Glutamate release in experimental ischaemia of the retina: an approach using microdialysis.
A rabbit eye model of neural ischaemia is described that uses an increased pressure in the anterior eye chamber to block the capillary supply to the retina. A microdialysis probe placed very close to the retinal surface was used to monitor release of amino acids during ischaemia. A large (two- to threefold) increase in the release of glutamate and O-phosphoserine (twofold), but not of six other amino acids monitored, occurred during initial ischaemia. During reperfusion after release of intraocular pressure, much larger (five- to 10-fold) increases in the release of these amino acids were observed. Parallel ischaemic retinal tissue damage was observed. This damage was prevented by ketamine applied locally via a superfusion needle, suggesting that glutamate released during ischaemia, and particularly during reperfusion, was responsible for cell death.
Louzada-Júnior
P
P
Department of Biochemistry, Faculdade de Medicina de Ribeirao Preto, Universidade de Sao Paulo, Brazil.
Dias
J J
JJ
Santos
W F
WF
Lachat
J J
JJ
Bradford
H F
HF
Coutinho-Netto
J
J
D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D003956:Dialysis / Q000379:methods; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D007511:Ischemia / Q000378:metabolism* / Q000473:pathology; D007649:Ketamine / Q000494:pharmacology; D008297:Male; D011817:Rabbits; D015424:Reperfusion; D012160:Retina / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D012164:Retinal Diseases / Q000378:metabolism / Q000473:pathology; D012171:Retinal Vessels
D000596:Amino Acids; D005971:Glutamates; D018698:Glutamic Acid; D007649:Ketamine