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Titolo:
VIRUS-INDUCED AIRWAY HYPERRESPONSIVENESS IN GUINEA RIGS IS RELATED TOA DEFICIENCY IN NITRIC-OXIDE
Autore:
FOLKERTS G; VANDERLINDE HJ; NIJKAMP FP;
Indirizzi:
UNIV UTRECHT,INST PHARMACEUT SCI,DEPT PHARMACOL,POB 80082 3508 TB UTRECHT NETHERLANDS
Titolo Testata:
The Journal of clinical investigation
fascicolo: 1, volume: 95, anno: 1995,
pagine: 26 - 30
SICI:
0021-9738(1995)95:1<26:VAHIGR>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
ASTHMA SYMPTOMS; PIG; INFLAMMATION; INFECTION; CELLS; EPITHELIUM; HISTAMINE; PRECIPITANTS; SYNTHASE; RELEASE;
Keywords:
L-ARGININE; PULMONARY RESISTANCE; PERFUSED TRACHEAL TUBE; PARAINFLUENZA 3 VIRUS; EPITHELIUM-DERIVED RELAXING FACTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
G. Folkerts et al., "VIRUS-INDUCED AIRWAY HYPERRESPONSIVENESS IN GUINEA RIGS IS RELATED TOA DEFICIENCY IN NITRIC-OXIDE", The Journal of clinical investigation, 95(1), 1995, pp. 26-30

Abstract

Intratracheal inoculation of parainfluenza type 3 virus to guinea pigs induces a marked increase in airway responsiveness in vivo and in vitro. In spontaneously breathing anesthetized guinea pigs inhalation ofan aerosol containing the nitric oxide (NO) precursor L-arginine (2.0mM) completely prevented the virus-induced airway hyperresponsivenessto histamine. In addition, perfusion of L-arginine (200 mu M) or the direct NO-donor S-nitroso-N-acetyl-penicillamine (SNAP, 1 mu M) through the lumen of tracheal tubes from infected animals prevented the increase in airway responsiveness to histamine or the cholinoceptor agonist methacholine. The NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME, 120 mu M) did not further increase the virus-induced airway hyperresponsiveness. In additional experiments, NO was measured with an Iso-NO nitric oxide meter and sensor. Stimulation of control tissues in vitro with histamine (10(-3) M) resulted in a contractionwith a simultaneous release of NO (44.5+/-5.4 nM). The release of NO was markedly reduced by 75% (P < 0.01, 11.4+/-3.1 nM) in tracheas fromvirus-infected animals that demonstrated enhanced contractile responses. Preincubation of tissues from virus-treated guinea pigs with L-arginine (200 mu M) completely prevented the enhanced contraction and simultaneously returned the NO production to control values (51.2+/-3.4 nM). An NO deficiency might be causally related to the development of airway hyperresponsiveness after a viral respiratory infection.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/10/20 alle ore 13:06:38