EEG power spectra changes and forebrain ischemia in rats.

نویسندگان

  • Giuseppina Mariucci
  • Maria Antonietta Stasi
  • Roberto Taurelli
  • Paolo Nardò
  • Michela Tantucci
  • Licia Pacifici
  • Paolo Carminati
  • Maria Vittoria Ambrosini
چکیده

BACKGROUND Several animal models of cerebral ischemia have been developed to investigate both pathophysiology and pharmacological treatment. The aim of this study was to verify the prognostic value of EEG power spectra analysis in a two-vessel plus hypotension rat model of transient global ischemia. METHODS Spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs) were subjected to 20 min bilateral common carotid artery occlusion plus hypotension by sodium nitroprusside followed by reperfusion for seven days. Sham-operated animals served as controls. The changes after ischemia in EEG power spectra, and their relations with neuronal damage and astrocytic response were investigated. RESULTS The EEG analysis revealed that in SHRs and WKYs, ischemia produced a dramatic increase in delta activity and a decrease in theta, beta and alpha activities derived from both cortical and hippocampal areas. EEG activity reverted to normal values more quickly in WKYs than in SHRs which did not recover cortical and hippocampal alpha and beta activities even at six days of reperfusion. SHRs presented more severe damage and intense astrocytosis than WKYs in almost all the brain regions analyzed. In SHRs, hippocampal delta activity was positively correlated with the degree of neuronal necrosis and astrocytic activation, whereas theta, alpha and beta activities correlated negatively. No correlations were found in WKYs. CONCLUSIONS These data indicate that the hippocampal bioelectrical activity recorded in SHRs from the beginning of reperfusion could be useful for predicting the ischemic outcome and evaluating the effects of pharmacological interventions.

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عنوان ژورنال:
  • The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques

دوره 30 1  شماره 

صفحات  -

تاریخ انتشار 2003