Recovery after hypoglycemic brain injury. Action of some biological substances on the cerebral metabolism.

Abstract:

:In artificially ventilated beagle dogs a severe hypoglycemic condition was induced by insulin injection, while the posthypoglycemic recovery was induced by glucose treatment at the end of a 20-min period of spontaneous electroencephalographic silence. The motor area of the cerebral cortex was analyzed for glycolytic metabolites, related amino acids, energy mediators, fatty acids, phospholipids and free fatty acids. The effects on the posthypoglycemic recovery of a intracarotid infusion with some agents (i.e. uridine, cytidine, DL-carnitine, DL-acetylcarnitine, papaverine) were tested. Severe hypoglycemia induced an extensive derangement of the brain metabolism, with partial restitution during the posthypoglycemic recovery. During this condition, the intracarotid perfusion with some biological pyrimidines (uridine, cytidine) interfered with the glycolytic and amino acid metabolites, inducing a decrease in glucose, pyruvate and lactate contents, and an increase in succinate, alanine and glutamine cerebral concns. The lipid carriers (DL-carnitine, DL-acetylcarnitine) interfered with the fatty acid degradation inducing a magnification of the decrease in the individual (palmitic acid, oleic acid) and total fatty acids, the vasodilating agent (papaverine) being practically inactive.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Benzi G,Gorini A,Dossena M,Taglietti M,Fulle D,Pastoris O

doi

10.1016/0006-2952(83)90629-9

subject

Has Abstract

pub_date

1983-03-15 00:00:00

pages

1083-91

issue

6

eissn

0006-2952

issn

1873-2968

pii

0006-2952(83)90629-9

journal_volume

32

pub_type

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