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Denervation deprives the heart of its normal adrenergic and cholinergic control via the sympathetic and parasympathetic pathways. In a heart which is blood supplied by a donor animal of the same species, normal contractility is maintained, probably by blood borne catecholamines or possibly by unknown inotropic agents of the donor. A heart receiving blood oxygenated by isolated lungs is in a state of failure. Substitution of blood by a cell and protein free solution diminishes oxygen availability in cardiac muscle, both in the perfused and bathed preparation. In the unphysiological environment, myocardial cells lose K+ and gain Na+. Under best possible conditions of oxygen supply but in a later stage of perfusion, contractility during rhythmical stimulation is depressed more at lower than at higher rates. Frequency potentiation and the inotropic effectiveness of noradrenaline is more pronounced in vitro than in situ. In excised papillary muscles and ventricular and atrial strips, the disarrangement and a more or less severe lesion of individual fibres accelerates the decay in mechanical performance. The role of endogenous catecholamines for the maintenance of normal contractility in situ and in vitro is still a matter of discussion.

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