[Tracking along the path toward ischemic XXXX ].

@entity308 @entity66 @entity63 @entity1358 @entity519 @entity204 @entity528
INTRODUCTION AND DEVELOPMENT: During episodes of @entity63 / @entity519 , the neurochemical and environmental changes considered toxic for nervous tissue lie behind the characteristic abrupt @entity1358 ( @entity1358 ). A strong resemblance with other pathologic events enable us to postulate that @entity1358 is a different state of the tissue that includes among others the anoxic depolarization and Le o s spreading @entity308 . @entity1358 is an active event. Neurons enter and leave @entity1358 suddenly and synchronously, and contrary to current belief, their membrane integrity is preserved and ion gradients are only reduced. Biophysical membrane properties are not compatible with some postulates based on endotoxines. There is a direct relation between @entity1358 susceptibility of the different neuron types/nuclei and their vulnerability to @entity63 / @entity519 . Two different substates can be distinguished in the associated interstitial potentials that are likely related to @entity66 , respectively. The different modes and timings of anoxic @entity528 depend on the duration of @entity1358 , the functional integrity of the glial network, and the history of previous insults. CONCLUSIONS: @entity1358 is a cellular state of risk bridging life and @entity204 . Neurons die if they cannot exit, but may recover if they do promptly, although still have to face subtle changes as well initiated during @entity1358 that will eventually lead them to a delayed @entity204 . Avoiding @entity1358 is escaping @entity204 . From a clinical point of view, the relevant point is that manipulating @entity1358 entails the simultaneous control of all toxic neurochemical concomitants. Reinforcing vulnerable neurons to avoid their falling into @entity1358 is possible
