Tortiglione A, Minale M, Pignataro G, Amoroso S, DiRenzo G, Annunziato L
University of Naples Federico II School of Medicine, Nuroscience Department, Via S Pansini 5, 80131, Naples, Italy.
Neuropharmacology. 2002 Sep;43(3):427-33. doi: 10.1016/s0028-3908(02)00093-x.
In this study, the temporal development of focal cerebral infarction induced by permanent middle cerebral artery occlusion (pMCAO) and the effects of piracetam, a derivative of gamma-aminobutyric acid widely used in clinical practice as a nootropic agent, on infarct area and volume were investigated. pMCAO caused a cerebral infarct whose size progressively increased after 3, 6, 9, and 24 h. Piracetam (125 mg/kg i.p.), administered 6, 9, and 22 h after pMCAO, did not reduce pMCAO-induced brain infarct area size detected at the 24th hour. By contrast, when this agent was administered at the doses of 250 and 500 mg/kg, it caused a marked reduction of the infarct area size. This reduction was observed in almost every brain slice affected by pMCAO, although statistical differences (p <0.05) were detected in slices located at 3-5.5 mm posterior to the anterior pole in animals treated with 250 mg/kg piracetam and in slices located at 3.5-5 mm in those receiving 500 mg/kg. When the mean total volumes of brain infarct resulting from pMCAO were calculated, it was observed that in animals which had received piracetam (250 or 500 mg/kg) infarction volume was markedly ( approximately 50%) and significantly (p <0.05) reduced in comparison with saline injected rats. Finally, piracetam (250 mg/kg administered i.p. 6, 9, and 22 h after the ischemic insult) significantly reduced brain infarct area evaluated 48 h and 7 days after pMCAO.
