AJP - Heart and Circulatory Physiology, Vol 250, Issue 1 7-15, Copyright © 1986 by American Physiological Society
Effect of hypoxia and hypercapnia on neurohypophyseal blood flow
D. F. Hanley, D. A. Wilson and R. J. Traystman
Neurohypophyseal blood flow responses to hypoxia and hypercapnia were
studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content
was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either
decreasing O2 tension (hypoxic hypoxia, HH) or by increasing
carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2
tension. In all animals HH and COH resulted in similar increases in total
cerebral blood flow (239 and 300%, respectively). Regional cerebral blood
flow showed a similar increase for all brain regions except the
neurohypophysis (NH). The NH increased its blood flow with HH
(approximately 320% of control) but was unchanged with COH (117% of
control). The responsiveness of NH blood vessels was tested under
conditions of hypercapnia (10% CO2) and HH with blood pressure controlled
by concurrent hemorrhage. The response of NH vessels to altered arterial O2
tension occurs independently of blood pressure. Systemic [H+] or CO2
tension produce only small changes in NH blood flow. These data suggest
that hypoxic and hypercapnic regulatory mechanisms for the NH are different
from those of other brain regions. The precise mechanism by which the NH
hypoxic response occurs remains unclear, but our data suggest an important
role for systemic arterial O2 tension and chemoreceptors.
