Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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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). ⋯ 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.
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To define multiple organ dysfunction in newborns, we established a sequential scoring system NEOMOD (Neonatal Multiple Organ Dysfunction Score). It was developed to describe the process of increasing physiologic derangement in critically ill newborns. It provides, during the first 28 days of life, information concerning function of organ systems having a primary influence on mortality in very low birth weight (VLBW) infants. ⋯ An analysis of specific organ dysfunctions in the non-survivors group (n = 16) disclosed, in all patients, dysfunction of more than two organ systems 24 h before death. Similar to critically ill adults, secondary multiple organ dysfunction can be described also in a majority of critically ill VLBW infants. NEOMOD scores may help to evaluate daily the severity of the syndrome and risk of death.
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We investigated relationships between visceral blood flow, intestinal wall carbon dioxide tension (PCO2), and sublingual PCO2 during hemorrhagic shock. In five pigs, cardiac output declined 81% and superior mesenteric blood flow 77% during hemorrhage. Duodenal PCO2 increased from an average of 50 to 121 mmHg and sublingual PCO2 concurrently increased from an average of 46 to 101 mmHg. ⋯ Decreases in mesenteric blood flow were correlated with increases in sublingual (r = 0.91; P < 0.001) and duodenal (r = 0.89; P < 0.001) tissue PCO2. In five randomized "sham hemorrhage" control animals, neither decreases in cardiac output or mesenteric blood flow nor increases in duodenal or sublingual PCO2 were observed. Decreases in mesenteric blood flow during hemorrhage were therefore associated with early and comparable increases in tissue PCO2 in both visceral and sublingual sites.
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We explored the effects of the nucleoside transport inhibitor draflazine on regional blood flow, O2 extraction capabilities, and tumor necrosis factor (TNF) release in acute endotoxic shock. Fourteen anesthetized and mechanically ventilated dogs received 2 mg/kg of Escherichia coli endotoxin and were divided into two groups. Seven dogs received 0.1 mg/kg of draflazine 30 min before endotoxin, and 7 dogs served as a control group. ⋯ TNF levels remained higher in the draflazine group than in the control group, particularly 3 and 4 h after endotoxin administration. We conclude that nucleoside transport inhibition with draflazine does not alter global and hepatosplanchnic hemodynamics but may decrease gut mucosal perfusion and renal blood flow. However, this intervention can improve liver O2 extraction capabilities in acute endotoxic shock.