Intraischemic mild hypothermia increases hippocampal CA1 blood flow duringforebrain ischemia

Citation
Lw. Jenkins et al., Intraischemic mild hypothermia increases hippocampal CA1 blood flow duringforebrain ischemia, BRAIN RES, 890(1), 2001, pp. 1-10
Citations number
53
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BRAIN RESEARCH
ISSN journal
00068993 → ACNP
Volume
890
Issue
1
Year of publication
2001
Pages
1 - 10
Database
ISI
SICI code
0006-8993(20010126)890:1<1:IMHIHC>2.0.ZU;2-2
Abstract
The hippocampal CA1 sector is selectively vulnerable to forebrain ischemia but protected by mild hypothermia. However, the consequence of intraischemi c hypothermia on CA1 blood flow during the insult has not been adequately c haracterized. The effects of mild intraischemic hypothermia on relative cha nges in regional hippocampal CA1 blood how were recorded continuously using laser Doppler flowmetry (LDF) during and 30 min after 6 min of forebrain i schemia. Six experimental groups (n=6/group) of fasted male Wistar rats wer e compared. Groups 1, 3 and 5 consisted of normothermic rats that underwent either 6 (for CBF measurements) and 6 or 10 (for 7 day survival-CA1 neuron al death measurements) min of transient forebrain ischemia using bilateral carotid clamping and hemorrhagic hypotension. Groups 2, 4 and 6 rats were s ubjected to mild hypothermia (34 degreesC) before, during, and 30 min after 6 (for CBF measurements) and 6 or 10 (for 7 day survival-CA1 neuronal deat h measurements) min of transient forebrain ischemia. CA1 blood Row and elec troencephalogram (EEG) were continuously recorded. During the ischemic insu lt there were intergroup differences in the magnitude of CBF decreases in t he CA1 region. In both groups 1 and 2, CBF returned to preischemic values w ithin 1 min of reperfusion but hypothermic rats had more sustained hyperemi a. Hypothermic rats had a quicker recovery of EEG activity and less delayed CA1 neuronal death (group 2 versus 4). These data suggest ischemic blood R ow to the CA1 sector was altered by intraischemic mild hypothermia which ma y contribute to the greater benefit of intraischemic hypothermic neuroprote ction. (C) 2001 Elsevier Science B.V. All rights reserved.