AJP - Heart and Circulatory Physiology, Vol 246, Issue 2 174-H179, Copyright © 1984 by American Physiological Society
Role of AVP in maintenance of circulatory homeostasis during hemorrhagic shock
C. E. Hock, J. Y. Su and A. M. Lefer
Hemorrhagic hypotension produces significantly increased plasma arginine
vasopression (AVP) concentrations. We have utilized a specific antagonist
(AVP-A) of the pressor effects of endogenous AVP to investigate the role of
this neurohypophyseal hormone on the pathogenesis of hemorrhagic shock.
Infusion of the AVP-A (2 micrograms/kg bolus + 2 micrograms X kg-1 X h-1
infusion) into sham-shocked animals produced no significant changes in any
of the observed experimental variables. Cats subjected to hemorrhagic shock
given AVP-A had final superior mesenteric artery flow (SMAF) values
significantly (P less than 0.05) higher than shock cats given vehicle (7.7
+/- 1.1 vs. 4.5 +/- 0.8 ml X kg-1 X min-1, respectively). Increases in
postreinfusion plasma cathepsin D activities were significantly blunted in
hemorrhaged animals treated with AVP-A (10.4 +/- 2.0 vs. 24.8 +/- 5.5 U/mg
protein; P less than 0.05). Plasma proteolysis as well as the plasma
accumulation of myocardial depressant factor (MDF) were also significantly
modulated by AVP-A treatment in hemorrhaged animals. MDF activities were 75
+/- 6 and 53 +/- 4 U/ml (P less than 0.02) for shock cats given vehicle or
AVP-A, respectively. However, these beneficial actions were not reflected
in any significant improvement in postreinfusion mean arterial blood
pressure (MABP). These findings suggest that endogenous AVP functions not
only as a potent splanchnic vasoconstrictor but also as a key humoral
factor in the maintenance of postreinfusion MABP, a profile that is
different from the role of angiotensin II, the other major splanchnic
vasoconstrictor, in shock.
