Role of carotid and aortic bodies in mediating the increase in cardiac output during anoxemia

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Abstract
In 14 anesthetized dogs the inhalation of 5% oxygen in nitrogen for 2.5 min caused an increase in cardiac output, measured by the dye dilution technique (16.8% ±6.1 se). After surgical carotid-aortic chemoreceptor denervation, anoxemia still increased cardiac output (27.1% ±6.7 se). An effect of chemoreceptor denervation was the reduction of the control level of cardiac output. In the presence of a similar reduction of cardiac output by bleeding (innervated animal) anoxemia caused a greater increase in cardiac output than in the control preparation. The increase in cardiac output was accompanied by a decrease in total peripheral systemic resistance in the denervated state as compared to an increase in the innervated state. The increase in cardiac output during anoxemia was not prevented by complete spinal anesthesia. A possible cause for the increase in the denervated animal is a combination of the increase in venous return and fall in total systemic peripheral resistance.

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