Dysregulation of oxygen hemodynamic responses to synaptic train stimulation in a rat hippocampal model of subarachnoid hemorrhage. Issue 4 (April 2016)

• Record Type: Journal Article
• Authors: Galeffi, Francesca; Degan, Simone; Britz, Gavin; Turner, Dennis A
• Is Part Of: Journal of cerebral blood flow & metabolism. Volume 36:Issue 4(2016)
• Page Start: 696
• Page End: 701
• Publication Date: 2016-04
• Subjects: Hippocampus -- tissue oxygen -- hyperemia -- physiological stimulation -- subarachnoid hemorrhage -- vasospasm -- optical imaging -- neurovascular coupling -- hemodynamics; Cerebral circulation -- Periodicals; Brain -- Metabolism -- Periodicals; Brain -- Blood-vessels -- Periodicals; Cerebrovascular disease -- Periodicals; 612.824
• DOI: 10.1177/0271678X15624699
• Languages: English
• ISSNs: 0271-678X

Abstract

We investigated microvascular reactivity to synaptic train stimulation after induction of subarachnoid hemorrhage in adult rats, analyzing tissue oxygen levels [pO2 ] in intact hippocampus. In control rats, hippocampal pO2 averaged 11.4 mm Hg whereas hemodynamic responses averaged 13.1 mm Hg (to a 25 s train). After subarachnoid hemorrhage (at 2 days), we recorded a dramatic elevation in baseline pO2 in the hippocampus (to 68.4 mm Hg) accompanied by inverted pO2 responses to synaptic train stimulation (−9.46 mm Hg). These significant changes in baseline hippocampal pO2 and inverted pO2 responses after subarachnoid hemorrhage indicate severe alterations of neurovascular coupling and neuronal viability.