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文献考察：ショック，脱水による腸管血流障害．
１）Shock. 2000;13(4):267-73.
Mesenteric vasoconstriction in response to hemorrhagic shock.
Toung T, Reilly PM, Fuh KC, Ferris R, Bulkley GB.
Previous studies indicate that cardiogenic shock (tamponade) in swine produces selective mesenteric ischemia due to disproportionate mesenteric vasospasm mediated primarily by the renin-angiotensin axis. Here, we characterized the systemic and mesenteric hemodynamic responses to hypovolemic shock to better understand the neurohumoral mechanisms controlling this response. Varying degrees of hypovolemic shock were produced by graded levels of hemorrhage, from 12.5 to 50% of the calculated blood volume. Systemic and mesenteric pressures and blood flows were measured, and corresponding vascular resistances were calculated. The hemodynamic responses of the mesenteric vascular bed were compared with those of the systemic (nonmesenteric) vasculature. These experiments were then repeated after confirmed blockade either of the alpha-adrenergic nervous system (phenoxybenzamine), of vasopressin (Manning compound), or of the renin-angiotensin axis (enalapril). Graded levels of hemorrhage produced corresponding graded, reproducible, steady-state levels of systemic hypotension, hypoperfusion, and peripheral vasoconstriction, i.e., hemorrhagic shock. This was associated with disproportionate degrees of mesenteric ischemia due to disproportionate mesenteric vasoconstriction. The selective component of this mesenteric vasoconstrictive response was not attenuated by a-adrenergic blockade nor by vasopressin blockade but was blocked by ablation of the renin-angiotensin axis with enalapril. Like cardiogenic shock, hemorrhagic shock generates selective mesenteric ischemia by producing a disproportionate mesenteric vasospasm that is mediated primarily by the renin-angiotensin axis.PMID: 10774614
２）Shock. 2001 May;15(5):329-43.
The mesenteric hemodynamic response to circulatory shock: an overview.
Reilly PM, Wilkins KB, Fuh KC, Haglund U, Bulkley GB.
The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post-capillary mesenteric venules and veins, mediated largely by the alpha-adrenergic receptors of the sympathetic nervous system, can effect an "autotransfusion" of up to 30% of the total circulating blood volume, supporting cardiac filling pressures ("preload"), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions 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 maintaining systemic arterial pressure and sustaining the perfusion of non-mesenteric 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 system and variably related to vasopressin, but mediated primarily by the renin-angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can 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. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock. PMID: 11336191
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