Critical care : the official journal of the Critical Care Forum
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The glucose paradox of cerebral ischemia (namely, the aggravation of delayed ischemic neuronal damage by preischemic hyperglycemia) has been promoted as proof that lactic acidosis is a detrimental factor in this brain disorder. Recent studies, both in vitro and in vivo, have demonstrated lactate as an excellent aerobic energy substrate in the brain, and possibly a crucial one immediately postischemia. ⋯ When an episode of cerebral ischemia in the rat coincided with glucose-induced elevated levels of corticosterone (CT), the main rodent glucocorticoid, an aggravation of the ischemic outcome was observed. Both the blockade of CT elevation by chemical adrenalectomy with metyrapone or the blockade of CT receptors in the brain with mifepristone (RU486) negated the aggravating effect of preischemic hyperglycemia on the postischemic outcome.
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Review
Clinical review: immunodepression in the surgical patient and increased susceptibility to infection.
Several studies indicate that organ failure is the leading cause of death in surgical patients. An excessive inflammatory response followed by a dramatic paralysis of cell-mediated immunity following major surgery appears to be responsible for the increased susceptibility to subsequent sepsis. In view of this, most of the scientific and medical research has been directed towards measuring the progression and inter-relationship of mediators following major surgery. ⋯ This article will focus on the effect of blood loss and surgical injury on cell-mediated immune responses in experimental studies utilizing models of trauma and hemorrhagic shock, which have defined effects on the immunoinflammatory response. Subsequently these findings will be correlated with data generated from surgical patients. The results of these studies may generate new approaches for the treatment of immunodepression following major surgery, thus reducing the susceptibility to infection and increasing the survival rate of the critical ill surgical patient.
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Lipopolysaccharide (endotoxin) from the cell wall of Gram-negative bacteria is a potent trigger for the release of host-derived inflammatory mediators. The relationship between endotoxaemia, Gram-negative infection and the clinical syndrome of sepsis has been difficult to establish, in part because of the limitations of available endotoxin assays. ⋯ Endotoxaemia is associated with Gram-negative infection from any source, and with a diagnosis of sepsis and leukocytosis. These correlations were not apparent using the LAL method. The EAA may be a useful diagnostic tool for the investigation of invasive Gram-negative infection and incipient sepsis.
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Treatment of patients with severe sepsis with agents antagonising the effects of C5a has been proposed based on beneficial effects in animal experiments and in vitro studies demonstrating upregulation of the C5a receptor (CD88) on granulocytes by endotoxin. ⋯ In contrast to the findings in animals, it is concluded that granulocyte CD88 expression is reduced at the time when the diagnosis of severe sepsis or septic shock can clinically be made. The reason for this needs further investigation but it may be due to a previous complement activation or to cytokine effects.