Mild traumatic brain injury does not modify the cerebral blood flow profile of secondary forebrain ischemia in Wistar rats.
The rat hippocampus is hypersensitive to secondary cerebral ischemia after mild traumatic brain injury (TBI). An unconfirmed assumption in previous studies of mild TBI followed by forebrain ischemia has been that antecedent TBI did not alter cerebral blood flow (CBF) dynamics in response to secondary ischemia. Using laser Doppler flowmetry (LDF), relative changes in regional hippocampal CA1 blood flow (hCBF) were recorded continuously to quantitatively characterize hCBF before, during, and after 6 min of forebrain ischemia in either normal or mildly traumatized rats. Two experimental groups of fasted male Wistar rats were compared. Group 1 (n = 6) rats were given 6 minutes of transient forebrain ischemia using bilateral carotid clamping and hemorrhagic hypotension. Group 2 (n = 6) rats were subjected to mild (0.8 atm) fluid percussion TBI followed 1 h after trauma by 6 min of transient forebrain ischemia. The laser Doppler flow probe was inserted stereotactically to measure CA1 blood flow. The electroencephalogram (EEG) was continuously recorded. During the forebrain ischemic insult there were no intergroup differences in the magnitude or duration of the decrease in CBF in CA1. In both groups, CBF returned to preischemic values within one minute of reperfusion but traumatized rats had no initial hyperemia. There were no intergroup differences in the CBF threshold when the EEG became isoelectric. These data suggest that the ischemic insult was comparable either with or without antecedent TBI in this model. This confirms that this model of TBI followed by forebrain ischemia is well suited for evaluating changes in the sensitivity of CA1 neurons to cerebral ischemia rather than assessing differences in relative ischemia.
Davis
K L
KL
Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555-0591, USA.
Jenkins
L W
LW
DeWitt
D S
DS
Prough
D S
DS
D000818:Animals; D001930:Brain Injuries / Q000209:etiology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D018450:Disease Progression; D006624:Hippocampus / Q000098:blood supply*; D008297:Male; D016548:Prosencephalon / Q000098:blood supply / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors