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Titolo:
Cardiac endothelial transport and metabolism of adenosine and inosine
Autore:
Schwartz, LM; Bukowski, TR; Revkin, JH; Bassingthwaighte, JB;
Indirizzi:
Univ Washington, Dept Bioengn, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 Dept Bioengn, Seattle, WA 98195 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 3, volume: 46, anno: 1999,
pagine: H1241 - H1251
SICI:
0363-6135(199909)46:3<H1241:CETAMO>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-TISSUE EXCHANGE; ISOLATED GUINEA-PIG; NUCLEOSIDE TRANSPORT; SPECIES-DIFFERENCES; NITROBENZYLTHIOINOSINE BINDING; VASCULAR ENDOTHELIUM; MYOCARDIAL-ISCHEMIA; HUMAN-ERYTHROCYTES; XANTHINE-OXIDASE; RABBIT HEART;
Keywords:
nucleoside transport; species specificity; biological transport; multiple-indicator dilution technique; capillary endothelial permeability; blood-tissue exchange; isolated heart; rabbit; guinea pig;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Bassingthwaighte, JB Univ Washington, Dept Bioengn, Box 357962, Seattle, WA 98195 USA Univ Washington Box 357962 Seattle WA USA 98195 5 USA
Citazione:
L.M. Schwartz et al., "Cardiac endothelial transport and metabolism of adenosine and inosine", AM J P-HEAR, 46(3), 1999, pp. H1241-H1251

Abstract

The influence of transmembrane flux limitations on cellular metabolism of purine nucleosides was assessed in whole organ studies. Transcapillary transport of the purine nucleosides adenosine (Ado) and inosine (Ino) via paracellular diffusion through interendothelial clefts in parallel with carrier-mediated transendothelial fluxes was studied in isolated, Krebs-Henseleit-perfused rabbit and guinea pig hearts. After injection into coronary inflow,multiple-indicator dilution curves were obtained from coronary outflow for90 s for I-131-labeled albumin (intravascular reference tracer), [H-3]arabinofuranosyl hypoxanthine (AraH; extracellular reference tracer and nonreactive adenosine analog), and either [C-14]Ado or [C-14]Ino. Ado or Ino was separated from their degradative products, hypoxanthine, xanthine, and uric acid, in each outflow sample by HPLC and radioisotope counting. Ado and Ino, but not AraH, permeate the luminal membrane of endothelial cells via a saturable transporter with permeability surface area product PSecl and also diffuse passively through interendothelial clefts with the same conductance (PSg) as AraH. These parallel conductances were estimated via fitting with an axially distributed, multi-pathway, four-region blood-tissue exchange model. PSg for AraH were similar to 4 and 2.5 ml.g(-1).min(-1) in rabbits andguinea pigs, respectively. In contrast, transplasmalemmal conductances (endothelial PSecl) were similar to 0.2 ml.g(-1).min(-1) for both Ado and Ino in rabbit hearts hut similar to 2 ml.g(-1).min(-1) in guinea pig hearts, anorder of magnitude different. Purine nucleoside metabolism also differs between guinea pig and rabbit cardiac endothelium. In guinea pig heart, 50% of the tracer Ado bolus was retained, 35% was washed out as Ado, and 15% waslost as effluent metabolites; 25% of Ino was retained, 50% washed out, and25% was lost as metabolites. In rabbit heart, 45% of Ado was retained and 5% lost as metabolites, and 7% of Ino was retained and 3% lost as metabolites. We conclude that endothelial transport of Ado and Ino is a prime determinant of their metabolic fates: where transport rates are high, metabolic transformation is high.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 15:07:39