INVESTIGADORES
DORFMAN Damian
artículos
Título:
Global and ocular hypothermic preconditioning protect the rat retina from ischemic damage
Autor/es:
SALIDO EM; DORFMAN D; BORDONE M; CHIANELLI MS; GONZÁLEZ FLEITAS MF; ROSENSTEIN RE
Revista:
PLOS ONE
Editorial:
PUBLIC LIBRARY SCIENCE
Referencias:
Lugar: San Francisco; Año: 2013 vol. 8 p. 61656 - 61667
ISSN:
1932-6203
Resumen:
PLoS One. 2013 Apr 23;8(4):e61656. doi: 10.1371/journal.pone.0061656. Print 2013.
Global and ocular hypothermic preconditioning protect the rat retina from ischemic damage.
Salido EM, Dorfman D, Bordone M, Chianelli M, González Fleitas MF, Rosenstein RE.
Source
Laboratory
of Retinal Neurochemistry and Experimental Ophthalmology, Department of
Human Biochemistry, School of Medicine, University of Buenos
Aires/CEFyBO, CONICET, Buenos Aires, Argentina.
Abstract
Retinal
ischemia could provoke blindness. At present, there is no effective
treatment against retinal ischemic damage. Strong evidence supports that
glutamate is implicated in retinal ischemic damage. We investigated
whether a brief period of global or ocular hypothermia applied 24 h
before ischemia (i.e. hypothermic preconditioning, HPC) protects the
retina from ischemia/reperfusion damage, and the involvement of
glutamate in the retinal protection induced by HPC. For this purpose,
ischemia was induced by increasing intraocular pressure to 120 mm Hg for
40 min. One day before ischemia, animals were submitted to global or
ocular hypothermia (33°C and 32°C for 20 min, respectively) and fourteen
days after ischemia, animals were subjected to electroretinography and
histological analysis. Global or ocular HPC afforded significant
functional (electroretinographic) protection in eyes exposed to
ischemia/reperfusion injury. A marked alteration of the retinal
structure and a decrease in retinal ganglion cell number were observed
in ischemic retinas, whereas global or ocular HPC significantly
preserved retinal structure and ganglion cell count. Three days after
ischemia, a significant decrease in retinal glutamate uptake and
glutamine synthetase activity was observed, whereas ocular HPC prevented
the effect of ischemia on these parameters. The intravitreal injection
of supraphysiological levels of glutamate induced alterations in retinal
function and histology which were significantly prevented by ocular
HPC. These results support that global or ocular HPC significantly
protected retinal function and histology from ischemia/reperfusion
injury, probably through a glutamate-dependent mechanism.