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Titolo:
SPREADING DEPRESSION IN FOCAL ISCHEMIA - A COMPUTATIONAL STUDY
Autore:
REVETT K; RUPPIN E; GOODALL S; REGGIA JA;
Indirizzi:
UNIV MARYLAND HOSP,DEPT NEUROL,22 S GREENE ST BALTIMORE MD 21201 UNIV MARYLAND,INST ADV COMP STUDIES,DEPT NEUROL BALTIMORE MD 21201 UNIV MARYLAND,INST ADV COMP STUDIES,DEPT COMP SCI BALTIMORE MD 21201 TEL AVIV UNIV,DEPT COMP SCI IL-69978 TEL AVIV ISRAEL TEL AVIV UNIV,DEPT PHYSIOL IL-69978 TEL AVIV ISRAEL
Titolo Testata:
Journal of cerebral blood flow and metabolism
fascicolo: 9, volume: 18, anno: 1998,
pagine: 998 - 1007
SICI:
0271-678X(1998)18:9<998:SDIFI->2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBRAL-ARTERY OCCLUSION; BLOOD-FLOW; RAT; GLUTAMATE; PENUMBRA; STROKE; CORTEX; PATHOPHYSIOLOGY; THRESHOLDS; MIGRAINE;
Keywords:
FOCAL ISCHEMIA; CORTICAL SPREADING DEPRESSION; COMPUTATIONAL MODELS; STROKE; ISCHEMIC PENUMBRA; CALCIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
K. Revett et al., "SPREADING DEPRESSION IN FOCAL ISCHEMIA - A COMPUTATIONAL STUDY", Journal of cerebral blood flow and metabolism, 18(9), 1998, pp. 998-1007

Abstract

When a cerebral infarction occurs, surrounding the core of dying tissue there usually is an ischemic penumbra of nonfunctional but still viable tissue. One current but controversial hypothesis is that this penumbra tissue often eventually dies because of the metabolic stress imposed by multiple cortical spreading depression (CSD) waves, that is, by ischemic depolarizations. We describe here a computational model of CSD developed to study the implications of this hypothesis. After simulated infarction, the model displays the linear relation between finalinfarct size and the number of CSD waves traversing the penumbra thathas been reported experimentally, although damage with each individual wave progresses nonlinearly with time. It successfully reproduces the experimental dependency of final infarct size on midpenumbra cerebral blood flow and potassium reuptake rates, and predicts a critical penumbra blood flow rate beyond which damage does not occur. The model reproduces the dependency of CSD wave propagation on N-methyl-D-aspartate activation. It also makes testable predictions about the number, velocity, and duration of ischemic CSD waves and predicts a positive correlation between the duration of elevated potassium in the infarct coreand the number of CSD waves. These findings support the hypothesis that CSD waves play an important causal role in the death of ischemic penumbra tissue.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 18:37:23