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.
Department of Biochemistry, Faculdade de Medicina de Ribeirao Preto, Universidade de Sao Paulo, Brazil.
P
P
Louzada-Júnior
J J
JJ
Dias
W F
WF
Santos
J J
JJ
Lachat
H F
HF
Bradford
J
J
Coutinho-Netto
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