Cell sodium and the induction of myocardial injury after adrenaline.
Accumulation of calcium in cardiac cells during catecholamine induced injury is considered a major pathogenetic factor but its mechanism has not been defined. During initiation of injury in an intact canine model, cell sodium was enhanced fourfold in myocardium after a local infusion of epinephrine via the left anterior descending coronary artery for a 60 min period. Tissue calcium was enhanced and a major role for the Na-Ca carrier system is suggested. Regional myocardial function, blood flow and electrocardiogram responses to toxic levels of the catecholamine have been contrasted with ischaemic injury.
D000818:Animals; D001834:Body Water / Q000378:metabolism; D009202:Cardiomyopathies / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D003326:Coronary Circulation / Q000187:drug effects; D004285:Dogs; D004562:Electrocardiography; D004837:Epinephrine / Q000633:toxicity*; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D012964:Sodium / Q000378:metabolism*
D012964:Sodium; D004837:Epinephrine