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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Pharmacological therapy of surgical disease often involves manipulating the physiologic balance between pro- and anti-inflammatory responses. Many agents target only one aspect of the inflammatory cascade. Originally identified as a protein elaborated by T-lymphocytes, IL-10 appears to globally inhibit cytokine production. ⋯ IL-10 is elaborated from multiple sources and has diverse cellular effects to regulate immune and inflammatory responses. Accumulating evidence suggests that the anti-inflammatory influence of IL-10 observed at the cellular level may be manipulated to impact the immune and inflammatory-mediated responses associated with injury and sepsis, gastrointestinal and cardiovascular disease, and transplantation. In conclusion, IL-10 is an important mediator of immune and anti-inflammatory responses in surgical disease and, as such, has therapeutic promise as an immunomodulator and as an anti-inflammatory agent.
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The aim of this study was to assess the value of parameters of tissue oxygenation in monitoring the progression to irreversibility in a quantitative model of hemorrhagic shock. Rats were bled to a mean arterial pressure of 40 mmHg and were maintained at this level by further blood withdrawal until the compensation endpoint; this point was defined as the time at which the rat was no longer able to maintain its blood pressure at this level and shed blood was required for transfusion. The shock period was maintained until 0%, 20%, 40%, or 50% of the maximum shed blood volume (MBV) had been returned (n = 10 in each group, total n = 40). ⋯ Lactate levels only predicted irreversibility in late, severe shock. This quantitative model of hemorrhagic shock showed that tissue oxygenation parameters can be used to monitor the progression from the decompensated phase of hemorrhagic shock to irreversibility. Furthermore, this experimental study suggests that venous indices may be a valuable tool in reflecting the severity of hemorrhagic insult in a setting when arterial blood samples may not be easily available.
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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.