Regional Cerebral Blood Flow after Subarachnoid Hemorrhage (SAH) in the RAT

Nemoto, Edwin M.; Kofke, W. Andrew; Yonas, Howard; Williams, Donald S.; Rose, Marie E.; Rao, Gutti R.; Simplaceanau, Elena

doi:10.1007/978-1-4615-5865-1_38

Cited by 2 publications

(1 citation statement)

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“…Blood flow can change both immediately or in a delayed fashion following SAH. For example, using a middle cerebral rupture model of SAH, Nemoto et al (1997) showed that periods of both ischemic and hyperemic flow could occur temporally and regionally. Again, this finding has clinical relevance since it has been reported that within 3-5 days after bleeding, 20%-50% of patients who have suffered a traumatic brain injury or aneurysm rupture exhibit decreased cerebral blood flow (Zubkov et al, 1999;Turjman et al, 1999;Soustiel et al, 1998;Zurynski et al, 1995;.…”

Section: Cerebral Glucose Metabolism and Brain Injurymentioning

confidence: 99%

Subarachnoid Hemorrhage Induces Dynamic Changes in Regional Cerebral Metabolism in Rats

Glenn

Martin²,

Samii³

et al. 2002

Journal of Neurotrauma

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Following a subarachnoid hemorrhage (SAH), adult rats exhibit dynamic regional changes in cerebral glucose metabolism characterized by an increase in metabolic rates and a subsequent upregulation of cytochrome oxidase (CO). We evaluated both local cerebral metabolic rates for glucose (ICMRglc: (mol/100 g/min) and CO in 23 brain regions of interest (ROI). Sham animals underwent anesthesia and superficial surgery; saline-controls received an injection of 0.9% saline into the cisterna magna; and SAH rats received an injection of autologous blood into the cisterna magna. This blood, measured by albumin labeled with radioactive carbon 14, distributed throughout the brain but predominated ventrally. After experimental animals were sacrificed at day 0 (3 h), 1, 3, and 7 days postinjection, ROI were analyzed using [14C]2-deoxy-D-glucose autoradiography and CO histochemistry. ICMRglc in SAH rats increased in many regions (ranging from 0.7% to 32.2% above sham levels). Cytochrome oxidase also increased from 1% to 9% above sham levels, peaking on day 3. Conversely, saline-controls exhibited prolonged depression of ICMRglc (ranging from 11% to 35% below sham levels) and CO (ranging from 4% to 11% below sham levels) from day 0 through day 7. All saline-control ROI for all time points showed this metabolic depression, and between 91% and 95% of saline-control ROI presented lower CO levels as compared to sham. Overall, ICMRglc and CO levels were greater in SAH than in saline-control ROI. However, when considering the influence of subarachnoid blood on metabolic changes in SAH animals, both CO and 2DG levels did not correlate well with the amount of 14C-albumin binding. While previous studies have measured both metabolic rates of glucose and CO soon after SAH, this is the first to simultaneously conduct these measurements in the same SAH rat model.

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