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Thromboxane inhibitors attenuate pathological changes in alcoholic liver disease in the rat. | Thromboxane levels correlate with severity of liver injury in rats given alcohol. The aim of this study was to evaluate the effect of thromboxane inhibitors on pathological changes in experimental alcoholic liver disease.Male Wistar rats were given a liquid diet and ethanol intragastrically for 1 month. The thromboxane inhibitors tested were a thromboxane receptor antagonist (TXRA) and a thromboxane synthase inhibitor (TXSI). Pathological changes; liver and plasma thromboxane levels; 6-ketoprostaglandin F1 | 8978360 | [
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Thromboxane inhibitors attenuate pathological changes in alcoholic liver disease in the rat. | alpha levels; lipid peroxidation; and messenger RNA levels for tumor necrosis factor (TNF)-alpha and transforming growth factor (TGF) beta were evaluated.Treatment with thromboxane inhibitors prevented necrosis and inflammation. In the TXSI-treated group; fatty liver was also decreased. Ethanol administration led to a 3-4-fold increase in liver thromboxane levels; a reduction in thromboxane levels and lipid peroxidation was seen in the TXSI group. In all treatment groups; TNF-alpha and TGF-beta messenger RN | 8978360 | [
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Thromboxane inhibitors attenuate pathological changes in alcoholic liver disease in the rat. | A levels were decreased.The prevention of necroinflammatory changes in thromboxane-treated groups is related to a decrease in TNF-alpha levels. Inhibition of TGF-beta expression may also prevent fibrosis in ethanol-treated rats. | 8978360 | [
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8-Isoprostaglandin F2 alpha, a product of lipid peroxidation, increases portal pressure in normal and cirrhotic rats. | The F2-isoprostanes are a recently described class of prostaglandins formed by free radical-mediated lipid peroxidation. 8-Isoprostaglandin F2 alpha (8-iso-PGF2 alpha); an F2-isoprostane; has previously been shown to be a potent renal vasoconstrictor acting via a thromboxane-like receptor. The aim of this study was to investigate whether 8-iso-PGF2 alpha increases portal pressure.Livers from normal and bile duct-ligated cirrhotic rats were perfused; and portal pressure response to infused agonist was monito | 8978361 | [
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8-Isoprostaglandin F2 alpha, a product of lipid peroxidation, increases portal pressure in normal and cirrhotic rats. | red continuously.Infusion of 8-iso-PGF2 alpha increased portal pressure in both groups; with a significantly greater response in cirrhotic rats. At a dose of 2.5 nmol/min; the mean portal pressure increased from a baseline of 8.2 +/- 0.6 to 9.8 +/- 1.3 mm Hg; whereas in cirrhotic animals; the increase was from 12.0 +/- 0.9 to 18.6 +/- 1.8 mm Hg. This response was completely blocked by SQ29548; a thromboxane receptor antagonist. A similar response pattern was observed with the thromboxane receptor agonist U4 | 8978361 | [
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8-Isoprostaglandin F2 alpha, a product of lipid peroxidation, increases portal pressure in normal and cirrhotic rats. | 6619.8-iso-PGF2 alpha can increase portal pressure in cirrhotic rats. If extrapolated to patients with cirrhosis; lipid peroxidation secondary to alcoholic liver injury; sepsis; or other liver pathology may cause an acute increase in portal pressure such as that observed in acute liver injury. | 8978361 | [
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Bile acid concentrations in human and rat liver tissue and in hepatocyte nuclei. | Bile acids exert cellular and molecular effects in the liver; but little is known about tissue concentrations. The aim of this study was to characterize bile acid composition in human and rat liver tissue and hepatocyte nuclei and examine the effects of experimental cholestasis and bile acid administration.Bile acids were measured by gas chromatography-mass spectrometry.Liver tissue concentrations of sham-operated rats were 130.8 +/- 21.3 nmol/g; representing 2%-4% of the bile acid pool; cholic and delta 22 | 8978363 | [
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Bile acid concentrations in human and rat liver tissue and in hepatocyte nuclei. | -beta-muricholic acids were the major bile acids identified. Concentrations increased 7-8-fold with bile duct ligation; deoxycholate and hyodeoxycholate disappeared. Lithocholate concentrations were higher in ligated rats (6.4 +/- 0.4 vs. 3.9 +/- 0.5 nmol/g for sham-operated). Total bile acid concentrations in human liver tissue were 61.6 +/- 29.7 nmol/g and comprised mainly chenodeoxycholic and cholic acids. Concentrations were higher during ursodeoxycholate or tauroursodeoxycholate administration (157.2 + | 8978363 | [
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Bile acid concentrations in human and rat liver tissue and in hepatocyte nuclei. | /- 45.6 and 161.6 +/- 43.4 nmol/g; respectively); and liver tissue was enriched 30% in ursodeoxycholate at the expense of hydrophobic bile acids. Bile acids were identified in rat hepatic nuclei (50-110 pmol/4 x 10(7) nuclei); accounting for < 0.1% of liver tissue levels.Human and rat liver tissue bile acid concentrations are low; increase with bile acid administration or bile duct ligation; and account for only a small fraction of the bile acid pool. | 8978363 | [
