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Titolo:
Endogenous and exogenous coronary vasodilatation are attenuated in cardiachypertrophy: a morphological defect?
Autore:
Kingsbury, MP; Turner, MA; Flores, NA; Bovill, E; Sheridan, DJ;
Indirizzi:
Univ London Imperial Coll Sci Technol & Med, Sch Med, Div NHLI, Acad Cardiol Unit, London W2 1NY, England Univ London Imperial Coll Sci Technol & Med London England W2 1NY ngland
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 3, volume: 32, anno: 2000,
pagine: 527 - 538
SICI:
0022-2828(200003)32:3<527:EAECVA>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEFT-VENTRICULAR HYPERTROPHY; GUINEA-PIG HEART; SPONTANEOUSLY HYPERTENSIVE RATS; NITRIC-OXIDE; REACTIVE HYPEREMIA; VASCULAR RESERVE; ANGINA-PECTORIS; FLOW; PRESSURE; RESISTANCE;
Keywords:
adenosine; coronary circulation; endothelial-derived factors; hypertrophy; microcirculation; nitric oxide; vasodilatation; reactive hyperaemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Sheridan, DJ Univ London Imperial Coll Sci Technol & Med, Sch Med, Div NHLI, Acad Cardiol Unit, St Marys Campus,10th Floor,QEQM Wing,S Wharf Rd, London W2 1NY, England Univ London Imperial Coll Sci Technol & Med St Marys Campus,10th Floor,QEQM Wing,S Wharf Rd London England W2 1NY
Citazione:
M.P. Kingsbury et al., "Endogenous and exogenous coronary vasodilatation are attenuated in cardiachypertrophy: a morphological defect?", J MOL CEL C, 32(3), 2000, pp. 527-538

Abstract

Reactive hyperaemia (RH) following brief ischaemia is reduced in hypertrophied hearts, and this may contribute to reduced coronary now reserve. We studied vasodilatation during RH and in response to exogenous stimuli in control and hypertrophied hearts and explored the mechanisms underlying RH. Vascular reactivity was assessed in isolated hypertrophied hearts (55 +/- 3 days after aortic banding or sham operation) by constructing dose-response curves to acetylcholine (ACh), sodium nitroprusside (SNP) and adenosine. Reactive hyperaemic vasodilatation was assessed after global ischaemia (5-120 s) in the presence/absence of L-NAME, 8-phenyltheophylline (8-PT) and glibenclamide, Purine release and NO overflow in the coronary perfusate were analysed. Aortic constriction increased heart/body weight ratio (47%), myocyte size (19%) and arteriolar wall thickness (51%), all P<0.01. Coronary reserve was reduced in hypertrophy (105 +/- 8% v 182 +/- 12%, P<0.01). Dose response curves for ACh, SNP and adenosine were reduced in hypertrophy (69%, 86%and 68%, all P<0.01) v shams; however ED50 values were unchanged. The peakflow and duration of RH were also attenuated (50%, P<0.001) in hypertrophy. While purine washout during RH was related to the duration of preceding ischaemia, nitrate washout was not. RH experiments in the presence of L-NAME, 8-PT and glibenclamide indicated that RHI is mediated by combined actionsof K-ATP channels>adenosine>NO in both groups. RH is mediated by similar mechanisms in control and hypertrophied hearts. All vasodilatation was similarly attenuated in hypertrophy, independent of endothelial activation. We hypothesize that increased arteriolar wall thickness map limit vasodilator responses to all stimuli in hypertrophy. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 09:58:29