Dysregulation of oxygen hemodynamic responses to synaptic train stimulation in a rat hippocampal model of subarachnoid hemorrhage.

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM(2016)

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Abstract
We investigated microvascular reactivity to synaptic train stimulation after induction of subarachnoid hemorrhage in adult rats, analyzing tissue oxygen levels [pO(2)] in intact hippocampus. In control rats, hippocampal pO(2) averaged 11.4mm Hg whereas hemodynamic responses averaged 13.1mm Hg (to a 25 s train). After subarachnoid hemorrhage (at 2 days), we recorded a dramatic elevation in baseline pO(2) in the hippocampus (to 68.4mm Hg) accompanied by inverted pO(2) responses to synaptic train stimulation (-9.46mm Hg). These significant changes in baseline hippocampal pO(2) and inverted pO(2) responses after subarachnoid hemorrhage indicate severe alterations of neurovascular coupling and neuronal viability.
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Key words
Hippocampus,tissue oxygen,hyperemia,physiological stimulation,subarachnoid hemorrhage,vasospasm,optical imaging,neurovascular coupling,hemodynamics
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