The Journal of surgical research
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The purpose of this study was to determine the impact of perfusion pressure on cerebral blood flow (CBF) and metabolism during normothermic cardiopulmonary bypass (CPB) and after weaning. ⋯ Normothermic CPB initiated with a crystalloid prime and performed at the lower end of a 50-70 mm Hg perfusion window resulted in a highly significant increase in CBF in order to compensate for hemodilution, while at the same time reduced the perfusion pressure available to supply the increased CBF. Together, these two events create a hemodynamic paradox of hyperperfusion in the face of hypotension. The reduction in CMRO2 in Group A is yet to be explained but seems to remain coupled to CBF and could represent a previously undescribed protective mechanism of hibernating cerebral tissue, similar to the phenomena of ischemic preconditioning in the heart, where cerebral tissue is stimulated to lower metabolism in response to inadequate CBF.
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Pneumonia occurs in approximately 50% of incubated patients in burn intensive care units and carries a mortality as high as 40%. A model was developed to study altered cardiopulmonary function in burn complicated by pneumococcal pneumonia. Sprague-Dawley rats were given a 43% total body surface area scald burn or sham burn; 24 h later they were transtracheally inoculated with either 10(7) Streptococcus pneumoniae in 0.5 ml phosphate buffer solution (PBS) or 0.5 ml PBS alone. ⋯ Tumor necrosis factor-alpha (TNF-alpha) concentrations in serum, but not bronchoalveolar lavage, were greater in burned animals with aspiration pneumonia-induced sepsis than in animals with either burn alone or aspiration pneumonia-induced sepsis alone. While our data suggest that elevated circulating TNF-alpha levels may contribute, in part, to depressed cardiac function, further studies are needed to fully define the mechanisms underlying cardiac contractile deficits in this model. We speculate that depressed cardiopulmonary function due to burn complicated by pneumonia and sepsis contributes to the high mortality of this patient population.
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Diabetes has been shown to have a negative impact on mortality following coronary artery bypass graft (CABG) surgery. This analysis examines the impact of diabetes on additional clinical and economic outcomes. ⋯ Diabetics treated with oral hypoglycemic agents or with diet alone have clinical and economic outcomes similar to nondiabetics following CABG. Insulin-requiring diabetes, however, predicts significantly increased hospital resource utilization. Future outcome assessment and resource utilization analyses must stratify diabetes by treatment to be completely accurate.
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Lipopolysaccharide binding protein (LBP) markedly increases the sensitivity of immune cells to LPS and CD14 expression correlates with cellular responsiveness to LPS. LBP gene expression can be induced in multiple organs following injury and CD14 upregulation on monocytes correlates with the infection and mortality rates in severely injured patients. We sought to determine the time-course induction of LBP and CD14 gene expression following experimental peritonitis. ⋯ LBP, CD14, and IL-1 mRNA levels are induced concurrently in the lung, kidney, and liver after cecal ligation and puncture. Given the synergistic affect of LBP and CD14 in potentiating LPS-induced production of inflammatory cytokines and the hypothesized role of such cytokines in the etiology of MSOF following injury and sepsis, our findings suggest a mechanism by which these organs may be rendered more susceptible to a "second hit" from endotoxemia after initial injury.
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The biochemical and cellular pathways resulting in the production of proliferative scar in the thermally injured patient remain incompletely elucidated. A promising area of investigation is the phenomenon of programmed cell death and its modulation. The following study was designed to quantify differential levels of the bcl-2 protooncogene and the Fas cell surface receptor, two apoptosis-modulating proteins, in the peripheral blood mononuclear cell (PBMC) fractions of burn patients with hypertrophic scar versus those considered to have healed normally. The study also encompassed an immunohistochemical examination of fibroblasts in vitro, to identify differential levels of Fas, bcl-2, and interleukin converting enzyme (ICE). ⋯ Differential expression of the bcl-2 protooncogene and the Fas cell surface receptor in the PBMC fraction of patients with burn injuries may suggest a disequilibrium in a complex biochemical signaling mechanism mediating programmed cell death. The increased levels of bcl-2 could be responsible for delayed fibroblast apoptosis, resulting in the disruption of normal healing and subsequent hypertrophic scarring. This is confirmed by an in vitro examination of wound fibroblasts versus those from surrounding uninjured skin. This immunoperoxidase technique reveals a localized relative decrease in Fas and ICE, two apoptosis-inducing proteins, at the level of the fibroblast in the proliferative scar specimen.