AJP - Heart and Circulatory Physiology, Vol 245, Issue 6 962-H968, Copyright © 1983 by American Physiological Society
Mediation of pressor responses to cerebral ischemia by superficial ventral medullary areas
C. V. Rohlicek and C. Polosa
The effects on the pressor response to cerebral ischemia (CIR) of
superfusion of the ventral medullary surface with artificial cerebrospinal
fluid (CSF) containing local anesthetic was investigated in 10
sinoaortic-denervated, anesthetized cats. Prior to application of the local
anesthetic, occlusion of the common carotid and vertebral arteries caused
an increase in mean systemic arterial pressure (SAP) of 58 +/- 7 mmHg (+/-
SE) from an initial level of 98 +/- 6 mmHg. Following 108 +/- 15 s of
superfusion with artificial CSF containing 2% procaine, the CIR decreased
to 19 +/- 3 mmHg. At this time phrenic nerve activity had been eliminated
but basal SAP had only decreased by 14 +/- 2 mmHg, and significant
neurogenic vasomotor tone remained. The residual CIR can be accounted for
by the passive increase in systemic resistance due to occlusion of the
cerebral vascular bed. The effects of procaine were reversible. On
attenuation of the CIR, electrical stimulation of pressor points 2-4 mm
from the ventral medullary surface was still effective. Autoradiographic
analysis following application of 14C-labeled lidocaine showed that
attenuation of the CIR occurred when estimated concentrations of the
anesthetic sufficient to block nerve conduction extended 85 micron from the
ventral medullary surface. These results indicate that the CIR is mediated
by superficial structures in the ventral medulla that are not involved in
the generation of a major fraction of basal vasomotor tone.
