ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—Burn injury results in a rapid loss of intravascular volume as wound edema forms, which reduces the circulating blood volume and generates the need for fluid therapy to combat hypovolemia. Fluid resuscitation of a burn patient is usually carried out with isotonic, sodium- and chloride-containing fluids, such as lactated Ringer's solution. The initial 24 h resuscitation volume is based on the bum size and body weight of the patient. Following a successful resuscitation, the burn patient develops stereotypic neurohormonal and metabolic responses that, depending on the extent of injury, last for several weeks or months. Breathing of incomplete products of combustion by the fire victim produces inhalation injury, the incidence of which rises with increasing burn size and the severity of which is proportional to the duration of exposure. Systemic hypoxia from carbon monoxide toxicity causes early death; chemical airway injury increases mortality and predisposes to subsequent pneumonia that further reduces survival. The diagnosis of inhalation injury is made by bronchoscopy and/or xenon scan and therapy involves support of ventilation. Thermal destruction of the cutaneous mechanical bamier and the presence of nonviable avascular bum eschar as well as impaiment of other host defenses render the burn patient susceptible to local as well as systemic infections. Care following resuscitation is focused on topical antimicrobial therapy, bum wound excision, and wound closure by grafting. Nutritional support and the prevention and control of infection are constant themes in bum patient management. A progressive improvement in general care of the acutely injured patient, prevention of shock, effective means of maintaining organ function, prevention and control of burn wound and other infections, and physiologically based metabolic support have significantly increased burn patient survival in recent decades.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—The regulation of the intracellular pH (pHi) of phagocytic cells is critical to their function and viability. The acidic nature of the abscesses to which these cells migrate and the burden of acid that they generate in the activated state tend to perturb the pHioutside of the physiological range. Failure to maintain pHihomeostasis results in decreased cellular enzyme activity, cellular migration, and microbicidal function. Several pHiregulatory mechanisms, including the sodium-proton exchanger, proton conductive pathways, and a vacuolar type H+-ATPase exist in leukocytes and play an important role in preventing deviations in the pHiaway from the physiological range. The last of these mechanisms is central to the regulation of cytoplasmic pH, and is modulated by mediator molecules in the inflammatory mileu.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—The purpose of the present study was to determine whether insulin-like growth factor (IGF)-I would increase whole body and muscle glucose uptake in septic rats that are known to be insulin resistant. Animals were infused with either saline, low-dose IGF-I, high-dose IGF-I, or a maximally stimulating dose of insulin for 2 h, and the glucose metabolic response was assessed using a euglycemic clamp in combination with [3-3H]glucose. Under basal conditions, sepsis increased the rates of whole body glucose uptake, glycolysis, and hepatic glucose production. Under euglycemic hyperinsulinemic conditions, septic rats demonstrated a marked insulin resistance as evidenced by the impaired rate of insulin-stimulated glucose uptake and muscle glycogen synthesis. In contrast, the infusion of either dose of IGF-I increased total glucose uptake, glycolysis, and glycogen synthesis in both control and septic rats to the same extent. Furthermore, there was no difference in the IGF-I stimulation of glucose uptake (as determined by [14C]-2-deoxyglucose) in the gastrocnemius, soleus, and heart between control and septic rats. These results indicate that the glucose metabolic response to IGF-I is intact in insulin-resistant septic rats.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—The effects of intravenous immunoglobulin G (ivIG) on the hepatic microvascular inflammatory response to sepsis were studied in rats byin vivomicroscopy. High doses of ivIG (300 mg/kg bw) (Sandoglobulin or rat IgG) significantly improved the 48 h survival of septic rats from 25–66% when ivIG was given before or immediately after cecal ligation and puncture. Circulating endotoxin also was significantly reduced. Eight hours after inducing sepsis, the average number of leukocytes adhering to the sinusoidal endothelium increased 15-fold and the average decrease in the number of perfused sinusoids was 22%. IvIG administration minimized these responses. In both septic and nonseptic animals, ivIG also reduced the phagocytic activity of Kupffer cells. The results suggest that high doses of ivIG not only reduce lethality but also limit hepatic microcirculatory dysfunction during sepsis by minimizing leukocyte-endothelial interactions that may be a result of reducing circulating endotoxin and modifying Kupffer cell function.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—To study the role of Kupffer cells (KC) as a cellular source of proinflammatory cytokines in hepatic ischemia/reperfusion, Sprague-Dawley rats were subjected to 20 min global hepatic ischemia. Sham-operated animals served as controls. Blood levels of tumor necrosis factor-α (TNF-α), interleukin-1α (IL-α), and interleukin 6 (IL-6) were determined after 10, 30, 60, 120, and 240 min of reperfusion and compared with spontaneous cytokine release by KC isolated after 60 min of reperfusion. Hepatic ischemia/ reperfusion resulted in an enhanced (p< .01) spontaneous release of TNF-α (+482%), IL-1α (+33%), and IL-6 (+175%) by KC. Kinetic analysis of cytokinemia revealed an early increase (p< .01) of TNF-α and IL-1α within minutes upon reperfusion, while an elevation of IL-6 serum levels was observed with a delay of 2 h. Early cytokinemia was associated with dysfunction/injury of the liver, lung, and kidney after 4 and 24 h of reperfusion, respectively. These data indicate that hepatic ischemia/reperfusion results in Kupffer cell activation and increased cytokine levels, which may produce systemic inflammation and may be responsible for tissue injury locally and on remote sites.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—U46619, a thromboxane A2(TXA2) mimetic, inhibits human monocyte chemotactic responses, suggesting that TXA2, an arachidonic acid metabolite, may alter monocyte adhesion. We tested the hypothesis that TXA2alters Lipopolysaccharide (LPS)-induced adhesion of THP-1 cells, a human monocytic leukemia cell line.Salmonella enteritidisendotoxin (1 μg/mL) induced a significant (p< .05; n = 6) increase in the adherence of THP-1 cells (basal, 5.7 ± 1.8 μg/well; LPS, 78.8 ± 4.9 μg/well). Treatment of THP-1 cells with indomethacin or TXA2receptor antagonists before LPS stimulation significantly (p< .05) enhanced adhesion, suggesting that endogenously produced TXA2or prostaglandins alter LPS-induced THP-1 cell adhesion. TXA2mimetics significantly decreased (p< .05; n = 5 and n = 3, respectively) LPS-induced THP-1 cell adhesion. This effect was blocked by three structurally dissimilar TXA2receptor antagonists. These results support the hypothesis that TXA2alters LPS-induced adhesion of THP-1 cells.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

