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Titolo:
Airway vasculature after mycoplasma infection: chronic leakiness and selective hypersensitivity to substance P
Autore:
Kwan, ML; Gomez, AD; Baluk, P; Hashizume, H; McDonald, DM;
Indirizzi:
Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USAUniv Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, Dept Anat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 2, volume: 280, anno: 2001,
pagine: L286 - L297
SICI:
1040-0605(200102)280:2<L286:AVAMIC>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
RESPIRATORY-TRACT INFECTIONS; ENDOTHELIAL GROWTH-FACTOR; NEUROGENIC INFLAMMATION; RAT TRACHEA; MICROVASCULAR LEAKAGE; GUINEA-PIG; PLASMA EXTRAVASATION; PERMEABILITY; ASTHMA; ANGIOGENESIS;
Keywords:
angiogenesis; beta(2)-adrenoceptor agonists; endothelial cells; Evans blue; inflammation; Mycoplasma pulmonis; salmeterol; vascular permeability; Wistar rats; Fischer 344 rats;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: McDonald, DM Univ Calif San Francisco, Cardiovasc Res Inst, Box 0130,Rm S-1363, San Francisco, CA 94143 USA Univ Calif San Francisco Box 0130,Rm S-1363 San Francisco CA USA 94143
Citazione:
M.L. Kwan et al., "Airway vasculature after mycoplasma infection: chronic leakiness and selective hypersensitivity to substance P", AM J P-LUNG, 280(2), 2001, pp. L286-L297

Abstract

Angiogenesis and microvascular remodeling are features of chronic airway inflammation caused by Mycoplasma pulmonis infection in rats. As airway blood vessels undergo remodeling, they become unusually sensitive to substance P-induced plasma leakage. Here we determined whether the remodeled vessels are leaky under baseline conditions, whether their heightened sensitivity is specific to substance P, and whether the leakage is reversible. Four weeks after infection, the amount of baseline leakage of Evans blue in the tracheal mucosa was two to five times the normal level. Gaps < 1 <mu>m in diameter were located between endothelial cells in some remodeled vessels. Substance P, but not platelet-activating factor or 5-hydroxytryptamine, producedan exaggerated leakage response. Inhalation of the beta (2)-adrenergic receptor agonist salmeterol reduced the leakage by <60%. We conclude that the blood vessel remodeling after M. pulmonis infection is associated with microvascular leakiness due, in part, to the formation of endothelial gaps. This leakage is accompanied by an abnormal sensitivity to substance P but not to platelet-activating factor or 5-hydroxytryptamine and can be reduced by <beta>(2)-agonists.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 07:31:49