The mesenteric hemodynamic response to circulatory shock is characteristic
and profound; this vasoconstrictive response disproportionately affects bot
h the mesenteric organs and the organism as a whole. Vasoconstriction of po
st-capillary mesenteric venules and veins, mediated largely by the a-adrene
rgic receptors of the sympathetic nervous system, can effect an "autotransf
usion" of up to 30% of the total circulating blood volume, supporting cardi
ac filling pressures ("preload"), and thereby sustaining cardiac output at
virtually no cost in nutrient flow to the mesenteric organs. Under conditio
ns of decreased cardiac output caused by cardiogenic or hypovolemic shock,
selective vasoconstriction of the afferent mesenteric arterioles serves to
sustain total systemic vascular resistance ("afterload"), thereby maintaini
ng systemic arterial pressure and sustaining the perfusion of non-mesenteri
c organs at the expense of mesenteric organ perfusion (Cannon's "flight or
fight" response). This markedly disproportionate response of the mesenteric
resistance vessels is largely independent of the sympathetic nervous syste
m and variably related to vasopressin, but mediated primarily by the renin-
angiotensin axis. The extreme of this response can lead to gastric stress e
rosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepat
itis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock ca
n produce decreased or increased mesenteric perfusion, but is characterized
by an increased oxygen consumption that exceeds the capacity of mesenteric
oxygen delivery, resulting in net ischemia and consequent tissue injury. M
esenteric organ injury from ischemia/reperfusion due to any form of shock c
an lead to a triggering of systemic inflammatory response syndrome. and ult
imately to multiple organ dysfunction syndrome. The mesenteric vasculature
is therefore a major target and a primary determinant of the systemic respo
nse to circulatory shock.