Effect of a xanthine oxidase inhibitor on adenine nucleotide degradation in hemorrhagic shock.
Biochemical effects of treatment with a xanthine oxidase inhibitor (allopurinol) were investigated in an experimental hemorrhagic shock procedure. Allopurinol pretreatment abolished the increase in plasma uric acid which occurs in untreated dogs during hemorrhagic hypotension and resulted in a much lesser increase in plasma allantoin. The pancreatic, liver and duodenal adenosine triphosphate (ATP) and total adenine nucleotides of untreated dogs were severely reduced, while those of allopurinol-pretreated dogs were essentially normal 2 h following reinfusion. Pretreatment with allopurinol resulted in a significantly lesser release of the lysosomal enzymes, acid phosphatase and beta-glucuronidase, following reinfusion. When treatment was delayed until after reinfusion, an infusion of hypoxanthine + allpurinol restored normal ATP concentrations. The role of adenine nucleotide breakdown in irreversible shock is discussed.
D000135:Acid Phosphatase / Q000097:blood; D000227:Adenine Nucleotides / Q000378:metabolism*; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000481:Allantoin / Q000097:blood; D000493:Allopurinol / Q000494:pharmacology*; D000818:Animals; D004285:Dogs; D004386:Duodenum / Q000378:metabolism; D005966:Glucuronidase / Q000097:blood; D008099:Liver / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism; D012771:Shock, Hemorrhagic / Q000378:metabolism*; D014527:Uric Acid / Q000097:blood; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors
D000227:Adenine Nucleotides; D014527:Uric Acid; D000481:Allantoin; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000493:Allopurinol; D000255:Adenosine Triphosphate; D014969:Xanthine Oxidase; D000135:Acid Phosphatase; D005966:Glucuronidase