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Hepatocyte transport of bile acids and organic anions in endotoxemic rats: impaired uptake and secretion. | In sepsis; intrahepatic cholestasis occurs frequently; suggesting impaired hepatocyte transport of bile acids and organic anions. The aim of the study was to define the magnitude; time course; and the site of impaired biliary secretion in a rat sepsis model.Maximal transport for two bile acids (cholyltaurine and chenodeoxycholyltaurine) and two organic anions (sulfobromophthalein and sulfolithocholyltaurine) was measured in isolated perfused livers at various times after lipopolysaccharide injection. Basola | 8978362 | [
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Hepatocyte transport of bile acids and organic anions in endotoxemic rats: impaired uptake and secretion. | teral and canalicular liver plasma membrane vesicles were used to characterize the impairment in hepatocyte transport.Maximal hepatocyte transport was reduced for all compounds by 60%-81% compared with controls. Bile acid-independent bile flow was reduced by 51%. Impairment was maximal 12 hours after endotoxin injection and recovered thereafter. In basolateral plasma membrane vesicles; sodium-dependent transport for bile acids was reduced by 36%-47%. Sodium-independent transport of organic anions was reduce | 8978362 | [
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Hepatocyte transport of bile acids and organic anions in endotoxemic rats: impaired uptake and secretion. | d by 40%-55%. Adenosine triphosphate-stimulated transport was greatly decreased in canalicular vesicles prepared from endotoxemic animals for all four compounds probably because of a reduced number of transport molecules; based on kinetic studies.Basolateral and canalicular bile acid and organic anion transport are markedly impaired in endotoxemia. These mechanisms may contribute to the cholestasis of sepsis. | 8978362 | [
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Fatal hyperammonemia following orthotopic lung transplantation. | There have been anecdotes of unexplained coma and death in patients after otherwise successful orthotopic lung transplantation. A patient with primary pulmonary hypertension who underwent a technically uncomplicated single orthotopic lung transplantation is described. The patient developed intractable status epilepticus 4 days after surgery in association with the presence of a markedly elevated plasma ammonium level. Despite multiple therapeutic interventions; the hyperammonemia ultimately resulted in the | 8978364 | [
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Fatal hyperammonemia following orthotopic lung transplantation. | patient's death. Both metabolic and enzymatic studies showed that the unique physiological disturbance in this disorder results at least in part from defective in vivo conversion of waste nitrogen to urea and increased production of waste nitrogen. Although the rate of hepatic ureagenesis was therefore insufficient to prevent accumulation of ammonium; the cause was not severe liver disease. Liver histology showed widespread; microvesicular steatosis on light-microscopic examination; but only electron-micros | 8978364 | [
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Fatal hyperammonemia following orthotopic lung transplantation. | copic examination showed severe microvesicular steatosis with severe mitochondrial injury. As in Reye's syndrome; it was unclear whether the hepatic mitochondrial injury played a role in development or if it was the result of hyperammonemia. We recommended that any patient with an unexplained alteration of mental status after solid organ transplantation be evaluated for hyperammonemia. | 8978364 | [
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Basidiobolomycosis: an unusual fungal infection mimicking inflammatory bowel disease. | Basidiobolus ranarum is a fungus belonging to the Entomophthoraceae family and is mainly associated with subcutaneous soft tissue infection. The disease is usually characterized by an insidious onset of massive induration of the subcutaneous tissue involving the limbs; trunk; or buttocks. Most cases of basidiobolomycosis have been reported from Africa; South America; and tropical Asia. Visceral involvement is extremely rare. Only 4 cases with involvement of the gastrointestinal tract; including 1 fatal case | 8978366 | [
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Basidiobolomycosis: an unusual fungal infection mimicking inflammatory bowel disease. | originating in the United States; have been well documented in the English-language literature. This case report describes the first successfully treated patient residing in the United States who had B. ranarum infection involving the gastrointestinal tract. | 8978366 | [
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A new syndrome of Crohn's disease and pachydermoperiostosis in a family. | Few syndromic associations with Crohn's disease are described. The aim of this study was to characterize a new syndrome of Crohn's disease associated with pachydermoperiostosis in 3 brothers. Three probands; 6 siblings; both parents; 20 of 21 third-generation relatives; and 9 spousal controls were evaluated. Serological evaluation for antineutrophil cytoplasmic antibodies and human leukocyte antigens as well as genetic testing for tumor necrosis factor microsatellites; intercellular adhesion molecule 1 poly | 8978365 | [
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A new syndrome of Crohn's disease and pachydermoperiostosis in a family. | morphisms; the interleukin 1 receptor antagonist gene; and the interleukin 1 beta gene were performed. Only the 3 probands were affected and developed pachydermoperiostosis between ages 14 and 17 years. Pachydermoperiostosis preceded Crohn's ileocolitis by 6 and 20 years in two probands; excluding secondary hypertrophic osteoarthropathy. Two probands were antineutrophil cytoplasmic antibody positive vs. 1 of 27 unaffected relatives (P < 0.001; chi 2). Haplotypes for human leukocyte antigen and tumor necrosi | 8978365 | [
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