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Energy metabolism in the conscious gerbil during recirculation following transient ischemia: Effects of RU 24722 and vincamine
Author(s) -
Formento Maria Luisa,
Barzaghi Fernando,
Mantegazza Paolo
Publication year - 1988
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430130108
Subject(s) - phosphocreatine , ischemia , gerbil , glutamate receptor , alanine , medicine , chemistry , endocrinology , metabolism , energy charge , energy metabolism , biochemistry , amino acid , receptor , adenylate kinase
In the present study, cerebral energy metabolism and the alanine/glutamate ratio were evaluated in gerbils at the end of or 6, 24, or 48 hr after ischemia (10 min) induced by clamping both common carotid arteries. At the end of ischemia, the energy substrates were dramatically reduced, while lactate and pyruvate levels and the alanine/glutamate ratio were increased. During 48 hr of recirculation, the high‐energy phosphate increased but never to normal values; lactate, which is low in the early postischemic period, progressively increased; pyruvate fell but without returning to normal; the alanine/glutamate ratio decreased without reaching normal value. RU 24722 (vindeburnol) or vincamine were administered subcutaneously 15 min, 10, 24, and 34 hr after ischemia. RU 24722 completely inhibited the increase in lactate levels observed 24 and 48 hr after ischemia, improved pyruvate recovery, and normalized the alanine/glutamate ratio, but vincamine did not. Neither compound had any effect on the tissue concentrations of phosphocreatine, ATP, ADP, or AMP. The ability of RU 24722 to prevent the postischemic lactate accumulation associated with the normalization of the alanine/glutamate ratio indicates that it should improve the capacity for postischemic cerebral metabolic recovery and that it also has a different biochemical profile from that of vincamine.