Effects of calcium ions and atropine on endotoxin-induced contractility deficit in rat atrial muscle.

Isolated atrial muscle preparations obtained from rats injected (ip) with 3.7 x 10(9) per kg/body weight heat killed pure E. coli (endotoxin) were used to investigate the severity of induced mycocardial inotropic dysfunction and the effects of some autonotic agents and calcium. Both atrial strips were removed from endotoxin-shock rats at 48 and 72 hours post treatment. The control groups were given (ip) 0.2ml of isotonic saline and sacrificed at the same period as the treated groups. Maximum developed contractile force (amplitude) were significantly depressed in atrial strips of shock rats (p < 0.05). Maximum deficit in atrial contractility was characterised by altered responsiveness to low extra cellular Ca2+ (0.12mM) concentration. Increasing Ca2+ concentration by 1-3 mM in a normal Ca2+ medium significantly enhanced the contractile force by an increase of 88 +/- 5.9% (p < 0.005). Atropine (5 x 10(-7) - 1.5 x 10(-6)M) produced positive intropic effect with a maximum increase of 80 +/- 7.1% (p < 0.05) in the shock atrial strips. Noradrenaline (1 x 10(-7)-10(-6)) on the other hand, did not produce any significant inotropic effect. Concomitant administration of noradrenaline (1 x 10(-6)M) and atropine (1.5 x 10(-5)M) produced positive inotropic effect which is not greater in magnitude compared with atropine (5 x 10(-7)M). This study suggests that Ca2+ and atropine may provide beneficial effects in endotoxin-induced shock state. It also confirms the involvement of myocardium in the pathogenesis of this condition.