XANTHINE-OXIDASE MEDIATES MYOCARDIAL INJURY AFTER HEPATOENTERIC ISCHEMIA-REPERFUSION

Objectives: To determine if myocardial injury results from hepatoenter ic ischemia reperfusion. We also proposed to determine if this remote heart injury is mediated by a xanthine oxidase-dependent mechanism. De sign: Randomized, controlled animal study. Setting: University based a nimal research facility. Subjects: Thirty six New Zealand white male r abbits, weighing 1.8 to 3 kg. Interventions: Anesthetized rabbits were randomly assigned to one of four groups (n = 9 per group): a) a sham- operated group; b) a sham operated group pretreated with sodium tungst ate (xanthine oxidase inactivator); c) an aorta occlusion group; and d ) an aorta occlusion group pretreated with sodium tungstate, Descendin g thoracic aorta occlusion was maintained for 40 mins with a 4-Fr Foga rty embolectomy catheter, followed by 2 hrs of reperfusion. Measuremen ts and Main Results: Myocardial injury, manifested by increased circul ating crestine kinase-MB fraction activity, was significantly associat ed with aortic occlusion and reperfusion (p < .05). Sodium tungstate p retreatment significantly (p < .05) reduced circulating and myocardial xanthine oxidase activity, Xanthine oxidase inactivation by sodium tu ngstate significantly decreased circulating creatine kinase-MB fractio n activity after hepatoenteric ischemia-reperfusion (p < .05). Finally , circulating creatine kinase-MB fraction activity was significantly a ssociated with circulating xanthine oxidase activity (r(2) = .85; P < .001). Conclusions: We conclude that remote myocardial injury is cause d by hepatoenteric ischemia reperfusion. The pathoetiology of this myo cardial injury involves a xanthine oxidase-dependent mechanism.