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Titolo:
Mechanisms of Helicobacter pylori-induced rat gastric mucosal microcirculatory disturbances in vivo
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:
DIGESTIVE DISEASES AND SCIENCES
fascicolo: 4, volume: 45, anno: 2000,
pagine: 763 - 772
SICI:
0163-2116(200004)45:4<763:MOHPRG>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET-ACTIVATING FACTOR; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; MAST-CELLS; MICROVASCULAR PERMEABILITY; EICOSANOID SYNTHESIS; SURFACE-PROTEINS; DUODENAL-ULCER; HISTAMINE; NEUTROPHILS; RELEASE;
Keywords:
gastric mucosal microcirculation; fluorescent in vivo microscopy; platelet aggregation; mast cells; histamine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
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., "Mechanisms of Helicobacter pylori-induced rat gastric mucosal microcirculatory disturbances in vivo", DIG DIS SCI, 45(4), 2000, pp. 763-772

Abstract

The exact mechanisms by which Helicobacter pylori infection results in gastric mucosal injury are unclear. However, it has been demonstrated that surface protein extracts of the bacterium can induce a number of disturbances within the rat gastric mucosal microcirculation, including platelet aggregation and macromolecular leakage (MML) of labeled albumin. This study aimed to determine the mechanisms involved in inducing these events using the technique of fluorescent in vivo microscopy. Male Wistar rats were pretreated with either ketotifen, a mast cell stabilizer (1 mg/kg), pyrilamine, an H-1-receptor antagonist (30 mg/kg), hexanolamine-PAF, a PAF-receptor antagonist (10 mu g/kg), L-arginine, the nitric oxide precursor (300 mg/kg) or vehicle, saline. Then 0.5 mi of H. pylori extract was administered to the exteriorized gastric mucosa of the anesthetized rat. Alterations in fluorescein-labeled albumin leak, vessel diameters, and acridine red-labeled leukocyte and platelet activity were determined over a 2-hr period. Saline pretreated animals demonstrated significant MML with a peak at 5 min (11%, P < 0.02). This was prevented with ketotifen and pyrilamine, but not with hexanolamine-PAF (17.5%, P < 0.05) and L-arginine (13%, P < 0.05). Significant numbers of platelet emboli and thrombi were observed within mucosal capillaries andpostcapillary venules with vehicle pretreatment; this was prevented with hexanolamine-PAF and L-arginine, but not with ketotifen and pyrilamine. In conclusion, these studies demonstrate that more than one mediator is involved in inducing the rat gastric mucosal microcirculatory disturbances associated with H. pylori administration. Mast cells and histamine are linked to MML, with PAF, probably not derived from mast cells, involved in platelet activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 11:59:56