kidney (218.49 +29.50 ti mol kg-1) compared with the control group(121.63+28.82,141.19+14.68,114.39+11.12umol kg-1) in the delayed phase of shock,which suggested that kidney,liver and spleen might be responsible for the increase of NO during traumatic shock.. 3. Effects of NOS inhibitor and L-arginine on the survival rate of traumatic shock rats.During rescuscitation,10 mg kg-1 L-NAME,100 mg kg-1 AG,10 mg kg-1,100 mg kg'and 300 mg kg-1 L-Arg were infused to traumatic shock rats. The results showed that there was no significant changes of survival time and 24 h survival rate between L-NAME and control group;the survival time of AG group (28.72 +6.25 h) and all L-Arg groups( 27.03 + 4.37 h,30.64 +8.77 h,38.03 +8.62 h) prolonged apparently(p<0.05),and their 24 h survival rates (80%,80%,80%,100%) were also increased(p<0.01),while control group is only 10%. The survival time of L-Arg(300 mg kg-1) group is longer than that of AG,L-Arg (10 mg kg-1) and L-Arg(100 mg kg-1) groups,and the 36 h survival rate of L-Arg (300 mg kg-1) (70%) group is higher than that of control group(0%) and L-Arg (10 mg-kg-1) group(0%)(p<0.01).ConclusionNo significant alterations of serum NO level was observed during traumatic shock.,NO level first decreased transiently and then increased after resuscitation. There were no significant changes of serum NO levels in those traumatic shock rats without rescuscitation,which indicate that NO synthase during traumatic shock might be caused by reperfusion injury. Tissues NOlevels increased significantly in liver,spleen,kidney in the delayed phase of shock.Kidney,liver,spleen are responsible for the increase of NO during traumatic shock. L-NAME,a nonselective NOS inhibitor,did not enhance the survival time,but iNOS inhibitor AG and L-Arg exert benefitial effects on traumatic shock rats. T...
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