Vagotomy alters regional blood flow distribution by interrupting the t
onic central inhibitory effect of cardiopulmonary vagal afferent nerve
s on sympathetic outflow predominantly to the renal, splanchnic, and c
utaneous circulations. We hypothesized that the alteration of blood fl
ow distribution by vagotomy would lead to disruption of the oxygen con
sumption-oxygen delivery relationship (VO2/DO2), increase critical DO2
(DO2Crit), and decrease whole-body oxygen extraction ratio (O(2)ER).
Nineteen chloralose-anesthetized, paralyzed, splenectomized dogs were
submitted to either bilateral vagosympathectomy (n = 7), bilateral vag
otomy (n = 6), or sham denervation (n = 6) following baseline cardiore
spiratory parameter measurement. VO2 was measured by indirect calorime
try and carotid blood flow by ultrasonic flow probe. Incremental hemor
rhages (1-5 mL/kg) were performed to determine the VO2/DO2 relationshi
p. Cardiorespiratory parameters were measured after each hemorrhage at
steady-state VO2. DO2Crit was derived from the VO2/DO2 relationship u
sing a best-fit regression analysis technique. The average DO2Crit val
ues 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 decr
eased mean arterial pressure to approximately 70 mmHg from baseline va
lues, carotid blood flow in the vagosympathectomy group was significan
tly greater than the control group. We conclude that vagotomy disrupts
the VO2/DO2 relationship. Vagosympathectomy causes a severe disruptio
n of the VO2/DO2 relationship, probably by the combined effect of vago
tomy and interruption of sympathetic nervous system control of blood f
low to the head and neck.