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Nitric oxide synthesis inhibition does not improve the hemodynamic response to hemorrhagic shock in dehydrated
I P Brown1, R L Williams, M D McKirnan
1Department of Pathology, University of California-San Diego 92093, USA.
Abstract:
Nitric oxide (NO) may influence the hemodynamic response to hemorrhage. To test this hypothesis, the NO synthesis inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) was administered to conscious, dehydrated swine during a 37% blood volume hemorrhage and a 180 min recovery period without fluid resuscitation. L-NAME (.75 mg/kg bolus plus constant infusion of .75 mg/kg/h) was given via a central intravenous catheter during the bleed. The selectivity and specificity of L-NAME as a NO synthesis inhibitor in pigs was validated in pilot studies. The present study shows that inhibition of NO synthesis with L-NAME had no significant effect on the major hemodynamic parameters during and after hemorrhage when compared to dehydrated and euhydrated control groups. Only stroke volume and A-VO2 were significantly different from controls. Mortality was 83% for the L-NAME group and 44% for controls at 180 min of recovery (NS). The results suggest that NO synthesis inhibition provides no hemodynamic benefit during hemorrhage in dehydrated, conscious swine.