Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Protection of ischemic myocardium in diabetics by inhibition of electroneutral Na+-K+-2Cl(-) cotransporter
Autore:
Ramasamy, R; Payne, JA; Whang, J; Bergmann, SR; Schaefer, S;
Indirizzi:
Columbia Univ, Coll Phys & Surg, Div Cardiol, Dept Med, New York, NY 10032USA Columbia Univ New York NY USA 10032 diol, Dept Med, New York, NY 10032USA Univ Calif Davis, Dept Internal Med, Div Cardiovasc Med, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 v Cardiovasc Med, Davis, CA 95616 USA Univ Calif Davis, Dept Human Physiol, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 pt Human Physiol, Davis, CA 95616 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: H515 - H522
SICI:
0363-6135(200108)281:2<H515:POIMID>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERFUSED RAT-HEART; CYTOSOLIC FREE CALCIUM; INTRACELLULAR PH; NA+/H+ EXCHANGE; GLOBAL-ISCHEMIA; SODIUM; INJURY; REPERFUSION; CONTRACTURE; MODULATION;
Keywords:
diabetes; ischemic injury; sodium transporters;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Ramasamy, R Columbia Univ, Coll Phys & Surg, Div Cardiol, Dept Med, PH 3-342,630 W 168th St, New York, NY 10032 USA Columbia Univ PH 3-342,630 W 168th St New York NY USA 10032 SA
Citazione:
R. Ramasamy et al., "Protection of ischemic myocardium in diabetics by inhibition of electroneutral Na+-K+-2Cl(-) cotransporter", AM J P-HEAR, 281(2), 2001, pp. H515-H522

Abstract

Diabetes increases both the incidence of cardiovascular disease and complications of myocardial infarction and heart failure. Studies using diabetic animals have shown that changes in myocardial sodium transporters result inalterations in intracellular sodium (Na-i) homeostasis. Because the changes in sodium homeostasis can be due to increased entry of Na+ via the electroneutral Na+-K+-2Cl(-) cotransporter (NKCC), we conducted experiments in acute diabetic hearts to determine if 1) net inward cation flux via NKCC is increased, 2) this cotransporter contributes to a greater increase in Nai during ischemia, and 3) inhibition of NKCC limits injury and improves function after ischemia-reperfusion. These issues were investigated in perfused type I diabetic and nondiabetic rat hearts subjected to ischemia and 60 min of reperfusion. A group of diabetic and nondiabetic hearts was perfused with5 muM of bumetanide, an inhibitor of NKCC. Flux via NKCC, Nai, and ATP wasmeasured in each group with the use of radiotracer Rb-86, Na-23, and P-31 nuclear magnetic resonance spectroscopy, respectively, whereas ischemic injury was assessed by measuring creatine kinase release on reperfusion. Cation flux via NKCC, as measured by Rb-86 uptake, was significantly increased in diabetic hearts. Inhibition of NKCC significantly reduced ischemic injuryin diabetic hearts, improved functional recovery on reperfusion, attenuated the ischemic rise in Na-i, and conserved ATP during ischemia-reperfusion. Parallel studies in nondiabetic hearts showed that NKCC inhibition was notcardioprotective. These findings demonstrate that flux via NKCC is increased in type I diabetic hearts and that inhibition with bumetanide attenuateschanges in Na-i and ATP during ischemia and protects against ischemic injury. The data suggest a therapeutic role for pharmacological agents that inhibit flux via NKCC in diabetic patients with myocardial ischemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/01/20 alle ore 12:16:23