PubMed Health⌕ Search

Biomedical subjects

L A Langdale

Publications and source records attributed to L A Langdale.

10 recordsLinked to original sources
PubMed1999

Effects of immunomodulation with interferon-gamma on hepatic ischemia-reperfusion injury.

The development of an inflammatory response after injury depends on the participation of a variety of cell populations and endogenous mediators. Interferon-gamma (IFN-gamma) is a potent cellular immunomodulating cytokine that contributes to acute and chronic inflammation. In this study, the effects of immunomodulation on ischemia-reperfusion injury were examined using increasing doses of recombinant, rabbit-specific IFN-gamma in an in situ model of hepatic ischemia-reperfusion. Pretreatment with low dose IFN-gamma augmented injury as measured by histology, aminotransferase concentrations, and myeloperoxidase activity. By contrast, high dose IFN-gamma pretreatment, equivalent to IFN-gamma supplements used in clinical trials, resulted in a lack of neutrophil infiltration and minimal progression of late phase, neutrophil-mediated reperfusion injury. These results suggest that immunomodulating mediators such as IFN-gamma may play a regulating role in the evolution of ischemia-reperfusion, contributing to the development and resolution of acute hepatic injury.

Adjuvants, Immunologic↗
PubMed1993

Neutrophils contribute to hepatic ischemia-reperfusion injury by a CD18-independent mechanism.

Hepatic ischemia-reperfusion injury is reported to be modulated by neutrophils (PMNs). The adhesion and emigration of PMNs that precede tissue inflammation and necrosis in other organs are mediated, in part, by the leukocyte adhesion complex CD11/CD18. In this study, the role of PMN adhesion via CD11/CD18 in isolated liver ischemia-reperfusion injury was examined in rabbits using a blocking monoclonal antibody (mAb 60.3) specific for the CD18 receptor. Vinblastine-induced neutropenia provided significant protection, confirming participation of neutrophils in the pathogenesis of hepatic injury. Inhibition of PMN adherence with mAb 60.3 did not ameliorate injury, as measured by aminotransferase concentrations or a histologic scoring system for injury severity. Histologic sections were scored for pattern and extent of injury as well as neutrophil association with injury. These results suggest a CD18-independent mechanism of neutrophil adhesion in the evolution of isolated hepatic ischemia-reperfusion injury.

Animals↗
PubMed1992

Liposome-encapsulated hemoglobin inhibits tumor necrosis factor release from rabbit alveolar macrophages by a posttranscriptional mechanism.

Macrophages contribute to the systemic inflammatory response that characterizes the sepsis syndrome through the production of inflammatory cytokines such as tumor necrosis factor (TNF). Liposome-encapsulated hemoglobin (LEH), a potential red cell substitute, is cleared by fixed tissue macrophages. In these studies, in vitro incubation of alveolar macrophages with stored LEH was shown to inhibit the expression of TNF induced by endotoxin (lipopolysaccharide, LPS) stimulation. This effect was dependent on LEH dose but independent of the period of exposure to the LEH. Despite inhibition of TNF expression, Northern blot analysis of total cellular RNA from LPS-stimulated macrophages revealed accumulations of TNF-specific transcripts in cells treated with or without LEH. Thus the mechanism of LEH inhibition of TNF expression appears to involve a posttranscriptional event. Although these results suggest a potential advantage of resuscitation with LEH when sepsis complicates hemorrhagic shock, immunomodulation in vivo remains to be defined.

Animals↗
PubMed1992

Tuberculosis and the surgeon.

With the resurgence of active tuberculosis in the United States, surgeons may be called upon to participate in the management of primary tuberculosis as well as major complications of the disease. To define the role of surgery in the diagnosis and treatment of tuberculosis in the 1990s, a 5-year retrospective review of 121 tuberculosis patients requiring invasive procedures in the course of their work-up was performed. Mycobacterium tuberculosis was cultured in 68% of patients, and atypical mycobacteria in 19%. Tissue was required to achieve the definitive diagnosis in 36%. Of the 93 patients with pulmonary evidence of tuberculosis, 54% presented with a pulmonary complication, 19 of whom required operative intervention. Extrapulmonary tuberculosis affected 45% of patients, including nine with miliary tuberculosis. Patients testing seropositive for human immunodeficiency virus accounted for 11% of the patients seen, emphasizing that the re-emergence of tuberculosis is not confined to the immunosuppressed.

Adolescent↗
PubMed1992

Infectious complications of blood transfusions.

