MILD TRAUMATIC BRAIN INJURY DOES NOT MODIFY THE CEREBRAL BLOOD-FLOW PROFILE OF SECONDARY FOREBRAIN ISCHEMIA IN WISTAR RATS

Citation
Kl. Davis et al., MILD TRAUMATIC BRAIN INJURY DOES NOT MODIFY THE CEREBRAL BLOOD-FLOW PROFILE OF SECONDARY FOREBRAIN ISCHEMIA IN WISTAR RATS, Journal of neurotrauma, 15(8), 1998, pp. 615-625
Citations number
43
Categorie Soggetti
Neurosciences,"Clinical Neurology","Emergency Medicine & Critical Care
Journal title
ISSN journal
08977151
Volume
15
Issue
8
Year of publication
1998
Pages
615 - 625
Database
ISI
SICI code
0897-7151(1998)15:8<615:MTBIDN>2.0.ZU;2-X
Abstract
The rat hippocampus is hypersensitive to secondary cerebral ischemia a fter mild traumatic brain injury (TBI), An unconfirmed assumption in p revious studies of mild TBI followed by forebrain ischemia has been th at antecedent TBI did not alter cerebral blood flow (CBF) dynamics in response to secondary ischemia, Using laser Doppler flowmetry (LDF), r elative changes in regional hippocampal CA1 blood flow (hCBF) were rec orded continuously to quantitatively characterize hCBF before, during, and after 6 min of forebrain ischemia in either normal or mildly trau matized rats. Two experimental groups of fasted male Wistar rats were compared. Group 1 (n = 6) rats were given 6 minutes of transient foreb rain ischemia using bilateral carotid clamping and hemorrhagic hypoten sion. Group 2 (n = 6) rats were subjected to mild (0.8 atm) fluid perc ussion TBI followed 1 h after trauma by 6 min of transient forebrain i schemia, The laser Doppler flow probe was inserted stereotactically to measure CA1 blood flow. The electroencephalogram (EEG) was continuous ly recorded. During the forebrain ischemic insult there were no interg roup differences in the magnitude or duration of the decrease in CBF i n CA1, In both groups, CBF returned to preischemic values within one m inute of reperfusion but traumatized rats had no initial hyperemia, Th ere were no intergroup differences in the CBF threshold when the EEG b ecame isoelectric. These data suggest that the ischemic insult was com parable either with or without antecedent TBI in this model. This conf irms that this model of TBI followed by forebrain ischemia is well sui ted for evaluating changes in the sensitivity of CA1 neurons to cerebr al ischemia rather than assessing differences in relative ischemia.