The influence of venous return on cardiac mechanical and sarcoplasmic reticulum function during endotoxemia.
E. coli endotoxin (0.03 mg/ml) added to blood perfusing a heart-lung preparation with a venous return of 600 ml/min produced a significant depression in ventricular function within 4 hours. Fragmented sarcoplasmic reticulum isolated from the myocardium of the endotoxin-perfused heart-lung preparations showed depressed calcium uptake rates and ATPase activity. When venous return was increased to 1,200 ml/min, gram-negative endotoxin had no effect on ventricular function, isolated fragmented sarcoplasmic reticulum calcium uptake, or ATPase activity. These observations suggest that gram-negative endotoxin or a product thereof acts in synergism with low venous return in order to depress myocardial function.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D009206:Myocardium / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects* / Q000378:metabolism; D012772:Shock, Septic / Q000378:metabolism
D004731:Endotoxins; D000251:Adenosine Triphosphatases; D002118:Calcium