XXXX in sepsis: clinical and experimental investigations.

@entity296 @entity5691 @entity326 @entity63 @entity16 @entity2348 @entity2554 @entity281 @entity842 @entity299 @entity67 @entity669
OBJECTIVE: To review the clinical manifestations and mechanisms of @entity299 in @entity326 . METHODS: Literature review of selected clinical studies and animal models. RESULTS: Depressed myocardial contractile function is a common consequence of severe @entity281 . Bacterial factors, in conjunction with host inflammatory mediators, produce a profile of reversible @entity299 manifested by a decrease in ventricular ejection fraction, @entity2554 , and @entity5691 . Global @entity63 is not the major mechanism that mediates @entity299 during sepsis. Inflammatory mediators contribute to @entity296 by damaging the coronary microcirculation and contributing to @entity296 and @entity16 . However, trials of anti-inflammatory agents have not prevented or increased the rate of reversal of @entity326 or improved survival. The link between @entity842 and clinical @entity296 remains unclear, as nonselective @entity842 synthase inhibition does not block the development of @entity67 . CONCLUSIONS: Serious @entity2348 result in inflammatory injury to the heart manifested by a common profile of @entity299 . Therapy remains limited to treatment of the infection with antibiotics and supportive care, with fluid resuscitation and selective use of inotropes and vasopressors. Experimental models suggest that new anti-inflammatory strategies (e.g. @entity669 kinase inhibitors) may offer some advantages over those that target a single mediator; these agents remain to be clinically evaluated.
