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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Several studies indicate that norepinephrine (NE) may be more effective than dopamine for the treatment of septic shock. Nonetheless, many consider dopamine to be the pressor of choice for shock refractory to volume resuscitation. Owing to fear of excessive vasoconstriction, accentuated end-organ hypoperfusion, and the development of multiple organ dysfunction syndrome (MODS), it is contended that NE may be deleterious. ⋯ In addition, whereas survivors showed significant improvement by Day 5 (p < .01), MOD amongst nonsurvivors remained unchanged (p = .993). Although critically ill surgical patients requiring NE support have significantly greater degrees of organ dysfunction than patients not requiring pressors, much of the organ dysfunction is present on admission. The data contradict the notion that NE facilitates the development of MODS.
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Gut mucosal hypoperfusion plays a major role in the pathogenesis of ongoing sepsis and multiple organ dysfunction syndrome. Traditionally, therapy included increasing systemic flow, thus secondarily augmenting blood flow to the gut. Direct manipulation of the gut mucosal microcirculation avoiding systemic effects, i.e., selective gut microcirculatory control (SGMC), has not been tested with a clinically available vasodilating drug. ⋯ SNP normalized (to SC saline values, 14.5 +/- .6 microm) the CLP arteriolar diameters, from 11 +/- 6 to 14.6 +/- .3 microm (p < .05), while mean arterial pressure (MAP) was stable. Flowmotion patterns were also normalized by SNP, and intercapillary areas (i.e., diffusion distance) were decreased. We conclude that SNP exerted beneficial effects on gut mucosal microcirculation without affecting MAP; therefore, SGMC may be a novel way to affect the course of sepsis.
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Neutrophil (PMN) influx into the peritoneal cavity in response to bacterial peritonitis is an indispensable aspect of host defense. PMNs also are responsible for the remote organ injury observed after major abdominal infection. The aim of this study was to examine the effect of selectin blockade on PMN migration into the peritoneum and on PMN sequestration in the lungs, early in the course of peritonitis. ⋯ In conclusion, P-selectin mediates PMN influx into the peritoneal cavity, while E- and L-selectins do not appear to play any significant role in the 6 h time period following CLP. Lung PMN sequestration, after CLP, occurred independent of P-, E-, or L-selectin expression. Blockade of P-selectin during peritonitis appears to be potentially deleterious by preventing early PMN influx into the compartment containing the septic focus.