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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In the intensive care unit (ICU) of our tertiary care university medical center, central venous pressure (CVP) measurements derived from bedside monitors differ considerably from measurements by trained intensivists using paper tracings. To quantify these differences, printed CVP tracings and concurrent respiratory waveforms were collected from 100 consecutive critically ill patients along with the corresponding monitor-displayed CVP. Four blinded intensivists interpreted the tracings. ⋯ To determine the potential clinical impact of these differences, we used the original Surviving Sepsis Campaign Guidelines for fluid administration based upon the measurement of CVP. For individual physicians, protocol-driven fluid management strategy would have differed in 19.2% to 25.3% of cases, dependent upon which measured value was chosen. Although protocol-driven strategies to direct fluid infusion therapy may improve outcomes, these interventions in a specific patient are dependent upon the method by which the CVP is measured.
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We previously demonstrated that hearts from Brown Norway (BN) rats were more resistant to ischemic injury than hearts from Dahl S (SS) rats. Here we determined the susceptibility to LPS-induced cardiomyopathy in these rats and examined the involvement of inflammatory signaling. Both strains were treated with LPS (20 mg/kg) via i.p. injection for 6 h. ⋯ LPS notably up-regulated the expression of proinflammatory enzymes, iNOS and cyclooxygenase 2, in SS hearts but not in BN hearts. Interestingly, LPS did not stimulate Toll-like receptor 4 or its adaptor myeloid differentiation factor 88 expression in the hearts of either strain but did increase IkappaB and P65 phosphorylation, less prominently in BN hearts than in SS hearts. These data indicate that reduced production of proinflammatory cytokines and diminished nuclear factor kappaB activation are major mechanisms by which BN hearts are more resistant to LPS-induced myocardial dysfunction than SS hearts.
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Glucocorticoid and epinephrine are important stress hormones secreted from the adrenal gland during critical illness. Adrenal glucocorticoid stimulates phenylethanolamine N-methyltransferase (PNMT) to convert norepinephrine to epinephrine in the adrenal medulla. Glucocorticoid is sometimes used in catecholamine-resistant septic shock in critically ill patients. ⋯ We conclude that without stress, when adrenocorticotropic hormone is low, high doses of exogenous dexamethasone stimulate PNMT and catecholamine synthesis, likely independently of adrenal corticosterone concentration. After stress, adrenocorticotropic hormone levels are elevated, and exogenous dexamethasone suppresses endogenous corticosterone and PNMT production. Nonetheless, catecholamines increase, possibly due to direct neural stimulation, which may override the hormonal regulation of epinephrine synthesis during stress.
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There are only few strategic and therapeutic options to improve the functional outcome of patients after cardiac arrest and resuscitation (CPR). The pathophysiology of reperfusion injury after global ischemia is not completely understood. We present here a murine model of cardiac arrest and resuscitation that allows an analysis of the pathophysiology of reperfusion injury, especially focusing on survival, tissue damage, and functional neurological parameters. ⋯ Histological examinations and blood analyses of CPR animals revealed significant leukocyte tissue infiltration and morphological damage of brain, lung, and kidneys. In summary, mice undergoing CPR after cardiac arrest present distinct neurological deficits, marked organ damage, and a 54% mortality rate. Our highly standardized and reproducible model of mice resuscitation provides a means for a better understanding of the post-CPR pathophysiology and thus opens new perspectives to develop relevant therapeutic approaches to minimize global I/R injury.