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Titolo:
Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs
Autore:
Ogasa, T; Nakano, H; Ide, H; Yamamoto, Y; Sasaki, N; Osanai, S; Akiba, Y; Kikuchi, K; Iwamoto, J;
Indirizzi:
Asahikawa Med Coll, Sch Nursing, Dept Med, Asahikawa, Hokkaido 0788510, Japan Asahikawa Med Coll Asahikawa Hokkaido Japan 0788510 kkaido 0788510, Japan Asahikawa Med Coll, Sch Nursing, Div Appl Physiol, Asahikawa, Hokkaido 0788510, Japan Asahikawa Med Coll Asahikawa Hokkaido Japan 0788510 kkaido 0788510, Japan
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 1, volume: 91, anno: 2001,
pagine: 363 - 370
SICI:
8750-7587(200107)91:1<363:FRONOI>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
PULMONARY CIRCULATION; RELAXING FACTOR; L-ARGININE; ENDOTHELIUM; ACETYLCHOLINE; VASCULATURE; GENERATION; EXERCISE; INVIVO; SITE;
Keywords:
pulmonary endothelium; shear stress; recruitment;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Nakano, H Asahikawa Med Coll, Dept Internal Med, 1-1 Higashi 2-1, Asahikawa, Hokkaido 0788510, Japan Asahikawa Med Coll 1-1 Higashi 2-1 Asahikawa Hokkaido Japan 0788510
Citazione:
T. Ogasa et al., "Flow-mediated release of nitric oxide in isolated, perfused rabbit lungs", J APP PHYSL, 91(1), 2001, pp. 363-370

Abstract

The effects of changing perfusate flow on lung nitric oxide (NO) production and pulmonary arterial pressure (Ppa) were tested during normoxia and hypoxia and after N-G-monomethyl-L-arginine (L-NMMA) treatment during normoxiain both blood- and buffer-perfused rabbit lungs. Exhaled NO (eNO) was unaltered by changing perfusate flow in blood-perfused lungs. In buffer-perfused lungs, bolus injections of ACh into the pulmonary artery evoked a transient increase in eNO from 67 +/- 3 (SE) to 83 +/- 7 parts/billion with decrease in Ppa, whereas perfusate NO metabolites (pNOx) remained unchanged. Stepwise increments in flow from 25 to 150 ml/min caused corresponding stepwiseelevations in eNO production (46 +/- 2 to 73 +/- 3 nl/min) without changesin pNOx during normoxia. Despite a reduction in the baseline level of eNO,flow-dependent increases in eNO were still observed during hypoxia. L-NMMAcaused declines in both eNO and pNOx with a rise in Ppa. Pulmonary vascular conductance progressively increased with increasing flow during normoxia and hypoxia. However, L-NMMA blocked the flow-dependent increase in conductance over the range of 50-150 ml/min of flow. In the more physiological conditions of blood perfusion, eNO does not reflect endothelial NO production. However, from the buffer perfusion study, we suggest that endothelial NO production secondary to increasing flow, may contribute to capillary recruitment and/or shear stress-induced vasodilation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 18:23:00