Abstract
In anesthetized dogs, monophasic action potentials from the right atrium and the right ventricle were recorded by an intracardiac suction electrode technique, together with the electrocardiogram (standard lead II). The animals were subjected by ventilation with 100% nitrogen to periods of severe, systemic hypoxia. The separate effects of myocardial oxygen deficiency and increased autonomic influence on the myocardial excitation were studied, using animals with (1) intact autonomic innervation of the heart, (2) parasympathetically denervated hearts and (3) parasympathetically and sympathetically denervated hearts. During severe, systemic hypoxia the parasympathetic influence predominated over the sympathetic and induced a pronounced shortening of the duration of the atrial monophasic action potential whereas the increased sympathetic activity induced no alteration of the duration of the ventricular monophasic action potential. The myocardial oxygen deficiency induced a shortening of the duration of the atrial monophasic action potential which appeared earlier than that of the duration of the ventricular monophasic action potential when the autonomic influences were excluded. During the recovery from myocardial oxygen deficiency, the duration of the atrial monophasic action potential was normalized earlier than that of the ventricular monophasic action potential. Pronounced ST‐segment and T‐wave elevations in the ECG were in general recorded when the period of severe, systemic hypoxia exceeded 2 min.

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