Current opinion in critical care
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The mesenteric hemodynamic response to circulatory shock is substantial and asymmetrical; the vasoconstrictive response disproportionately affects the mesenteric organs. The cardiac output is sustained partially, at no cost in nutrient flow to the mesenteric organs, by vasoconstriction of the mesenteric veins, resulting in the "autotransfusion" of up to 30% of the circulating blood volume into the systemic circulation. ⋯ The response to any of these conditions can, variably and unpredictably, cause hemorrhagic gastric stress erosions, nonocclusive mesenteric ischemia of the small bowel, ischemic colitis, ischemic hepatitis, acalculous cholecystitis, and/or ischemic pancreatitis. Injury to the mesenteric organs can also initiate the systemic inflammatory response syndrome and, consequently, multiple organ failure.
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Curr Opin Crit Care · Apr 2003
ReviewSedation in neurointensive care: advances in understanding and practice.
To evaluate the rationale and the pharmacologic options for sedating neurointensive care patients. ⋯ The pharmacokinetic and pharmacologic effects of the available sedatives used in neurointensive care patients are reviewed.
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Curr Opin Crit Care · Apr 2003
ReviewIntestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness.
Tight junctions between adjacent epithelial cells are essential for the maintenance of compositionally distinct fluid compartments in various organs, such as the liver, lungs, kidneys, and intestine. These epithelial organs are commonly affected in the condition known as multiple organ dysfunction syndrome, which can complicate the clinical course of patients with sepsis or other conditions associated with poorly controlled systemic inflammation. The gut serves as a useful model for this problem, and studies using reductionist in vitro models and experiments carried out using laboratory animals are starting to clarify the cellular and biochemical mechanisms that are responsible for intestinal epithelial hyperpermeability secondary to critical illness. ⋯ Epithelial dysfunction may be a common final pathway contributing to organ dysfunction in sepsis and other forms of critical illness.
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Curr Opin Crit Care · Apr 2003
ReviewRole of poly(adenosine diphosphate-ribose) polymerase 1 in septic peritonitis.
Peritonitis generally results from gastrointestinal perforation, with systemic sepsis developing over hours or days from an initially localized nidus of infection. The consecutive inflammatory response induces the widespread generation of oxidants and free radicals, which are potent inducers of breaks and nicks in double-stranded DNA. ⋯ In parallel, poly(ADP-ribose) polymerase 1 positively regulates inflammatory signal transduction pathways through a functional association with the transcription factor nuclear factor kappaB, resulting in a progressive amplification of local inflammation. Recent data indicate that these molecular mechanisms are instrumental in the development of cardiovascular collapse and multiple organ dysfunction in sepsis, supporting the view that pharmacologic inhibitors of poly(ADP-ribose) polymerase 1 may represent useful tools for the treatment of this condition.