Abstract

In the anaesthetized, open-chest rat, electrical stimulation of the sympathetic or parasympathetic nerves in the cervical area produced significant changes in the heart rate. The subsequent alterations in cardiac output and in total peripheral resistance did not alter the oxygenation of resting skeletal muscle. This means that the skeletal muscle of intact rats provided sufficient O2 to withstand shortlasting changes in hemodynamics. The increase in mean tissue PO2 on the heart after the bilateral vagotomy was the consequence of an increased perfusion due to the increased heart rate. The absence of vasoconstrictor nerve impulses after the bilateral dissection of the sympathetic cord induced a dilation of the vascular bed and therefore an increase in the tissue PO2 of the heart.

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