Contractility of endotoxic atria.
Previous studies showed that atria of guinea pigs pretreated with endotoxin had a reduced sensitivity to norepinephrine. Since accumulation of [3H]norepinephrine was reduced in atria from endotoxin-treated guinea pigs, the reduced responsiveness of such atria to norepinephrine cannot be explained on the basis of endotoxin effect on the uptake of the amine. In the present study, the relative enhancement of the contractile force of the atria during paired stimulation in endotoxic and control animals was of equal magnitude. The results indicate that reduced sensitivity to norepinephrine may not be related only to endotoxin effect on the contractility of the myocardium. Endotoxin treatment may induce certain changes in the sequence of steps involved in the process of excitation-contraction coupling in the myocardium. The most likely locus of endotoxin action appears to be the heart cell membrane.
D000818:Animals; D002415:Cats; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology*; D006168:Guinea Pigs; D006325:Heart Atria / Q000187:drug effects* / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects*; D009638:Norepinephrine / Q000378:metabolism / Q000494:pharmacology*; D012772:Shock, Septic / Q000503:physiopathology; D013268:Stimulation, Chemical
D004731:Endotoxins; D009638:Norepinephrine