Stroke, Vol 16, 855-860, Copyright © 1985 by American Heart Association
EF Lundy, J Dykstra, B Luyckx, GB Zelenock and LG D'Alecy
The objective of this study was to determine if 1,3-butanediol would reduce
a neurologic deficit in rats exposed to ischemic-hypoxia (Levine rats). Age
and weight matched male Sprague-Dawley rats were anesthetized with 2%
halothane. The right common carotid and external jugular vein were ligated
and cannulated and EEG screws were implanted followed by a 2 hour recovery
period. Thirty minutes prior to exposure the rats received either
1,3-butanediol (47 mmole/kg i.v.; n = 11) or an equal volume of saline (n =
10). The rats were then exposed to 4.5% O2 until mean arterial blood
pressure fell to 70 mm Hg. The oxygen level was then increased to 8% for 30
minutes, after which the rats were returned to room air. Posture,
hemiparesis, circling, shuffling, activity, and ability to hang on to a
vertical screen were scored 1 (normal) to 5 (severe deficit) at 2 and 20
hours after insult. The time to 70 mm Hg was extended from 7.9 +/- 0.9 min
for saline treated rats to 19.0 +/- 2.3 min for the 1,3-butanediol treated
rats (p less than 0.001). All eleven 1,3-butanediol treated rats survived
the hypoxic insult; 90% (9/10) saline treated rats died. In an attempt to
reduce the insult, six additional saline treated rats were switched to 8%
O2 at 75 mm Hg and still 4/6 died. The mean score at 20 hours for three
surviving saline treated rats was 3.4. A significantly better (p less than
0.002) mean 20 hour score for the surviving 8/11 1,3-butanediol treated
rats was 1.2. 1,3-butanediol increases survival and decreases the
neurologic deficits associated with this ischemic-hypoxic insult.
ARTICLES
Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats
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