The protective effect of adenosine A2A receptor antagonism in cerebral ischemia.
OBJECTIVE
We reviewed our most recent work on the protective effect of adenosine A(2A)antagonism in cerebral ischemia.


METHODS
Focal ischemia was produced in rats by introducing a nylon monofilament pre-coated with silicone through the external carotid artery to occlude the right MCA at its origin.


RESULTS
A(2A) antagonism was found protective in the model of permanent focal ischemia induced by the monofilament technique. This methodology provides the possibility of evaluating the protection against the outflow of excitatory amino acids and against an acute motor disturbance, i.e.contralateral turning to the ischemic side in the first hours after ischemia in awake rats. Hours later, a definite neurological deficit and necrotic neuronal damage can be evaluated.


CONCLUSIONS
Our results suggest that A(2A) antagonism may be protective from the earliest up to several hours after the ischemic event.
Pedata
F
F
Department of Preclinical and Clinical Pharmacology, University of Florence, V.le Pieraccini 6, 50139 Florence, Italy. felicita.pedata@unifi.it
Gianfriddo
M
M
Turchi
D
D
Melani
A
A
D058917:Adenosine A2 Receptor Antagonists; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications / Q000517:prevention & control*; D004195:Disease Models, Animal; D018698:Glutamic Acid / Q000378:metabolism; D002534:Hypoxia, Brain / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D043705:Receptor, Adenosine A2A / Q000502:physiology; D013997:Time Factors
D058917:Adenosine A2 Receptor Antagonists; D018696:Neuroprotective Agents; D043705:Receptor, Adenosine A2A; D001224:Aspartic Acid; D018698:Glutamic Acid