Chronic alcohol intoxication attenuates human immunodeficiency virus-1 glycoprotein 120-induced superoxide anion release by isolated Kupffer cells.

This work tests the hypothesis that chronic alcohol intoxication suppresses the microbicidal activity of Kupffer cells by modulating the expression of cell surface receptors associated with respiratory burst and the release of potent microbicidal agents [i.e., reactive oxygen species (ROS)].

[The absence of interference between GSM mobile telephones and implantable defibrillators: an in-vivo study. Groupe Systèmes Mobiles].

Introduction And Objectives: The electromagnetic field created by mobile telephones can cause pacemaker dysfunction. Although implantable cardioverter defibrillators are also susceptible to electromagnetic interference, few studies have addressed this issue and compatibility with the GSM mode has not been tested. This study was developed to detect possible "in vivo" interference between GSM mobile telephones and implantable cardioverter defibrillators.

Chronic alcohol intoxication induces hepatic injury through enhanced macrophage inflammatory protein-2 production and intercellular adhesion molecule-1 expression in the liver.

This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP2) and up-regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter-receptor, intercellular adhesion molecule-1 (ICAM-1), on hepatic cells.

Cross-tolerance between acute alcohol intoxication and endotoxemia.

This study tests two hypotheses: (1) prior exposure to LPS induces cross-tolerance for the hepatic effects of subsequent short-term alcohol intoxication; and (2) short-term alcohol intoxication renders the liver resistant to the effects of acute endotoxemia, resulting in reduced production of superoxide and tumor necrosis factor. In the first group of experiments, male Sprague-Dawley rats were treated intravenously with E. coli lipopolysaccharide (LPS) (0.

Motor function of the esophagus after caustic burn.

During the subacute and chronic phases of esophagitis due to ingestion of a caustic substance, the patient commonly displays stricture, esophageal rigidity and dysphagia. We used esophageal manometry, radiology, pH monitoring and 99mTc scintigraphy to investigate esophageal motor function in 25 children (mean age 24 +/- 7 months) with chronic esophagitis after second- and/or third-degree caustic burns. The results were compared with those for a control group of 12 children (mean age 32 +/- 19 months) under surveillance for suspected gastroesophageal reflux (GER) but for whom this pathology was later ruled out.

Effects of prednisolone and dexamethasone in children with alkali burns of the oesophagus.

We compared the efficacies of prednisolone and dexamethasone for treatment of children with oesophageal burns due to ingestion of caustic substances. The criteria of efficacy used were a) stricture severity by 3 weeks post-ingestion, b) reduction in burn severity by 3 weeks post-ingestion and c) number of dilatations required over the first year post-ingestion. Thirty-six children (24 boys and 12 girls; mean age 23.

Postbinge effects of acute alcohol intoxication on hepatic free radical formation.

The present studies were performed to test the hypothesis that Kupffer and endothelial cells are activated after recovery from an acute alcohol binge, which is accompanied by formation of oxygen-derived radicals. These radicals have been implicated in the pathogenesis of alcohol-mediated tissue injury in a number of organs. Male Sprague-Dawley rats received an intravenous injection of 20% ethanol in saline (1.

Effects of prednisolone and dexamethasone on alkali burns of the esophagus in rabbit.

Steroids have been widely used to prevent the severe secondary strictures that inevitably follow accidental ingestion of caustic substances by children, though with controversial results. To confirm the efficacy of large early doses of dexamethasone, we conducted an experimental study in rabbits. A cotton swab soaked in sodium hydroxide was placed on the esophageal mucosa of 30 rabbits.

Chronic alcohol intoxication enhances the expression of CD18 adhesion molecules on rat neutrophils and release of a chemotactic factor by Kupffer cells.

Chronic alcohol intoxication has been associated with increased migration of inflammatory leukocytes to the liver that may contribute to the development of alcoholic hepatitis in susceptible individuals. Thus, this work was performed to examine the mechanism by which neutrophils [polymorphonuclear neutrophils (PMNS)] are sequestered in the liver during prolonged consumption of alcohol. Male Sprague-Dawley rats were fed with Sustacal supplemented by 36% alcohol, or isocaloric diet for 16 weeks.

Acute endotoxin tolerance downregulates superoxide anion release by the perfused liver and isolated hepatic nonparenchymal cells.

This work is based on the hypothesis that low-dose lipopolysaccharide (LPS) suppresses the stimulatory and priming effects of a subsequent high-dose endotoxin on the formation of toxic oxygen-derived radicals by the perfused liver and isolated hepatic nonparenchymal cells. Such effects may in turn contribute to hyposensitivity to the lethal effect of large doses of endotoxin. Male Sprague-Dawley rats received a nonlethal ("low-dose") intravenous injection of Escherichia coli LPS (0.

Generation of a CD11b/c upregulating and chemotactic factor by hepatocytes of endotoxic rats--nonidentity with interleukin-8.

To further clarify the mechanism of polymorphonuclear leukocyte (PMN) recruitment into the liver associated with short term endotoxin infusion (1), we investigated the effect of a noval factor generated by hepatocytes of such endotoxic rats on the expression of PMN adhesion molecules CD11b/c and chemotactic activity. Conditioned medium of hepatocytes from endotoxin-infused rats shows a fast induction and dose-dependent activity for upregulating CD11b/c expression in and chemotactic activity for blood PMN of naive rats. Supernatants of naive control rats cultured in the presence of endotoxin and Kupffer cells and liver PMNs of endotoxic rats also produce activation, but to a much lesser extent.

Inhibition of nitric oxide formation in vivo enhances superoxide release by the perfused liver.

