ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;Burn patients, multiple trauma patients, and patients undergoing major surgical operations often suffer from acquired immunologic deficits that predispose them to life‐threatening sepsis. This paper reviews the current research in this area, with emphasis on identifying the components of the immune response affected by injury, elucidating the mediators of immunologic change, and determining new therapeutic approaches for correcting immunologic deficits. Lessons learned from the study of immune deficiency disease are reviewed, as are basic observations of burn‐ and trauma‐induced immune depression.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;That the lymphatic vessel participates in the regulation of interstitial dynamics through its ability to contract and propel fluid and protein from the extravascular tissues back to the bloodstream has not been fully appreciated. The “lymph pump” appears to be regulated by local physiologic forces as well as neurogenic and humoral factors. We have dassessed the effects of hemorrhage and endotoxin on the ability of the lymph vessel to propel fluid in sheep using a model system that permits the quantitation of lymphatic pumping in vivo without the complication of variable lymph inputs. A major blood loss was found to enhance lymphatic contractile activity and fluid pumping. Considering the large reservoir of fluid and protein in the interstitium and lymph, we speculate that stimulation of the “lymph pump” after hemorrhage might help to re‐expand the vascular space. On the other hand, the intravenous administration of endotoxin inhibited lymphatic pumping, suggesting that impaired lymph propulsion in sepsis may contribute to edema by reducing the ability of the lymphatic vessel to remove extravasated protein from the tissues.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;Bacterial infection is a common and serious problem in burn victims who survive the shock phase of thermal injury. Our experimental work, plus the clinical studies of others, suggests that the gut can serve as a reservoir for systemic infections caused by bacteria that cross (translocate) the gastrointestinal (GI) epithelium. Bacterial translocation from the GI tract does not normally occur in the healthy animal owing to (1) the presence of an indigenous GI microflora preventing bacterial overgrowth, (2) an intact intestinal epithelial barrier, and (3) normal host immune defenses. However, a thermal injury, as well as other stressors, can result in the disruption or impairment of any of these protective mechanisms, potentially leading to lethal systemic infections with bacteria colonizing the gut.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;While the direct effects of anesthesia on immunological competence have not yet been fully elucidated, it is clear that the use of certain anesthetics and anesthetic procedures contributes to reduced immune function, as demonstrated by such clinical markers as increased infection and tumor growth. This review evaluates evidence of the participation of anesthesia in suppression or activation of the immune systemd, and discusses the implications of these changes to patient care and outcome.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;This short review focuses on the immunological functions of iron‐containing compounds. Five such compounds—transferrin, haptoglobin, hemopexin, albumin, and lactoferrin—are thought to contribute to normal infection resistance. Experimental results that demonstrate the ability of these compounds to inhibit the growth of an important pathogen,Klebsiella pneumoniae, are discussed.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;Granulocytes, predominantly polymorphonuclear neutrophils, are the major components of the body's defense against acute infections. Starting from pioneering work done 20 years ago by Alexander and cowokers,1,2neutrophil dysfunction after major thermal injury has been well documented. Defects in neutrophil function have been recognized as being serum‐borne3Additionally, a review of granulocyte function in burns was presented in 1984, at the Conference on the Immune Consequences of Thermal and Traumatic Injuries.14Because of methodologic difficulties, however, our knowledge of granulocyte kinetics has increased very slowly. Although the bone marrow produces 1.5 billion granulocytes per kg body weight per day5and the marrow granulocyte reserve is enormous, the hematopoietic tissues, along with the release, distribution, and possible role of granulocytes in the pathophysiology of burns, have not been studied thoroughly. This article presents a current review of our knowledge of granulocyte kinetics in burns and the production and possible fate of granulocytes in tissues.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;The increased susceptibility to infection of patients with thermal injury is related to loss of host defense, which is reflected, in part, by the temporal loss of chemotactic function of leukocytic phagocytes. Our studies of patient neutrophils to define the mechanism of this phenomenon involved evaluation of both random and chemotactic migratory functions of patient neutrophils, measurement of receptors for chemotactic ligands, and measurement of receptors mediating substrate adherence of the cells. Measurements of migratory functions were made using the under‐agarose techniques and measurements of receptor expression were accomplished by flow cytometry using fluorescein‐labeled ligand or receptor‐specific antibody. We conclude that loss of chemotaxis in response to C5a/C5adesArg is the result of downregulation of receptors for C5a and of reduced motility, and that loss of chemotaxis in response to the tripeptide FMLP is the result of reduced motility alone. Measurements of changes in the expression of “adherence” (iC3b) receptors revealed that up‐regulation occurs early and can be sustained for weeks after injury. These results are taken to suggest that either hyper‐ or hypoadherence could explain the loss of random migratory function observed for patient cells. Evidence of auto‐oxidative alteration of cytoskeletal elements, to produce loss of random migratory function, also is reviewed. Considering the evidence for activation of the complement cascade after thermal injury C5a and C5adesArg are likely primary factors in effecting the down‐regulation of C5a receptors, stimulation of secreation to mobilize iC3b receptors, and stimulation of respiration to auto‐oxidize cell components. Such evidence of injury‐mediated complement activation included data derived from application of a novel immunoassay for iC3b.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID

摘要:

&NA;Sepsis is responsible for 75% of late deaths after major thermal or traumatic injury. In the clinical setting, efforts to prevent or control sepsis, or both, should include an understanding of normal host resistance, proper resuscitation techniques, and nutritional support. Previous studies have identified T suppressor cell abnormalities following thermal injury and have suggested macrophage defects after traumatic injury. Although major thermal injury is easier to quantify than mechanical trauma, both insults can stress patients host resistance to a maximal degree, leading to profound and often fatal immunosuppression. Recent studies summarized in this paper have suggested that the macrophage and the interleukin system may play a major role an initiating some of these immune abnormalities following injury.

ISSN:0273-8481    

出版商:OVID    

年代:1987

数据来源: OVID