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We studied the effects of the nitric oxide donor, S-nitroso-N-acetylpenicillamine (SNAP), in rat traumatic shock characterized by hypotension, increases in plasma free amino-nitrogen (5.3 ± 0.5 U/ml vs. 2.5 ± 0.3 U/ml controls) and intestinal myeloperoxidase activities (2.7 ± 1.0 U/100 mg vs. 0.2 ± 0.1 U/100 mg controls), and a survival time of 143 ± 20 min. Moreover, superior mesenteric artery rings isolated from rats in traumatic shock relaxed to the endothelium-dependent vasodialator acetylcholine only 21 ± 6% of U-46619 induced contraction. Administration of 100 μg/kg SNAP 10 min post-trauma followed by 10 μg/kg/h infusion prolonged survival time to 273 ± 18 min (p < .05), attenuated the increases in plasma free aminonitrogen (3.1 ± 0.4 U/ml, p < .05) and tissue myeloperoxidase activities (0.6 ± 0.3 U/100 mg, p < .05). Moreover, SNAP significantly preserved superior mesenteric artery endothelial function; the vasorelaxation to acetylcholine was 54 ± 4% (p < .01). Protective effects were not seen in traumatic shock rats treated with the non-NO-donating parent compound N-acetylpenicillamine. These results indicate that SNAP affords significant protection in murine traumatic shock which may be achieved through maintenance of systemmic blood pressure, preservation of vascular endothelial integrity, and inhibition of neutrophil-endothelial interaction and the resultant reduced microvascular leakiness.