Nitric oxide, a known scavenger of toxic oxygen-derived radicals, has been shown to have a protective effect against tissue injury in endotoxemia. Based on the hypothesis that under normal physiological conditions, a balance between superoxide and nitric oxide exists in vivo, this work examines hepatic superoxide release after nitric oxide formation is inhibited in vivo. Male Sprague-Dawley rats were treated intravenously with N omega-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg body wt), an inhibitor of nitric oxide synthase.

Antineutrophil monoclonal antibody (1F12) alters superoxide anion release by neutrophils and Kupffer cells.

The formation of oxygen-derived radicals by phagocytes is regulated by chemotactic agents, cytokines, and adhesion molecules, such as CD11b/CD18 (Mac-1). In the rat system, we investigated the effect of monoclonal antibody 1F12 against rat neutrophils on hepatic sequestration of neutrophils and superoxide release by hepatic phagocytes. Within 15 min after 1F12 injection, there was profound neutropenia, which persisted for 24 h.

Acute ethanol intoxication regulates f-met-leu-phe-induced chemotaxis and superoxide release by neutrophils and Kupffer cells through modulation of the formyl peptide receptor in the rat.

This study was performed to assess alcohol-induced alterations in superoxide release and chemotaxis by Kupffer cells and blood neutrophils. Male Sprague-Dawley rats received a bolus injection of alcohol (1.75 g/Kg) followed by an intravenous infusion (250-300 mg/Kg/hr).

Primed pentose cycle activity supports production and elimination of superoxide anion in Kupffer cells from rats treated with endotoxin in vivo.

Glucose use and pentose cycle activity were determined in freshly isolated rat Kupffer cells 3 h after an i.v. injection of Escherichia coli endotoxin (0.

Clastogenic effect of extracts obtained from Crotalaria retusa L. and Crotalaria mucronata Desv. on mouse bone marrow cells.

This work has evaluated the clastogenicity of six extracts (tea and aqueous extract of leaves, tea, aqueous and methanolic extracts of dried fruit, and tea of unripe fruit) obtained from Crotalaria retusa L. and three extracts (tea and methanolic extract of dried fruit, and tea of unripe fruit) obtained from Crotalaria mucronata Desv. The extracts were injected intraperitoneally into mice, and the animals were killed 24 h after treatment for preparation of bone marrow cells.

Functional inactivation of neutrophils with a Mac-1 (CD11b/CD18) monoclonal antibody protects against ischemia-reperfusion injury in rat liver.

The role of neutrophil CD11b/CD18 (Mac-1) adhesion proteins in the pathogenesis of hepatic reperfusion injury was investigated in an experimental model. Male Fischer rats were treated with a CD11b monoclonal antibody or an isotype-matched IgM control antibody and subjected to 45 min of hepatic ischemic followed by 24 hr of reperfusion. Large numbers of neutrophils were present in postischemic liver lobes (1,241 +/- 64 polymorphonuclear cells/50 high-power fields) compared with numbers in baseline measurements (14 +/- 3 polymorphonuclear cells/50 high-power fields), and severe liver injury was observed after 24 hr of reperfusion (hepatic necrosis: 88% +/- 2%).

Monoclonal antibody against the CD18 adhesion molecule stimulates glucose uptake by the liver and hepatic nonparenchymal cells.

Neutrophils and macrophages play an important role in the body's microbicidal defense and have been implicated in the induction of tissue injury in reperfusion, endotoxemia and septic shock. Cellular host defense is accompanied by enhanced glucose use. In this study we examined the effect of monoclonal antibody 1F12 on in vivo glucose use by selected tissues and hepatic phagocytes.

Complement activates Kupffer cells and neutrophils during reperfusion after hepatic ischemia.

The hypothesis that complement factors may be involved in the postischemic activation of Kupffer cells (KC) and polymorphonuclear neutrophils (PMN) was investigated in a model of hepatic ischemia (45 min) and reperfusion in male Fischer rats in vivo. Depletion of serum complement before ischemia resulted in a significant attenuation of the KC-induced oxidant stress (enhanced oxidation of plasma glutathione) and also prevented the accumulation of PMNs in the liver during the initial reperfusion period of 1 h. Complement activation through injection of cobra venom factor (CVF; 75 micrograms CVF/kg) also induced enhanced oxidation of plasma glutathione and accumulation of PMNs in the liver.

Superoxide generation by neutrophils and Kupffer cells during in vivo reperfusion after hepatic ischemia in rats.

Kupffer cells and polymorphonuclear leukocytes (PMNs) contribute to the severe reperfusion injury of the liver after ischemia at different time points. The objective of this study was to identify the cellular source(s) of reactive oxygen formation during the PMN-induced injury phase. Kupffer cells and PMNs were isolated from the liver after 45 min of ischemia and 5 h or 24 h of reperfusion using collagenase-pronase digestion and a centrifugal elutriation method.

Modulation of f-met-leu-phe induced chemotactic activity and superoxide production by neutrophils during chronic ethanol intoxication.

Chronic alcohol consumption has been associated with increased migration of neutrophils into liver that could contribute to the development of alcoholic liver disease. Mild endotoxemia may be at least partially responsible for this condition since endotoxemia was shown to be present in virtually all chronic alcoholics. This study examines the release of superoxide anion and chemotactic activity by Kupffer cells and sequestered hepatic as well as blood neutrophils during chronic alcohol intoxication (16 weeks) alone, and following an intravenous injection of Escherichia coli lipopolysaccharide (LPS) (1 mg/kg) 3 hr before cell isolation.