[On line monitoring of SvO2 during combined anesthesia. Preliminary observations].
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Biomedical subjects
Publications and source records attributed to A F Sabato.
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Acute hypoxia was induced by keeping guinea pigs in an atmosphere of 5% O2/95% N2 for 20 min. Four groups of 10 guinea pigs each were used: (A) control; (B) after 20 min of hypoxia; (C) after 20 min of hypoxia and 20 min of oxygen therapy (100%); (D) pretreatment with phenobarbital (100 mg/kg body wt) and 20 min of hypoxia, followed by 20 min of oxygen therapy. The histological study did not show significant differences between barbiturate-treated and untreated hypoxic brains. In fact, the severity of ischemic-hypoxic damage as well as its distribution were similar in all the experimental groups of animals. Lesions predominated in the regions which are known to be more sensitive to hypoxia (3rd and 4th layers of parieto-occipital cortex, Sommer's fields, cerebellum). It is considered that in the experimental conditions barbiturates did not act as a protective agent--at least as assessed morphologically.
An experimental study was carried out on 50 guinea pigs to evaluate the amino acid pattern in the whole brain after a toxic dose of phenytoin (1 g . kg-1 body wt). One group of 25 guinea pigs was treated with the drug which made them comatose, and their brains removed by craniotomy and frozen in liquid nitrogen; 25 guinea pigs were used as a control group. The brain amino acid pattern was determined by ion-exchange chromatography. All the amino acids, except threonine and methionine, decreased. Hypotheses about the particular cerebral metabolic pathways involved are discussed.