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        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Se revisa el papel que desempe&#241;an los astrocitos en la progresi&#243;n del da&#241;o cerebral isqu&#233;mico&#46; Evidencias recientes obtenidas con cultivos de astrocitos han revelado que estas c&#233;lulas se encargan de amortiguar las tres alteraciones principales del medio extracelular inducidas por la isquemia&#58; i&#41; la elevaci&#243;n del K<span class="elsevierStyleSup">&#43;</span> que impide una transmisi&#243;n adecuada de los potenciales de acci&#243;n&#44; ii&#41; la elevaci&#243;n hasta niveles neurot&#243;xicos del glutamato que desencadena la muerte neuronal y iii&#41; la acidosis que interfiere negativamente en el metabolismo neuronal&#46; La hiperactividad de estos mecanismos de compensaci&#243;n durante las isquemia origina un edema citot&#243;xico glial&#46; A pesar de ello&#44; los astrocitos resisten mejor el insulto isqu&#233;mico que las neuronas permaneciendo viables y metab&#243;licamente activos durante un periodo m&#225;s prolongado&#46; Las interacciones metab&#243;licas entre neuronas y c&#233;lulas gliales en el foco isqu&#233;mico resultan esenciales en la supervivencia neuronal&#46; Recientemente ha sido posible explorar estas interacciones empleando la espectroscopia de resonancia magn&#233;tica de <span class="elsevierStyleSup">13</span>C&#46; Los resultados obtenidos &#8220;in vivo&#8221; son consistentes con el mantenimiento del edema citot&#243;xico glial y un mayor consumo del exceso de glutamato durante las primeras veinticuatro horas del insulto isqu&#233;mico&#46; Estos datos revelan un papel fundamental de las c&#233;lulas gliales en la fisiopatologia de la isquemia cerebr&#46;al&#46;</p>"
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        "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">The role played by astrocytes in the development of ischemic brain damage is reviewed&#46; Recent evidences obtained with astrocytes in culture reveal that these cells buffer the three major changes in the extracellular fluid occuring during the ischemic injury&#58; i&#41; the rise in K<span class="elsevierStyleSup">&#43;</span> concentration which hamper adequate transmission of action potentials&#44; ii&#41; the increase in glutamate concentration up to neurotoxic levels inducing neuronal death and iii&#41; the increased acidosis which inteferes negatively in neuronal metabolismo Hyperactivity of these compensatory mechanisms during ischemic episodes causes glial swelling&#46; In spite of this&#44; astrocytes show better resistance to ischemic damage than neurons&#44; remaining viable and metabolicalIy active during a longer periodo Metabolic interactions between neurons and glial celIs in the ischemic area are essential to maintain neuronal survival&#46; RecentIy&#44; it has been possible to explore these interactions in vivo using <span class="elsevierStyleSup">13</span>C magnetic resonance spectroscopy&#46; Results obtain &#8220;in vivo&#8221; are consistent with glial swelling caused by increased glutamate metabolism is maintained during the first twenty four hours after the ischemic insul&#237;&#46; Present data reveal a fundamental role of glial cells in the patophysiology of cerebral ischemia&#46;</p>"
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Vol. 11. Núm. 4.
Páginas 247-258 (enero 1999)
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Vol. 11. Núm. 4.
Páginas 247-258 (enero 1999)
Fisiopatología de las células gliales en la isquemia cerebral
Physiopathology of glial cells in cerebral ischemia
Visitas
3078
J.M. Pascual, F. González-Llanos, F. Carceller, J.M. Roda
Unidad de Investigación Cerebrovascular, Hospital Universitario La Paz
S. Cerdán*
* Instituto de Investigaciones Biomédicas.C.S.I.C
Este artículo ha recibido
Información del artículo
Resumen

Se revisa el papel que desempeñan los astrocitos en la progresión del daño cerebral isquémico. Evidencias recientes obtenidas con cultivos de astrocitos han revelado que estas células se encargan de amortiguar las tres alteraciones principales del medio extracelular inducidas por la isquemia: i) la elevación del K+ que impide una transmisión adecuada de los potenciales de acción, ii) la elevación hasta niveles neurotóxicos del glutamato que desencadena la muerte neuronal y iii) la acidosis que interfiere negativamente en el metabolismo neuronal. La hiperactividad de estos mecanismos de compensación durante las isquemia origina un edema citotóxico glial. A pesar de ello, los astrocitos resisten mejor el insulto isquémico que las neuronas permaneciendo viables y metabólicamente activos durante un periodo más prolongado. Las interacciones metabólicas entre neuronas y células gliales en el foco isquémico resultan esenciales en la supervivencia neuronal. Recientemente ha sido posible explorar estas interacciones empleando la espectroscopia de resonancia magnética de 13C. Los resultados obtenidos “in vivo” son consistentes con el mantenimiento del edema citotóxico glial y un mayor consumo del exceso de glutamato durante las primeras veinticuatro horas del insulto isquémico. Estos datos revelan un papel fundamental de las células gliales en la fisiopatologia de la isquemia cerebr.al.

Palabras clave:
Isquemia cerebral
Astrocitos
Metabolismo cerebral
Interacciones
Neurona-glía
Espectroscopia de Resonancia Magnética 13C
Summary

The role played by astrocytes in the development of ischemic brain damage is reviewed. Recent evidences obtained with astrocytes in culture reveal that these cells buffer the three major changes in the extracellular fluid occuring during the ischemic injury: i) the rise in K+ concentration which hamper adequate transmission of action potentials, ii) the increase in glutamate concentration up to neurotoxic levels inducing neuronal death and iii) the increased acidosis which inteferes negatively in neuronal metabolismo Hyperactivity of these compensatory mechanisms during ischemic episodes causes glial swelling. In spite of this, astrocytes show better resistance to ischemic damage than neurons, remaining viable and metabolicalIy active during a longer periodo Metabolic interactions between neurons and glial celIs in the ischemic area are essential to maintain neuronal survival. RecentIy, it has been possible to explore these interactions in vivo using 13C magnetic resonance spectroscopy. Results obtain “in vivo” are consistent with glial swelling caused by increased glutamate metabolism is maintained during the first twenty four hours after the ischemic insulí. Present data reveal a fundamental role of glial cells in the patophysiology of cerebral ischemia.

Key words:
Cerebral ischemia
Astrocytes
Brain metabolism
Neuronal-glial interactions, 13C NMR spectroscopy

Artículo

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