Though the increased heart rate which accompanies acute hypoxia is well known, the mechanism of its genesis is incompletely understood. Sands and DeGraff (1) and Wiggers(2) have shown that it depends chiefly upon reduced tonic activity of the vagal cardio-inhibitory center and in lesser degree upon increased activity of the sympathetic cardio-accelerator center. However, the channels through which hypoxia operates when it alters the action of these centers have not been demonstrated.The suggestion has been made repeatedly (3-5) that the changes in heart rate which accompany alterations of arterial oxygen tension are initiated at the chemoreceptors of the carotid and aortic bodies. Thus, it has been assumed either that hypoxic stimulation of these chemoreceptors would reflexly accelerate the heart or, conversely, that hyperoxic diminution of their tonic activity would do the reverse, Since the literature seemed devoid of experimental evidence bearing directly upon these assumptions, we have performed experiments to determine the chemoreflex response of heart rate to hypoxia. The results do not support the suggestion that hypoxic cardiac acceleration is initiated at the carotid or aortic bodies. of recording heart rate during the application of hypoxic stimuli carefully restricted to the carotid chemoreceptor region. Dogs were anesthetized with morphine sulphate (4 mg/ kilo) and urethane (1 g/kilo) and their heart rates recorded from a carotid artery with a membrane manometer. Breathing was recorded to indicate the intensity of chemoreceptor stimulation. While preserving Hering's nerves, all vessels efferent to each carotid bifurcation were ligated a few millimeters beyond their origin, The vascularly isolated carotid regions were then supplied with blood from a perfusion source, the blood entering through cannulae placed in the commun carotid arteries and leaving through cannulae in the external carotid arteries from which it returned to the perfusion source through an adjustable resistance. Duri'ng controlled periods, normally aerated heparinized blood flowing in this circuit was rendered hypoxic in known degree. I n some instances, the perfusion source was a donor animal inhaling a gas mixture low in partial pressure of oxygen for short periods. I n other experiments, autoperfusion apparatus was used (9). Cyanide was administered by injecting directly into the carotid perfusion circuit, I n most experiments, arterial blood pressure compensators (9 ) minimized variations of pressoreceptor stimulation. I n some experiments, natural breathing was allowed. I n others, constant artificial pulmonary ventilation with open pneumothorax was imposed.Results and discussion. Representative responses of eight animals are summarized in Table I which gives only the maximum deviation of heart rate from control values during each hypoxic episode. In Fig. 1, plotted summaries of the heart rate during 3 complete hypoxic episodes and one cyanide administration are given in order to show the pattern and time relationships of the res...

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