The Journal of surgical research
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Previous studies on patients with hip fractures and in patients with colorectal cancer have documented that perioperative transfusion is associated with a significant increase in postoperative infection rate. Therefore, we sought to investigate the incidence of preoperative and postoperative anemia in noncardiac surgical patients and to determine if transfusion is an independent risk factor for infection and adverse outcome postoperatively. ⋯ There is a high incidence of preoperative and postoperative anemia in surgical patients, with a coincident increase in blood utilization. These factors are associated with increased risk for perioperative infection and adverse outcome (mortality) in surgical patients. Consideration should be given to preoperative diagnosis and correction of anemia with iron, vitamin B12, folate supplementation, or administration of recombinant human erythropoietin.
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Tumor necrosis factor (TNF)-alpha is a critical effector of lipopolysaccharide (LPS)-induced acute lung injury, and its effects are mediated by two structurally related receptors, RI and RII. Cellular adhesion molecules and C-X-C chemokines (Keratinocyte chemoattractant (KC) and macrophage inflammatory protein [MIP]-2) regulate tissue neutrophil polymorphonuclear neutrophil (PMN) accumulation in a multitude of inflammatory states. We hypothesized that TNFRI signaling dictates PMN accumulation in the lung via regulation of chemokine molecule production. Therefore, the purposes of this study were to (1) delineate LPS-induced lung TNF-alpha production and (2) characterize the contribution of both TNF receptors to lung chemokine production and neutrophil influx following systemic LPS. ⋯ Acute lung injury following systemic LPS administration is characterized by increased lung (1) TNF-alpha production, (2) C-X-C chemokine production, and (3) neutrophil accumulation. The maximal effect of LPS-induced lung neutrophil accumulation appears to be dependent upon the TNFRI receptor but not the TNFRII receptor. .
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After cutaneous burn injury, an area of tissue 1-2 mm thick surrounding the wound is the site of a pronounced inflammatory response where blood flow is reduced. This "zone of stasis" undergoes progressive necrosis within 24-48 h, resulting in an expansion of the burn wound. Poloxamer-188 (P-188) is a surfactant that has been shown to prevent cell death due to electrical injury in vivo and heat shock in vitro. ⋯ Beyond 3 mm from the center of the burn, red blood speed was equal to the preburn levels in saline controls, while it increased by about 10% in P-188 animals. Twenty-four hours after administration of burn, the "zero red blood cell speed zone," termed as the zone of coagulation, became smaller in P-188-treated animals, with an area of 2.4 +/- 0.5 mm(2) (n = 5) compared to 3.5 +/- 0.5 mm(2) (n = 4) in saline controls (P < 0.01). These results suggest that P-188 prevented the formation of a zone of stasis within 2 h after the burn injury and reduced the area of coagulation observed 24 h after cutaneous burn injury.
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Cardiopulmonary bypass (CPB) is associated with poorly understood alterations in gastrointestinal (GI) perfusion. Intestinal fatty acid binding protein (IFABP), a cytosolic protein uniquely located in mature small-intestinal enterocytes, has been shown to be a sensitive biochemical marker of early intestinal ischemia when assayed in urine. We hypothesized that if significant small-intestinal ischemia occurs with CPB, then urine IFABP levels should be concomitantly elevated. ⋯ In low-risk bypass patients, small-bowel mucosal perfusion appeared to be maintained, while in the high-risk population, 21% of the patients sustained clinically significant mucosal compromise. In this pilot study, urine IFABP was 100% sensitive and 92% specific with respect to GI complications. Since elevated urine IFABP concentrations appeared to correlate with clinical GI complications, urine IFABP may be a useful marker to identify the patient at risk for postbypass GI complications.
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There have been many studies on anti-lipopolysaccharide (LPS) agents and LPS-neutralizing agents; however, there have been no reports on the changes in clinical status and mediators that occur when these agents are used. Polymyxin (PMX) (treatment using a column containing polymyxin B-immobilized fiber) removed circulating endotoxin, and reduced various cytokines within 120 min, even in patients with high levels of plasma cytokines. Our purpose was examine the mechanisms of PMX treatment by which plasma cytokines are reduced by endotoxin neutralization with polymyxin B, even during therapy for sepsis and/or endotoxin shock. ⋯ These findings may indicate one of the mechanisms operating in the clinical changes that occur after circulating endotoxin removal, and are likely to have therapeutic value, even for patients with high proinflammatory cytokine levels.