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Titolo:
HYPOXIC AND ISCHEMIC HYPOXIA EXACERBATE BRAIN INJURY ASSOCIATED WITH METABOLIC ENCEPHALOPATHY IN LABORATORY-ANIMALS
Autore:
VEXLER ZS; AYUS JC; ROBERTS TPL; FRASER CL; KUCHARCZYK J; ARIEFF AI;
Indirizzi:
4 BROMPTON COURT HOUSTON TX 77024 UNIV CALIF SAN FRANCISCO,NEURORADIOL SECT SAN FRANCISCO CA 94143 BAYLOR COLL MED,DEPT MED HOUSTON TX 77024 VET AFFAIRS MED CTR,DEPT MED,GERIATR SECT SAN FRANCISCO CA 94121 UNIV CALIF SAN FRANCISCO SAN FRANCISCO CA 94121
Titolo Testata:
The Journal of clinical investigation
fascicolo: 1, volume: 93, anno: 1994,
pagine: 256 - 264
SICI:
0021-9738(1994)93:1<256:HAIHEB>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-BRAIN; HYPONATREMIC ENCEPHALOPATHY; CEREBRAL-ISCHEMIA; PATHO-PHYSIOLOGY; VASOPRESSIN; SYNAPTOSOMES; EDEMA; MORBIDITY; CHANNEL; DAMAGE;
Keywords:
METABOLIC ENCEPHALOPATHY; HYPOXIA; HYPONATREMIA; SYNAPTOSOMES; SODIUM TRANSPORT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
Z.S. Vexler et al., "HYPOXIC AND ISCHEMIC HYPOXIA EXACERBATE BRAIN INJURY ASSOCIATED WITH METABOLIC ENCEPHALOPATHY IN LABORATORY-ANIMALS", The Journal of clinical investigation, 93(1), 1994, pp. 256-264

Abstract

Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairsbrain adaptation to hyponatremia, worsening brain edema, we performedin vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was0%; with hyponatremia, 22%; and with hyponatremia + hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transportwas significantly altered such that brain cell osmolality would decrease: 44% increase in Na+-K+-ATPase transport activity(ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change inveratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 22:59:11