Journal article
Interactions between hypothermia and the latency to ischemic depolarization: implications for neuroprotection
Anesthesiology, Vol.88(5), pp.1266-1273
05/1998
DOI: 10.1097/00000542-199805000-00018
PMID: 9605687
Abstract
The authors postulated that hypothermic neuroprotection can be attributed to a delayed onset of ischemic depolarization. Halothane-anesthetized rats were prepared for near-complete forebrain ischemia. Direct current (DC) potential microelectrodes were placed in hippocampal CA1. The pericranial temperature was maintained at 31 degrees C, 33 degrees C, 35 degrees C, or 37 degrees C (n = 6 per group). Bilateral carotid occlusion with systemic hypotension was initiated for 10 min. The time to onset of the DC shift was recorded. In a second experiment, rats were assigned to 37 degrees C or 31 degrees C for 10 min of ischemia, or to 31 degrees C for 14 min of ischemia (n = 8 per group). These durations of ischemia were defined to allow 9 min of ischemic depolarization in the 37 degrees C-10 min and 31 degrees C-14 min groups. Neurologic and histologic outcomes were examined 7 days later. Hippocampal CA1 time to depolarization increased with decreasing temperature (P < 0.0001). Time to depolarization was increased by approximately 4 min in the rats maintained at 31 degrees C compared with those at 37 degrees C. Time to repolarization during reperfusion was not affected by temperature. Increasing the duration of ischemia from 10 min to 14 min with the pericranial temperature maintained at 31 degrees C resulted in a duration of depolarization that was equivalent in the 37 degrees C-10 min and 31 degrees C-14 min groups. However, hippocampal CA1 damage was not increased (31 degrees C-10 min = 4 +/- 1% dead neurons; 31 degrees C-14 min = 6 +/- 1% dead neurons, 95% CI, -1% to 3%; 37 degrees C-10 min = 90 +/- 17% dead neurons). Despite similar durations of DC depolarization, outcome in hypothermic rats was markedly improved compared with normothermic rats. This indicates that hypothermic neuroprotection can be attributed to mechanisms other than the delay in time to onset of ischemic depolarization.
Details
- Title: Subtitle
- Interactions between hypothermia and the latency to ischemic depolarization: implications for neuroprotection
- Creators
- Robert D Bart - Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710, USASeiji TakaokaRobert D PearlsteinFranklin DexterDavid S Warner
- Resource Type
- Journal article
- Publication Details
- Anesthesiology, Vol.88(5), pp.1266-1273
- DOI
- 10.1097/00000542-199805000-00018
- PMID
- 9605687
- NLM abbreviation
- Anesthesiology
- ISSN
- 0003-3022
- eISSN
- 1528-1175
- Publisher
- United States
- Grant note
- R01 GM39771-11 / NIGMS NIH HHS
- Language
- English
- Date published
- 05/1998
- Academic Unit
- Health Management and Policy; Anesthesia
- Record Identifier
- 9983806385502771
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