The mesenteric hemodynamic response to circulatory shock: An overview

Citation
Pm. Reilly et al., The mesenteric hemodynamic response to circulatory shock: An overview, SHOCK, 15(5), 2001, pp. 329-343
Citations number
112
Categorie Soggetti
Aneshtesia & Intensive Care","Cardiovascular & Hematology Research
Journal title
SHOCK
ISSN journal
10732322 → ACNP
Volume
15
Issue
5
Year of publication
2001
Pages
329 - 343
Database
ISI
SICI code
1073-2322(200105)15:5<329:TMHRTC>2.0.ZU;2-I
Abstract
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.