ALLOPURINOL PLUS STANDARD RESUSCITATION PRESERVES HEPATIC BLOOD-FLOW AND FUNCTION FOLLOWING HEMORRHAGIC-SHOCK

To determine the contribution of ischemia-reperfusion injury (IRI) to the blood flow deficit and hepatocellular dysfunction seen after resus citation from hemorrhagic shock, the xanthine oxidase inhibitor allopu rinol was given to rats as a 50 mg/kg bolus after shock but before res uscitation and continued as a 25 mg/kg/h infusion. Resuscitation with shed blood and lactated Ringer's restored cardiac output and blood pre ssure in both groups. Control animals demonstrated a reduction in tota l hepatic and effective hepatic blood flow to 59% and 43% of baseline values, respectively. Allopurinol resulted in a return to baseline val ues of both variables. Allopurinol treatment resulted in a 350% increa se in xanthine, a 630% increase in hypoxanthine, and a 70% reduction i n uric acid concentrations. These data suggest that IRI contributes to the organ dysfunction and blood flow deficits seen after resuscitated hemorrhagic shock the effect of which can be attenuated by the additi on of the xanthine oxidase inhibitor allopurinol to standard resuscita tion.