Use of selective mesenteric dilator peptides to examine the role of the intestine in experimental hemorrhagic shock.

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.