Search PubMed⌕ Search

Biomedical subjects

A F Sabato

Publications and source records attributed to A F Sabato.

At least 37 records · Page 2Linked to original sources
PubMed1984

Experimental acute hypoxia. Brain preservation by phenobarbital pretreatment. Histological study in guinea pigs.

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.

Animals↗
PubMed1984

The brain amino acid pattern in experimental coma due to phenytoin in guinea pigs.

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.

Amino Acids↗
PubMed1984

The amino acid cerebral pool after toxic doses of lidocaine and mexiletine. An experimental study on guinea pigs.

Lidocaine and Mexiletine are two anti-arrhythmic drugs which when administered in toxic doses cause alterations in the central nervous system (convulsions, tremors, coma). An experimental study was carried out to clarify some neurological side-effects caused by these two drugs, by studying the variations of the brain amino acid pool. With Lidocaine one can observe an increase of phenyl-alanine and tyrosine, a decrease of glycine, GABA, alanine, aspartate and glutamate, while taurine and ammonia showed no significant changes. After Mexiletine one can observe an increase of ammonia, a decrease of GABA, glutamine, glycine and alanine, while glutamate, taurine, phenyl-alanine and tyrosine remain within normal values. In conclusion, on the basis of the data obtained by comparing the two drugs, one could say that Lidocaine has a greater interference on the catecholaminic precursors which are little influenced by Mexiletine. For the rest, the data obtained are practically super- imposable .

Amino Acids↗
PubMed1983

The effect of five drugs in coma doses on neurotransmitter amino acids in the brains of guinea pigs.

The study has been carried out in order to investigate the effects of some drugs in coma doses on the concentration in brain of some amino acids involved in brain function. Six groups of 25 guinea pigs each were utilized. In each of the five groups a subcutaneous dose of diazepam, flunitrazepam, phenobarbital, phenytoin or alfaxalone, was injected and one group was utilized as control. Some neurotransmitter amino acids (glutamate, aspartate, glycine and taurine) and precursors of neurotransmitters (phenylalanine and tyrosine) were determined in brain preparations. The results are discussed.

Amino Acids↗
PubMed1981

Biochemical changes in acute respiratory failure.

A study has been carried out on patients presenting respiratory failure from chronic obstructive lung disease. Acid-base balance, electrolytes and amino acids levels have been studied in plasma and in cerebrospinal fluid (CSF) of patients in hypercapnic coma and results compared with those observed in patients with primary acute hypercapnia. Additional cardiopulmonary measurements were made. The study has shown evidence of significant modification of the distribution ratios of plasma and CSF electrolytes and amino acids, particularly in the patients with coma. The changes seem to be related to variations of the transmembrane potentials and alterations of some metabolic pathways involved in the homeostasis and in neurotransmission. Finally some of the changes of amino acid in plasma and CSF appear significantly correlated to variations in pulmonary function and to modification of acid-base balance observed both in plasma and CSF.

Amino Acids↗