title: Metabolic effects of hyperbaric oxygen in postischemic muscle.
abstract: In traumatic injuries to the extremities, with a circulatory insufficiency, the resultant ischemia leads to decreasing levels of the energy-rich compounds adenosine triphosphate (ATP) and phosphocreatine (PCr) and increasing levels of lactate in muscle. A tourniquet model for temporary ischemia was used to determine if hyperbaric oxygen treatment could enhance the cellular metabolic restitution when the circulation was restored. The circulation of the rat hindlimb was interrupted for 1.5 and 3 hours. After 1.5 hours of ischemia, the levels of adenosine triphosphate, phosphocreatine, and lactate were restored to normal in muscle biopsies taken 5 hours after the ischemia. After 3 hours of ischemia, there were marked reductions of adenosine triphosphate and phosphocreatine and elevated lactate values in the postischemic muscle, indicating severe ischemic damage. Hyperbaric oxygen treatment at 2.5 atm for 45 minutes reduced these changes significantly. A certain number of hyperbaric oxygen treatments were necessary to maintain this effect. It is concluded that repeated hyperbaric oxygen treatments in the postischemic phase stimulate aerobic metabolism.
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006614:Hindlimb; D006931:Hyperbaric Oxygenation; D007511:Ischemia / Q000628:therapy*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009132:Muscles / Q000098:blood supply* / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow; D013997:Time Factors; D014111:Tourniquets
chemical_list: D007773:Lactates; D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate