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Titolo:
ROLE OF K-FLOW IN THE RAT - EFFECT OF GLIBENCLAMIDE AND OUABAIN( IN REGULATING HYPOXIC CEREBRAL BLOOD)
Autore:
REID JM; PATERSON DJ;
Indirizzi:
UNIV OXFORD,PHYS LAB,PARK RD OXFORD OX1 3PT ENGLAND UNIV OXFORD,PHYS LAB OXFORD OX1 3PT ENGLAND
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 1, volume: 39, anno: 1996,
pagine: 45 - 52
SICI:
0363-6135(1996)39:1<45:ROKITR>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXTRACELLULAR POTASSIUM; HIPPOCAMPAL SLICES; NEURONS INVITRO; ANOXIA; BRAIN; RELEASE; SULFONYLUREAS; CHANNEL; CORTEX;
Keywords:
HYPOXIA; SODIUM-POTASSIUM-ADENOSINE-TRIPHOSPHATASE SULFONYLUREA; ARTERIAL BLOOD FLOW;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
J.M. Reid e D.J. Paterson, "ROLE OF K-FLOW IN THE RAT - EFFECT OF GLIBENCLAMIDE AND OUABAIN( IN REGULATING HYPOXIC CEREBRAL BLOOD)", American journal of physiology. Heart and circulatory physiology, 39(1), 1996, pp. 45-52

Abstract

We assessed the role of extracellular potassium ([K+](e)) on the increase in cerebral blood flow (CBF) during hypoxia, and we tested whether it was affected by glibenclamide or ouabain. Cortical CBF was measured using the hydrogen clearance technique in enflurane-anesthetized rats, and local [K+](e) was measured with K+ microelectrodes adjacent tothe hydrogen electrode. Eucapnic hypoxia (arterial P-O2 similar to 35-40 Torr) increased CBF twofold and caused a modest rise in [K+](e) (from 2.9 +/- 0.2 to 3.7 +/- 0.2 mM; mean arterial blood pressure, ABP, 86 +/- 5 mmHg). If ABP fell <70 mmHg during hypoxia, no increase in CBF was seen, whereas [K+](e) increased to >20 mM. Glibenclamide (10-100mu M intracortically) attenuated [K+](e) and CBF during hypoxia (ABP similar to 75 mmHg, P < 0.01). Ouabain (20-1,000 mu M) increased [K+](e); however, it did not remove the hypoxic-induced rise in [K+](e). Weconclude that glibenclamide-sensitive potassium channels contribute to the accumulation of [K+](e) during hypoxia, although an increase in CBF during hypoxia can occur without a marked rise in [K+](e). Furthermore, if ABP falls below the lower limit of autoregulation during hypoxia, there is no increase in CBF, yet there is a large increase in [K+](e).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 03:42:58