作者: Thomas F. Lindsay , Shinta Liauw , Alex D. Romaschin , Paul M. Walker
DOI: 10.1016/0741-5214(90)90360-M
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摘要: Prolonged ischemia to skeletal muscle as occurs after an acute arterial occlusion results in alterations adenine nucleotide metabolism. Adenosine triphosphate continues be used for cellular functions, and ischemia-induced degradation of phosphorylated nucleotides is initiated. In this experiment we demonstrated the time-dependent aspect depletion during production large quantities soluble precursors. addition, studied rate conversion xanthine dehydrogenase oxidase, a potential source oxygen-free radicals, controlled periods total normothermic (4 hours 5 hours) reperfusion phase. During complete creatine phosphate occurred both groups, adenosine fell from 22.1 +/- 1.3 10.3 1.4 mumol/gm dry weight 4 21.6 0.7 3.9 0.8 (p less than 0.05). reperfusion, phosphokinase resynthesis but levels were not significantly increased greater A washout lipid products metabolism equally groups. The relationship between measured by energy charge groups 0.05), shorter period it returned normal early did ischemia. There was 21% 4% necrosis 51% 8% ischemic stress when assessed at 48 hours. conclusion, degree degeneration determined primarily length period, may most important determinant ultimate extent that interruption circulation.