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钙离子和阿托品对大鼠心房肌内毒素诱导的收缩功能障碍的影响。

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

作者信息

Ashorobi R B, Kpohraror B O

机构信息

Department of Pharmacology, College of medicine, University of Lagos, Nigeria.

出版信息

East Afr Med J. 1995 Apr;72(4):263-6.

PMID:7621764
Abstract

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.

摘要

从经腹腔注射每千克体重3.7×10⁹热灭活的纯大肠杆菌(内毒素)的大鼠身上获取离体心房肌标本,用于研究诱导的心肌收缩功能障碍的严重程度以及一些自主神经药物和钙的作用。在治疗后48小时和72小时从内毒素休克大鼠身上取出两条心房肌条。对照组腹腔注射0.2ml等渗盐水,并在与治疗组相同的时间段处死。休克大鼠心房肌条的最大收缩力(振幅)显著降低(p<0.05)。心房收缩力的最大缺陷表现为对低细胞外Ca²⁺(0.12mM)浓度的反应性改变。在正常Ca²⁺培养基中将Ca²⁺浓度增加1 - 3mM可使收缩力显著增强,增加88±5.9%(p<0.005)。阿托品(5×10⁻⁷ - 1.5×10⁻⁶M)在休克心房肌条中产生正性肌力作用,最大增加80±7.1%(p<0.05)。另一方面,去甲肾上腺素(1×10⁻⁷ - 10⁻⁶)未产生任何显著的肌力作用。去甲肾上腺素(1×10⁻⁶M)和阿托品(1.5×10⁻⁵M)联合给药产生的正性肌力作用在幅度上与阿托品(5×10⁻⁷M)相比并无更大。本研究表明,Ca²⁺和阿托品可能在内毒素诱导的休克状态中发挥有益作用。它还证实了心肌参与了这种疾病的发病机制。

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