ABSTRACT—Resolution of acute inflammation requires the removal of sequestered neutrophils (PMN) from the inflammatory site by apoptosis and ingestion by tissue macrophages; however, sequestered PMN are prevented from undergoing programmed cell death by some of the mediators of the acute inflammatory process, including lipopolysaccharide (LPS), granulocyte-macrophage colony-stimulating factor, and interleukin 2. This delay in apoptosis could lead to necrosis resulting in tissue damage. Tumor necrosis factor-α (TNF-α),Escherichia coliingestion resulting in a respiratory burst, and heat have been shown to induce PMN apoptosis. The effects of TNF-α,E. coliingestion, and heat shock on the one hand and LPS on the other, on PMN apoptosis are unknown. The aim of this study was to determine if TNF-α,E. coliingestion, and heat shock, which have been shown to induce PMN apoptosis, could override the delay in apoptosis associated with LPS. PMN (106) isolated from 10 healthy volunteers were cultured in either medium alone or PMN cultured with LPS (10 ng/mL/1 h). PMN activation was assessed subsequently by phagocytosis ofE. coliand CD11b expression. PMN were then further studied under four cuiture conditions: medium alone, TNF-α (100 U/mL).E. coli(1:25, PMN:E. coli), and heat shock (42±C for 45 min). Apoptosis was assessed over time by propidium iodide staining of DNA and FcyRIII receptor expression. The results demonstrate, for the first time, that the mechanisms by which LPS delays PMN apoptosis are overridden by the mechanisms by which TNF-α,E. coliingestion, and heat shock induce programmed cell death. Factors regulating PMN apoptosis have an important role to play in the resolution of acute inflammation. Identification of these factors and their interaction have important implications for the development of therapeutic strategies aimed at modulating the acute inflammatory response.

ISSN:1073-2322    

出版商:OVID    

年代:1996

数据来源: OVID