Endotoxin and myocardial failure: role of the myofibril and venous return.
The effects of gramnegative endotoxin-induced myocardial failure in the pentobarbital-anesthetized dog were examined by monitoring its influence on cardiac myofibrillar ATPase activity. Myofibrils were isolated from endo- and epicardial portions of the left ventricular wall. ATPase activities were determined in animals treated with 4 mg/kg endotoxin and monitored 5 h, in animals monitored for 5 h without endotoxin (controls), and in animals implanted with a unilateral femoral shunt and given endotoxin. No differences were seen in the activities between the endo- and epicardial portions of any preparation. Activity was significantly depressed in endotoxemic animals. Increasing venous return by 313 +/- 71 ml/min significantly increased coronary flow by reducing coronary vascular resistance and prevented any observed depression of myofibrillar ATPase activity. In in vitro studies, adding endotoxin directly to a myofibril preparation did not modify normal activity. It appears that the mechanical and myofibrillar dysfunctions are due to the action of endotoxin at sites not associated with the actomyosin ATPase, but may be due to the production of an intermediary agent in concert with a decreased venous return.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001163:Arteriovenous Anastomosis; D002118:Calcium / Q000378:metabolism; D004285:Dogs; D005260:Female; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism*; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D009210:Myofibrils / Q000378:metabolism*; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism*
D000251:Adenosine Triphosphatases; D008274:Magnesium; D002118:Calcium