[Focal cerebral ischaemia induced by middle cerebral artery occlusion and the neuroprotective effect of ketoprofen in rats].
Cerebral ischaemia is eventualy observed during neurosurgical procedures and in several clinical entities that may cause severe neurological deficits and even death. Because it is a severe and complex problem, several studies have been done aiming to elucidate the mechanisms of the ischemic phenomenon and aiming to abolish or to diminish its effects, using drugs that protect the neurons from ischaemia-induced damage. Several neurotransmitters play a role in cerebral ischaemia with emphasis to glutamate by its high concentration in the central nervous system. The purpose of this study was to evaluate the effect of focal cerebral ischaemia in the rat through the dosage of the glutamate and morphological findings, and to evaluate a possible protective effect of the ketoprofen to ischemic neurons. Thirty-six rats Wistar were divided into four groups. The first was a control group, the second a sham group and the animals of the third and fourth groups were submitted to induced cerebral ischaemia through selective obstruction of the midlle cerebral artery during 15, 30 and 45 minutes. Animals of the fourth group were previously treated with ketoprofen 15 minutes before the ischaemia. The ischaemia was evaluated through the histopathological examination and through dosage of the extracellular glutamate in vitro. The histopathological examination showed that there was no difference between the animals of the control and of the sham groups. In the animals submitted to ischemia histopathological alterations appeared at 30 minutes and become more intense at 45 minutes of ischaemia. The main findings were interstitial edema, chromatinic disorganization, vacuolization and nuclear desintegration. The animals treated with ketoprofen showed similar alterations, but they were less intense. Decrease in the dosage of glutamate in the parietal cortex of the animals submitted to ischaemia started at 30 minutes and became more intense at 45 minutes of ischaemia and was similar for animals previously treated or not with ketoprofen, indicating that this drug seems not to interfere with the metabolism of the glutamate at the synapses. The morphological findings in the parietal cortex of the animals submitted to ischaemia, previously treated or not with ketoprofen, suggest that this drug has a neuroprotective effect.
Dias
L A
LA
Departamento de Cirurgia, Hospital das Clínicas, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brazil.
Colli
B O
BO
Coutinho Netto
J
J
Lachat
J J
JJ
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications* / Q000473:pathology; D002545:Brain Ischemia / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D016022:Case-Control Studies; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D018698:Glutamic Acid / Q000032:analysis*; D007660:Ketoprofen / Q000627:therapeutic use*; D020768:Middle Cerebral Artery / Q000187:drug effects / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric
D016861:Cyclooxygenase Inhibitors; D018698:Glutamic Acid; D007660:Ketoprofen