Metabolic effects of fructose diphosphate in hypoxic and ischemic states.
A number of methods have been used to protect organ systems and cells from the ravages of ischemia and hypoxia. Some have attempted to reduce the metabolic needs, such as by hypothermia, cardioplegia, and slow calcium channel blockers. Others have attempted to provide the metabolic needs, such as by cold blood cardioplegia and solutions of readily metabolized substrates. Our work has centered on the use of fructose 1-6-diphosphate, which can be used anaerobically after glycolysis has been stopped by the effects of anoxia and acidosis. Fructose diphosphate has proved effective experimentally in ameliorating the effects of local and global ischemia of the heart. It has also been found to be of value in many hypoxic or ischemic states including traumatic, septic, endotoxic, and hypovolemic shock. The rationale and a survey of preliminary results are presented.
D000818:Animals; D004285:Dogs; D005635:Fructosediphosphates / Q000378:metabolism* / Q000627:therapeutic use; D006019:Glycolysis; D006598:Hexosediphosphates / Q000378:metabolism*; D000860:Hypoxia / Q000378:metabolism*; D007511:Ischemia / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D010732:Phosphofructokinase-1 / Q000378:metabolism; D012769:Shock / Q000188:drug therapy
D005635:Fructosediphosphates; D006598:Hexosediphosphates; D010732:Phosphofructokinase-1; C029063:fructose-1,6-diphosphate