If mesenteric vasoconstriction sets in motion the chain of events that leads to
shock, then the administration of a selective mesenteric
vasodilator (which has no other known cardiovascular actions) should prevent, or at least modify, the hemodynamic events in a standardized
shock preparation. We used the Wiggers model of experimental
hemorrhagic shock in 20
pentobarbital-anesthetized dogs, giving half the dogs a selective mesenteric dilator
peptide,
sauvagine, to produce selective dilatation of the superior (cephalic) and inferior (caudal) mesenteric circulations. (
Sauvagine does not dilate the coeliac vascular bed.) A third,
sham-operated group of four dogs served as a time control.
Sauvagine produced no observable beneficial effect in terms of hemodynamic measurements, intestinal
oxygen kinetics, or intestinal histology. Since we took the precaution of delivering the
peptide close-arterially (to ensure delivery during hypoperfusion), we conclude that mesenteric vasoconstriction per se is not the prime event in initiating
shock. Since reduced cardiac output during
hypovolemia led to diminished mesenteric flow (in spite of vasodilation), these experiments do not exclude the possibility of diminished intestinal blood flow being a central event in
shock.