Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats.
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.[1]References
- Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats. Lundy, E.F., Dykstra, J., Luyckx, B., Zelenock, G.B., D'Alecy, L.G. Stroke (1985) [Pubmed]
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