The use of blood and blood products has revolutionized medical care over the last century. Without this capacity, many medical and surgical procedures would not be possible. The safety of these procedures is predicated, in part, on an appreciation of the complications of transfusions, including transmission of infectious disease. Assuring that patients are adequately protected from these hazards while providing the products that they need is the responsibility of both blood banks and practitioners.

Acute Disease↗
PubMed1988

Emphysematous pyelonephritis in a xanthogranulomatous kidney. An unusual cause of pneumoperitoneum.

Emphysematous pyelonephritis is a rare, life-threatening suppurative infection of the renal parenchyma and perinephric tissues. The disease is encountered primarily in patients with diabetes mellitus or ureteral obstruction associated with perinephric and intrarenal gas. Causative organisms are those normally found in the urinary and gastrointestinal tracts; however, anaerobic bacteria have been demonstrated in only 1% of cases. We describe a case of emphysematous pyelonephritis, which presented as an acute abdomen with pneumoperitoneum in a nondiabetic patient. No visceral injury was found at laparotomy. Multiple gas-producing organisms, including Clostridium ramosum (not previously reported, to our knowledge), were the cause of the free intraperitoneal and perinephric air. Subsequent radical nephrectomy revealed a xanthogranulomatous kidney. An aggressive surgical approach combined with intensive antibiotic therapy, after aerobic and anaerobic culture of excised tissue, is lifesaving.

Adult↗
PubMed1986

Fluosol-DA as a red-cell substitute in acute anemia.

We assessed the safety and efficacy of Fluosol-DA as a red-cell substitute in acute anemia. Twenty-three surgical patients with blood loss and religious objections to receiving blood transfusions were evaluated. Fifteen moderately anemic patients with a mean hemoglobin level (+/- SE) of 7.2 +/- 0.5 g per deciliter had no evidence of a physiologic need for increased arterial oxygen content and did not receive Fluosol-DA. Eight severely anemic patients with a mean hemoglobin level of 3.0 +/- 0.4 g per deciliter met the criteria of need and received the drug until the physiologic need disappeared or a maximal dose of 40 ml per kilogram of body weight was reached. We observed no adverse reactions to Fluosol-DA. The average peak increment in arterial oxygen content with the drug was only 0.7 +/- 0.1 ml per deciliter. There were no appreciable beneficial effects of Fluosol-DA, perhaps because of the small increase in arterial oxygen content, the brief half-life of the drug (24.3 +/- 4.3 hours), and the limited total dose. Six of the eight patients receiving Fluosol-DA died. One of the survivors received red-cell transfusions against his wishes, under a court order, after his total Fluosol-DA dose. Fourteen of the 15 moderately anemic patients survived. The data in this select group of patients refusing blood products suggest that, after blood loss, Fluosol-DA is unnecessary in moderate anemia and ineffective in severe anemia.

Acute Disease↗
PubMed1983

Assessment of a 35% fluorocarbon emulsion.

We have previously reported on the efficacy of a 20% fluorocarbon emulsion (Fluosol-DA, 20%) as an acellular O2 carrier at an FIO2 = 1.0. We are concerned, however, about the potential O2 toxicity that may result from extended exposure to FIO2 = 1.0. The O2 content of the fluorocarbon phase is linearly related to both the FIO2 and the fluorocarbon concentration (Fct). It should therefore be possible to maintain the same O2 content by raising the Fct using a higher fluorocarbon concentration and lowering the FIO2. The purpose of this report is to assess the ability of a 35% fluorocarbon emulsion (Fluosol-DA, 35%) at an FIO2 = 0.6 to support hemodynamics and O2 transport. Five adult baboons were paralyzed, anesthetized, intubated, and mechanically ventilated at FIO2 = 0.6. An isovolemic total exchange transfusion (E.T.) with Fluosol-DA, 35% was performed. Measurements were made at Hct's of 20, 10, 5, and less than 2%. All animals survived the exchange. Total arterial O2 content fell from 17.4 +/- 0.7 to 3.3 +/- 0.2 vol% (p less than 0.01), and O2 delivery decreased from 21.8 +/- 2.2 to 5.1 +/- 0.7 cc/min-kg (p less than 0.01) during the exchange. There was no significant change in MAP, H.R., C.O., or VO2 during the exchange transfusion. Fluosol-DA, 35% maintains normal hemodynamics and O2 transport despite a marked fall in arterial O2 content and total O2 delivery. Fluosol-DA, 35% is thus an effective O2 carrier at the safe FIO2 of 0.6.

Animals↗