期刊
NEUROLOGICAL RESEARCH
卷 24, 期 2, 页码 161-168出版社
FOREFRONT PUBL GROUP
DOI: 10.1179/016164102101199710
关键词
brain oxygen; excitatory aminoacids; mild hypothermia; severe head injury
资金
- NINDS NIH HHS [NS 12587] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS012587, P01NS012587] Funding Source: NIH RePORTER
We studied brain temperature and the effect of mild hypothermia in 58 patients after severe head injury (SHI). Brain tissue oxygen tension (p(ti)O(2)), carbon dioxide tension (p(ti)CO(2)), tissuie pH (pH(ti)) and temperature (T-br) were measured using a multiparameter probe. Microdialysis was performed to measure glucose, lactate, glutamate, and aspartate in the extracellular fluid. Mild hypothermia (34degrees - 36degrees C) was employed in 33 selected patients who had persistent increased intracranial pressure (ICP > 20 mmHg). Mild induced hypothermia decreased brain oxygen significantly from 33 +/- 24 mmHg to 30 +/- 22 mmHg (p < 0.05). The p(ti)CO(2) (46 +/- 8 mmHg) was also significantly lower during mild hypothermia (40.4 +/- 4.0 mmHg), p < 0.0001). The pH(ti) increased from 7.13 +/- 0.15 to 7.24 +/- 0.10 (p < 0.0001) under hypothermic conditions. Induced hypothermia may protect patients from secondary ischemic events by lowering the critical p(ti)O(2) threshold, reducing anaerobic metabolism, and decreasing the release of excitatory aminoacids. However, patients with spontaneous brain hypothermia on admission (T-br < 36.0degrees C) showed significantly higher levels of glutamate as well as lactate, compared to all other patients, and had a worse outcome. Spontaneous brain hypothermia carries a poor prognosis, and was characterized by markedly abnormal brain metabolic indices.
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