In an in vivo dog model, intracoronary nicotine and acetylcholine increased myocardial contractile force, an effect modulated by adrenergic and cholinergic blockade.
May suggest adrenergic mediation of nicotine effects on contractility in dogs; leaves open human relevance.
In anaesthetized dogs intracoronary infusions of high doses of nicotine and acetylcholine increased myocardial contractile force and this could be prevented by pre-treatment with desmethylimipramine or phenoxybenzamine.2. The inotropic effect of nicotine was brief and subsided during the continuing infusion of the drug. The infusion of nicotine did not reduce the inotropic effects of cardiac sympathetic nerve stimulation.3. The motropic effect of intracoronary acetylcholine often fluctuated during prolonged infusions and was not altered by pretreatment with atropine. Acetylcholine infusions reduced the inotropic responses produced by cardiac sympathetic nerve stimulation and led to a substantial transient reduction in the associated pressor responses. Intracoronary acetylcholine also reduced the pressor and inotropic effect of intravenous noradrenaline. The attenuation of these adrenergic cardiovascular responses by acetylcholine was prevented by atropine.
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Gordon Ross (1973) studied this question.
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