Vagal innervation influences the whole body oxygen consumption-delivery relationship in the dog.

Abstract

Vagotomy alters regional blood flow distribution by interrupting the tonic central inhibitory effect of cardiopulmonary vagal afferent nerves on sympathetic outflow predominantly to the renal, splanchnic, and cutaneous circulations. We hypothesized that the alteration of blood flow distribution by vagotomy would lead to disruption of the oxygen consumption-oxygen delivery relationship (VO2/DO2), increase critical DO2 (DO2Crit), and decrease whole-body oxygen extraction ratio (O2ER). Nineteen chloralose-anesthetized, paralyzed, splenectomized dogs were submitted to either bilateral vagosympathectomy (n = 7), bilateral vagotomy (n = 6), or sham denervation (n = 6) following baseline cardiorespiratory parameter measurement. VO2 was measured by indirect calorimetry and carotid blood flow by ultrasonic flow probe. Incremental hemorrhages (1-5 mL/kg) were performed to determine the VO2/DO2 relationship. Cardiorespiratory parameters were measured after each hemorrhage at steady-state VO2. DO2Crit was derived from the VO2/DO2 relationship using a best-fit regression analysis technique. The average DO2Crit values of the vagotomy (9.1 +/- .54) and vagosympathectomy (11.5 +/- 1.2 mL/min/kg) groups were significantly greater than the control group (7.72 +/- .43). After hemorrhage had been performed to a point that decreased mean arterial pressure to approximately 70 mmHg from baseline values, carotid blood flow in the vagosympathectomy group was significantly greater than the control group. We conclude that vagotomy disrupts the VO2/DO2 relationship. Vagosympathectomy causes a severe disruption of the VO2/DO2 relationship, probably by the combined effect of vagotomy and interruption of sympathetic nervous system control of blood flow to the head and neck.