[The pathological and the compensatory in cerebral ischemia: molecular aspects].
BACKGROUND
An integral approach of the whole mechanisms involved during ischemic brain damage let us to realize that some phenomena, usually considered as 'pathological' make an integrate and harmonious response directed towards the preservation of neuronal survival and functional integrity of the whole system.


METHODS
It has been proposed that cellular lysis in a core of lesion may be protective for the surrounding tissue, as well as the development of vasoconstriction and cellular edema, in the face of the loss of intracellular calcium homeostasis. Some recent findings tend to support this hypothesis. Adaptative response to lower oxygen and glucose availability is linked with the inhibition of neuronal activity, and therefore, with their involved functions. Formation of prostanoids and hydrogen peroxide, and release of interleukin and neurotrophic factors are related to the expression of immediate early genes, the enhancement of cellular response during ischemic conditions and also related to the induction of mechanisms of repair and regeneration, where astroglial cells play a key role.


CONCLUSIONS
Pharmacological inhibition, hypothermia and hyperbaric oxygenation had been employed with a relative success in the clinical management of ischemic injured patients. That interventions are in agreement with some of these endogenous compensatory mechanisms, which become the brain less vulnerable that it is generally considered. The effectiveness of therapeutics in cerebrovascular disease must be increased if this compensatory response is adequately directed by physicians.
García-Salman
J D
JD
Departamento de Neurología Experimental, Instituto de Neurología y Neurocirugía, La Habana, Cuba.
Córdoba-Ramos
M
M
D000222:Adaptation, Physiological / Q000502:physiology; D001921:Brain / Q000098:blood supply* / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D010100:Oxygen / Q000378:metabolism; D018091:Receptors, AMPA / Q000378:metabolism; D018079:Receptors, GABA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
D015220:Calcium Channels; D018091:Receptors, AMPA; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; D010100:Oxygen
Lo patológico y lo compensatorio en la isquemia cerebral: aspectos moleculares.