Critical care medicine
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Critical care medicine · Oct 2005
Gut luminal microdialysis of glycerol as a marker of intestinal ischemic injury and recovery.
To evaluate microdialysis as a method to assess different degrees of intestinal damage and recovery during ischemia and reperfusion; to evaluate information obtained from microdialysis catheters in the peritoneum, the gut wall, and the gut lumen. ⋯ Microdialysis of glycerol provides information about the extent and severity of intestinal damage after ischemia and about the ensuing recovery. The gut lumen is to be preferred as a site for placement of microdialysis catheters.
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Critical care medicine · Oct 2005
Augmentation of hospital critical care capacity after bioterrorist attacks or epidemics: recommendations of the Working Group on Emergency Mass Critical Care.
The Working Group on Emergency Mass Critical Care was convened by the Center for Biosecurity of the University of Pittsburgh Medical Center and the Society of Critical Care Medicine to provide recommendations to hospital and clinical leaders regarding the delivery of critical care services in the wake of a bioterrorist attack resulting in hundreds or thousands of critically ill patients. In these conditions, traditional hospital and clinical care standards in general, and critical care standards in particular, likely could no longer be maintained, and clinical guidelines for U. S. hospitals facing these situations have not been developed. The Working Group offers recommendations for this situation.
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Critical care medicine · Oct 2005
Early changes in organ function predict eventual survival in severe sepsis.
Early identification and treatment of severe sepsis can significantly reduce mortality rate. We hypothesized that a risk prediction model based on early (baseline to day 1 of study) response to standard care should be significantly related to 28-day survival. ⋯ These analyses suggest that outcomes for patients with severe sepsis are closely related to early (baseline to day 1 here) improvement, or lack thereof, in organ function. Also, clinical improvement on subsequent days may have little additional impact on the likelihood of survival.
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Critical care medicine · Oct 2005
Effect of increased cardiac output on hepatic and intestinal microcirculatory blood flow, oxygenation, and metabolism in hyperdynamic murine septic shock.
Septic shock-associated organ dysfunction is attributed to derangements of microcirculatory perfusion and/or impaired cellular oxygen utilization. The hepatosplanchnic organs are regarded to play a pivotal role in the pathophysiology of sepsis-related organ failure. In a murine model of septic shock, we tested the hypothesis whether achieving normotensive, hyperdynamic hemodynamics characterized by a sustained increase in cardiac output would allow maintenance of regional microvascular perfusion and oxygenation and, thus, hepatic metabolic capacity. ⋯ During murine septic shock achieving normotensive hyperdynamic hemodynamics with fluid resuscitation and norepinephrine, exogenous glucose requirements together with the lack of norepinephrine-induced increase in the rate of gluconeogenesis mirror impaired metabolic capacity of the liver despite well-maintained hepatosplanchnic microvascular perfusion and oxygenation.
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Critical care medicine · Oct 2005
Carbon monoxide, but not endothelin-1, plays a major role for the hepatic microcirculation in a murine model of early systemic inflammation.
Endothelin-1 and carbon monoxide play a major role in the regulation of liver microcirculation in numerous disease states. During sepsis and endotoxemia, elevated formation of endothelin-1 results in reduced sinusoidal blood flow. However, the role of carbon monoxide and endothelin-1 and its receptors endothelin receptor A and endothelin receptor B in the deranged liver microcirculation during early systemic inflammation remains unclear. ⋯ These data suggest that endothelin-1 and the endothelin receptors A and B are not responsible for the observed hepatic microcirculatory and cellular dysfunction during early systemic inflammation, but exposure to exogenous carbon monoxide protected the hepatic microcirculation and improved the impaired hepatic cellular integrity and the hepatocellular redox status.