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Titolo:
INVOLVEMENT OF NITRIC-OXIDE IN THE PATHOGENESIS OF CYCLOPHOSPHAMIDE-INDUCED HEMORRHAGIC CYSTITIS
Autore:
SOUZA MVP; LIMA MVA; POMPEU MML; BALLEJO G; CUNHA FQ; RIBEIRO RD;
Indirizzi:
UFC,CCS,DEPT FISIOL & FARMACOL,HLTH SCI CTR,RUA CORONEL NUNES MELO 1127 BR-60430270 FORTALEZA CEARA BRAZIL UFC,CCS,DEPT FISIOL & FARMACOL,HLTH SCI CTR BR-60430270 FORTALEZA CEARA BRAZIL UFC,HLTH SCI CTR,DEPT PATHOL BR-60430270 FORTALEZA CEARA BRAZIL USP,FAC MED,DEPT PHARMACOL RIBEIRAO PRET BRAZIL
Titolo Testata:
The American journal of pathology
fascicolo: 1, volume: 150, anno: 1997,
pagine: 247 - 256
SICI:
0002-9440(1997)150:1<247:IONITP>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET-ACTIVATING-FACTOR; SYNTHASE; INHIBITION; CELLS; ALPHA; EDEMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
M.V.P. Souza et al., "INVOLVEMENT OF NITRIC-OXIDE IN THE PATHOGENESIS OF CYCLOPHOSPHAMIDE-INDUCED HEMORRHAGIC CYSTITIS", The American journal of pathology, 150(1), 1997, pp. 247-256

Abstract

The involvement of nitric oxide (NO) and the potential modulation of NO synthase (NOS) activity by platelet-activating factor were investigated in a rat model of cyclophosphamide-induced hemorrhagic cystitis, Male Wista rats received a single intraperitoneal injection of cyclophosphamide, and cystitis was evaluated 6, 12, 24, 48, and 72 hours later by determining the changes in bladder wet weight and plasma protein extravasation and the macro- and microscopic morphological alterations. In addition, NOS activity and NADPH-diaphorase histochemistry were studied in bladder tissues. Normal bladders showed extensizre NADPH-diaphorase staining and a high level of constitutive NOS whereas the activity of inducible NOS was almost undetectable, Cyclophosphamide dose- and time-dependently increased the bladder wet weight and bladder plasma protein extravasation. These events were accompanied at a microscopic level by urothelial necrosis, sloughing, ulceration, hemorrhage, and leukocyte infiltration, Cyclophosphamide also increased the levels of inducible NOS but reduced those of constitutive NOS. The NOS inhibitors L-N-G-nitroarginine methyl ester and L-N-G-nitroarginine significantly reduced the cyclophosphamide-induced plasma protein extravasationand urothelial damage, This reduction was completely reversed by L-arginine but not by D-arginine. The administration of the platelet-activating factor antagonist BN 52021 decreased the cyclophosphamide-induced plasma protein extravasation as well as the rise ill inducible NOS activity but had no effect on the fall in constitutive NOS activity, These results suggest that endogenous NO participates in the urothelial damage and in the inflanzmirtory events leading to cyclophosphamide-induced hemorrhagic cystitis. Platelet-activating factor also seems to be involved in the pathogenesis of this condition, possibly by inducingNOS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 10:49:34