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Titolo:
Mast cell stabilization prevents ethanol-induced rat gastric mucosal injury: Mechanisms of protection
Autore:
Kalia, N; Bardhan, KD; Reed, MWR; Jacob, S; Brown, NJ;
Indirizzi:
Royal Hallamshire Hosp, Dept Surg & Anaesthet Sci, Sheffield S10 2JF, S Yorkshire, England Royal Hallamshire Hosp Sheffield S Yorkshire England S10 2JF ire, England
Titolo Testata:
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
fascicolo: 2, volume: 15, anno: 2000,
pagine: 133 - 141
SICI:
0815-9319(200002)15:2<133:MCSPER>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
MICROVASCULAR PERMEABILITY; DAMAGE; HISTAMINE; SECRETION; FPL-52694; STOMACH; LESIONS;
Keywords:
gastric microcirculation; histamine; intravital microscopy; mast cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Kalia, N Royal Hallamshire Hosp, Dept Surg & Anaesthet Sci, K-Floor,Glossop Rd, Sheffield S10 2JF, S Yorkshire, England Royal Hallamshire Hosp K-Floor,Glossop Rd Sheffield S Yorkshire England S10 2JF
Citazione:
N. Kalia et al., "Mast cell stabilization prevents ethanol-induced rat gastric mucosal injury: Mechanisms of protection", J GASTR HEP, 15(2), 2000, pp. 133-141

Abstract

Introduction: We previously demonstrated that 60% ethanol increased macromolecular leakage and induced lesion formation in areas of permanent flow stasis within gastric mucosal vessels. Mast cells and their mediators have been implicated in acute mucosal injury. Fluorescent in vivo microscopy was used to assess the effects of ketotifen, a mast cell stabilizer, and pyrilamine, a histamine (H-1)-receptor antagonist, on ethanol-induced rat gastric mucosal injury. Methods: Experiments were carried out on anaesthetized rats pretreated orally with ketotifen (1 mg/kg) or pyrilamine (30 mg/kg). Fluorescein isothiocyanate-bovine serum albumin (FITC-BSA; 0.2 mL/100 g), a marker for quantitating macromolecular leakage was administered intra-arterially. Ethanol (60%) or distilled water was applied topically to the gastric mucosa. Macromolecular leakage of FITC-BSA, vessel diameters and leucocyte activity were quantified using image analysis. Results: Pretreatment with ketotifen or pyrilamine, followed by ethanol, caused no change in macromolecular leakage compared with controls. Both compounds prevented blood flow stasis in all areas and no lesion formation was observed. However, increased leucocyte activity and increases in vessel diameter were observed following pretreatment with ketotifen and pyrilamine, respectively. Conclusions: The data suggest that vasoactive substances released from mast cells may be involved in the aetiology of ethanol-induced gastric mucosaldamage. The prevention of these normal physiological responses to injury may lead to the employment of other microcirculatory mechanisms of defence. (C) 2000 Blackwell Science Asia Pty Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 15:49:13