Reduction of neurologic deficit by 1,3-butanediol induced ketosis in levine rats.
نویسندگان
چکیده
منابع مشابه
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 pr...
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15 صفحه اولButanediol induced ketosis increases tolerance to hypoxia in the mouse.
In previous studies from our laboratory a positive correlation between elevated blood ketone levels and the survival time (ST) during hypoxia (4-5% oxygen) was observed in fasted and alloxan diabetic mice. To test the hypothesis that ketosis was somehow increasing the tolerance of mice to hypoxia, we induced ketosis by either oral (PO), intraperitoneal (IP), or intravenous (IV) 1,3-butanediol (...
متن کاملButanediol induced cerebral protection from ischemic-hypoxia in the instrumented Levine rat.
To determine if 1,3-Butanediol (BD), which protects mice from hypoxia, would extend the tolerance of rats to ischemic-hypoxia, the Levine rat (unilateral carotid ligation and conscious hypoxic exposure) was modified to record mean arterial pressure (BP), heart rate (HR), central venous pressure (CVP), spontaneous respiration and EEG. Age and weight matched, male, Sprague-Dawley rats were anesth...
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Introduction: During hemorrhagic shock (HS), the kidneys are one of the primary target organs involved. Oxidative stress is shown to be enhanced in different models of acute kidney injury (AKI). Remote ischemic preconditioning (RPC) by brief limb ischemia is considered to be a safe method to protect different organs from further damage. In this study, we investigated the effects of brief hind l...
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ژورنال
عنوان ژورنال: Stroke
سال: 1985
ISSN: 0039-2499,1524-4628
DOI: 10.1161/01.str.16.5.855