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Exp Neurol. 2010 Jul;224(1):146-54. doi: 10.1016/j.expneurol.2010.03.004. Epub 2010 Mar 10.

The relationship between sudden severe hypoxia and ischemia-associated spreading depolarization in adult rat brainstem in vivo.

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Institute of Physiology I/Neurophysiology, University Hospital Jena, Teichgraben 8, D-07740 Jena, Germany.


Severe ischemia can induce spreading depolarization (SD) in the cerebral cortex, which is thought to contribute significantly to cerebral dysfunction. Whether the mature brainstem shows SD upon reduced oxygen supply has not been investigated although SDs may significantly influence brainstem functions. In anesthetized adult rats, we induced severe short-lasting hypoxia (SSH) by stopping artificial respiration for about 1 min or by ventilation with pure nitrogen for 1, 2 or 3 min, and milder hypoxia by ventilation with 6% O(2) in N(2) for 10 min. We measured DC potentials in the brainstem and cerebral cortex, systemic arterial blood pressure, heart rate and local blood flow at the brainstem or cerebral cortex surface. SSH lasting up to 1 min did not induce DC shifts in native brainstem but reduced heart rate, systemic blood pressure and blood flow in cortex and brainstem. Longer lasting SSH protocols both reduced systemic blood pressure and induced SD in the brainstem, but the magnitude of the cardiovascular response was not influenced by the simultaneous occurrence of SD. When neuronal excitability in the brainstem was artificially enhanced, SSH of 1 min evoked SD but again the magnitude of cardiovascular changes during SSH was not increased. SSH lasting 3 min evoked non-reversible sustained depolarization. SSH did not render the brainstem more excitable for classical SD evoked by local KCl application. Thus, sudden severe hypoxia/ischemia evokes SDs in the brainstem, but the occurrence of the so-elicited SD does not influence the immediate cardiovascular response to SSH.

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