作者: Kai U. Frerichs
DOI: 10.1007/978-3-7091-6391-7_9
关键词:
摘要: A myriad of mediators and mechanisms have been implicated as participants in the propagation damage following stroke traumatic brain injury. Effective neuroprotection for these conditions, however, remains elusive at clinical level. Adaptive strategies animal species that naturally endure severe reductions nutrient perfusion to may reveal new homeostatic control tolerance with potential usefulness. variety appear qualify models tolerance, including those are anoxia tolerant capable hibernation. Mammalian hibernation represents a state which global physiologic functions virtually arrested delivery glucose oxygen is minimal, yet maintained. The profound reduction cerebral would lead rapid autolysis tissue an unprotected state, but has no adverse effects on hibernators does not occur. In fact, even hippocampal slices from hibernating ground squirrels cerebellar anoxia-tolerant turtles show increased superimposed insult aglycemia hypoxia. Surprisingly, cellular signals trigger maintain adaptations remain unknown. Main targets current investigations regulation controlled metabolic suppression preservation cell structure membrane integrity despite reduced energy supplies. possibility induction similar humans by activation natural reversible arrest employed other states potentially far-reaching implications. This includes prevention secondary trauma ischemia well under conditions anticipated pressure, such arterial vasospasm after subarachnoid hemorrhage, or during surgical procedures require temporary circulatory arrest. Induction resistant could also provide additional time until specialized treatment re-open occluded blood vessels patients be administered.