[Prevention of heart damage of sodium oxybutyrate in terminal states caused by acute blood loss].
After clinical death caused by acute blood loss, hearts of rats were essentially damaged. In isolated hearts, these damages were manifested in the decrease of major contractility parameters with the preferential disturbance of relaxation, increased loss of enzymes (lactate dehydrogenase and creatine phosphokinase) into the perfusate and a significant decrease of the cardiac muscle resistance to hypoxia. All these effects could be, to a large extent, prevented by gamma-hydroxybutyric acid, an endogenous metabolite having central inhibitory effect, which was administered to the animals before the loss of blood.
D000208:Acute Disease; D000818:Animals; D003402:Creatine Kinase / Q000097:blood; D003643:Death; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D006339:Heart Rate / Q000187:drug effects; D006470:Hemorrhage / Q000150:complications* / Q000503:physiopathology; D006885:Hydroxybutyrates / Q000627:therapeutic use*; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D051381:Rats; D012151:Resuscitation; D012978:Sodium Oxybate / Q000627:therapeutic use*; D013997:Time Factors
D006885:Hydroxybutyrates; D012978:Sodium Oxybate; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase
Preduprezhdenie povrezhdeniĭ serdtsa oksibutiratom natriia pri terminal'nykh sostoianiiakh, vyzvannykh ostroĭ krovopotereĭ.