AJP - Heart and Circulatory Physiology, Vol 249, Issue 4 827-H833, Copyright © 1985 by American Physiological Society
Humoral factors may mediate increased rat hindquarter blood flow in portal hypertension
R. J. Korthuis, J. N. Benoit, P. R. Kvietys, M. I. Townsley, A. E. Taylor and D. N. Granger
Chronic portal hypertension is associated with systemic hypotension and
reduced peripheral vascular resistance. Although it is well established
that splanchnic and renal vascular resistances are reduced, the
contribution of possible alterations in skeletal muscle hemodynamics in
portal hypertension is unknown. The present study was designed to determine
if skeletal muscle vascular resistance was reduced and blood flow increased
in portal hypertensive rats. In portal hypertensive animals, hind-quarter
blood flow was significantly increased while vascular resistance was
significantly reduced. The fall in resistance in the portal hypertensive
animals was associated with an increase in the capillary filtration
coefficient, suggesting that an increase in functional exchange vessel
surface area occurred. Cross perfusion of control hindquarters with portal
hypertensive blood resulted in a 38% reduction in hindquarter vascular
resistance. Raising the plasma glucagon concentration to levels reported in
portal hypertensive animals resulted in no change in blood flow or vascular
resistance in control hindquarters. Skeletal muscle vascular sensitivity to
norepinephrine was assessed by constructing dose-response curves in control
and portal hypertensive animals. Mean ED50 values were not different. The
results of these studies indicate that skeletal muscle vascular resistance
is reduced in portal hypertension and humoral factors, but not glucagon,
are primarily responsible for the skeletal muscle hyperemia associated with
portal hypertension.
