Abstract
Steroids and barbiturates have been considered to be very reasonable drugs for cerebral protection from ischemic or traumatic insult. However, controversies on the effectiveness of these drugs have been growing [1–3]. On one hand there are experimental studies which strongly support the utility of these drugs for cerebral trauma or ischemia, but recent clinical studies based on randomized well-controlled trials have failed to show any advantages for these drugs [4–8]. The initial clinical enthusiasm for the widespread application of barbiturates to protects the brain from head injury, circulatory arrest, asphyxia, or ischemia has almost disappeared. Clinical and experimental data showed that complete global ischemic injury has not been favorably altered by barbiturate coma therapy, while barbiturates do appear to protect the brain damage from focal or incomplete ischemia/hypoxia [2,3]. If barbiturates are given before permanent occlusion, the size of the ensuing infarct is significantly reduced [9]. Barbiturate protection from cerebral ischemia/hypoxia is, at least partially, the result of a depressed metabolic demand for oxygen. Astrup demonstrated that the metabolic depression resulted from inhibition of neurotransmission [10].
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© 1991 Springer-Verlag Tokyo
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Manaka, S., Kirino, T., Sasaki, M. (1991). Cerebral Protection With Barbiturates, Nizofenone and Steroids. In: Takeshita, H., Siesjö, B.K., Miller, J.D. (eds) Advances in Brain Resuscitation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68538-8_14
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DOI: https://doi.org/10.1007/978-4-431-68538-8_14
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