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Titolo:
REDUCED PULMONARY METABOLISM OF ENDOTHELIN-1 IN CANINE TACHYCARDIA-INDUCED HEART-FAILURE
Autore:
DUPUIS J; MOE GW; CERNACEK P;
Indirizzi:
MONTREAL HEART INST,DEPT MED,5000 BELANGER ST E MONTREAL PQ H1T 1C8 CANADA ST MICHAELS HOSP TORONTO ON M5B 1W8 CANADA
Titolo Testata:
Cardiovascular Research
fascicolo: 3, volume: 39, anno: 1998,
pagine: 609 - 616
SICI:
0008-6363(1998)39:3<609:RPMOEI>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CIRCULATING ENDOTHELIN-1; RECEPTOR ANTAGONISTS; PLASMA ENDOTHELIN; ET(B) RECEPTORS; CLEARANCE; HYPERTENSION; SITE; RATS;
Keywords:
ENDOTHELIN; PULMONARY CIRCULATION; PACEMAKER; ENDOTHELIAL FUNCTION; HEART FAILURE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
J. Dupuis et al., "REDUCED PULMONARY METABOLISM OF ENDOTHELIN-1 IN CANINE TACHYCARDIA-INDUCED HEART-FAILURE", Cardiovascular Research, 39(3), 1998, pp. 609-616

Abstract

Objectives: Plasma endothelin-l (ET-1) increases in congestive heart failure (CHF). The pulmonary vascular bed could contribute to this increase through a reduced clearance. We evaluated the effect of tachycardia-induced CHF on pulmonary ET-1 kinetics. To discern between changesdue to variations in pulmonary hemodynamics from true alterations of endothelial cell functions, we quantified ET-I kinetics in isolated rat lungs under variable pressure and flow-rate conditions. Methods and Results: Indicator-dilution studies were performed in anesthetized dogs (n=14) before and 3 weeks after rapid ventricular pacing and in isolated lungs from healthy rats (n=4). In isolated lungs, graded increases in perfusion rate from 5-25 ml/min caused gradual reductions in ET-1extraction from 60+/-1.5% to 17+/-4.9% (mean+/-S.D.). The capacity toclear ET-1 from the circulation, as computed from the permeability-surface area product (PS), however did not vary over this range of hows. CHF increased plasma ET-I (11.2+/-11.4 vs. 5.2+/-1.6 fmol/ml, p<0.01), did not affect pulmonary ET-1 extraction (29.4+/-12.5% vs. 29.9+/-12.9%), but decreased the PS (8.3+/-5.4 cm(3)/s vs. 14.4+/-9.9 cm(3)/s, p=0.038). Contrary to the invariability of the PS in normal isolated rat lungs, CHF was associated with a positive relationship between the PS and pulmonary plasma flow (r=0.65, p<0.01). ET-1 binding studies inlung tissues showed no significant variations in ETA and ETB receptors densities but revealed a threefold decrease in binding affinity (p<0.01) that may explain the reduced clearance. Conclusion: CHF causes a reduction of pulmonary ET-1 clearance that likely contributes to the increased circulating ET-1 levels and reflects pulmonary metabolic dysfunction associated with this condition. (C) 1998 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 19:47:00