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  • Title: Role of xanthine oxidase and leukocytes in postburn cardiac dysfunction.
    Author: Horton JW, White DJ.
    Journal: J Am Coll Surg; 1995 Aug; 181(2):129-37. PubMed ID: 7627385.
    Abstract:
    BACKGROUND: Recent studies suggest that the cardiac dysfunction that occurs after a major burn is mediated by oxygen-derived free radicals. This hypothesis is based on the fact that superoxide dismutase and catalase, given with fluid resuscitation from burn injury, provided significant cardioprotection. STUDY DESIGN: In this present study, rats received either enteral allopurinol or tungsten-enriched diets to determine if xanthine oxidase mediates postburn defects in cardiac contraction and relaxation. Polymorphonuclear neutrophil (PMN) were depleted to examine the contribution of PMN-derived factors to postburn cardiac dysfunction. Rats were divided into eight groups: groups 1 to 6 received regular chow, and groups 7 and 8 received tungsten-enriched diets for 14 days before study. Groups 2, 4, 6, and 8 were given a third-degree burn comprising 43 +/- 2 percent total body surface area and were resuscitated with Ringer's lactated solution for 24 hours (4 mL/kg/percent burn). In group 2, burned rats received fluid resuscitation alone; in group 4 (n = 10), rats were given allopurinol, 10 mg/kg daily by gastric lavage for five days preburn, group 6 (n = 11) received vinblastine (0.75 mg/kg) four days preburn, and group 8 (n = 11) received tungsten-enriched diets for 14 days before burn; sham burn controls included vehicle-treated (n = 10), allopurinol-treated (n = 8), PMN-depleted (n = 8), and tungsten-fed rats (n = 11) (groups 1, 3, 5, and 7, respectively). RESULTS: Burn injury produced mild hypotension, hypothermia, bradycardia, and a significant decrease in left ventricular performance, despite aggressive fluid resuscitation (group 2). Allopurinol, tungsten-enriched diets, and PMN depletion partially attenuated burn-induced cardiac contractile dysfunction and improved left ventricular responsiveness to increases in preload, coronary flow rate and exogenous calcium. CONCLUSIONS: Our data suggest that xanthine oxidase-derived oxygen metabolites and PMN-derived mediators contribute to postburn cardiac contractile deficits.
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