Quantitative Electroencephalographic Changes Due To Middle Cerebral Artery Occlusion By Endothelin 1 In Conscious Rats

Abstract

The powerful vasoconstrictor peptide endothelin-1 (ET1) has been shown to reduce local cerebral blood flow in brain areas supplied by the middle cerebral artery (MCA) to a pathologically low level upon intracerebral injection adjacent to the MCA. This reduction manifests itself as an ischemic infarct, that is fully developed within 3 days after ET1 injection. The aim of the present study is to examine the effect of ET1 on electroencephalographic (EEG) activity. ET1 was microinjected unilaterally at a dose of 60 pmol in 3 microl of saline to the MCA in conscious rats. EEG signals were recorded from the frontoparietal cortical area, supplied by MCA, from the first up to the fourteenth day after ET1 injection. EEG activity was analyzed by the fast Fourier transformation. A significant shift to a lower EEG frequency, i.e., augmentation of slow waves and a reduction of alpha-like and faster EEG waves was found post-ET1. This effect was maximal after 3-7 days when the most severe destruction of neurons in this cortical area occurs, as has been previously demonstrated. The results suggest that the quantitative EEG analysis may provide useful additional information about the functional disturbances associated with focal cerebral ischemia.

Endothelin-1 induced MCAO: Dose dependency of cerebral blood flow

“…A model of reversible focal ischemia using ET1 was used as previously described (Moyanova et al, 1998;Biernaskie et al, 2001).…”

“…More recently, stereotaxic application of ET1 near the MCA (Robinson et al, 1990;Sharkey et al, 1993Sharkey et al, , 1994Sharkey and Butcher, 1995;Macrae et al, 1993;Moyanova et al, 1998;Biernaskie et al, 2001;Bogaert et al, 2000;Callaway et al, 2000) has been shown to produce a profound reduction of blood flow that leads to cerebral ischemic injury within the MCA territory. Several well-established models of ET1-induced MCA occlusion have been demonstrated (Robinson et al, 1990;Sharkey et al, 1993Sharkey et al, , 1994Sharkey and Butcher, 1995;Macrae et al, 1993;Moyanova et al, 1998;Biernaskie et al, 2001;Bogaert et al, 2000;Callaway et al, 2000).…”

“…Several well-established models of ET1-induced MCA occlusion have been demonstrated (Robinson et al, 1990;Sharkey et al, 1993Sharkey et al, , 1994Sharkey and Butcher, 1995;Macrae et al, 1993;Moyanova et al, 1998;Biernaskie et al, 2001;Bogaert et al, 2000;Callaway et al, 2000). In each case, a stereotaxic injection introduces a small amount of ET1 (60-120 pmol) in proximity to the MCA.…”

Ketanserin reduces the postischemic EEG and behavioural changes following Endothelin-1-induced occlusion of the middle cerebral artery in conscious rats

“…In the present study, ET1 was used as a tool to produce severe and sustained, but ultimately reversible unilateral MCA occlusion in order to provide an animal model of focal cerebral ischemia with reperfusion [14][15][16][17][18][19][20][21][22][23][24][25]. The quantitative EEG and the neurological examination both showed a substantial effect of ET1.…”

“…In this model, occlusion of the middle cerebral artery (MCAO) was induced in rats via intracerebral microinjection of Endothelin-1 (ET1) -the so-called EMCAO model. While some consequences of EMCAO on blood perfusion, behavior and histopathology have been explored in certain extent [14][15][16][17][18][19][20][21], the corresponding changes of bioelectrical activity are less investigated [22][23][24][25]. The brain electrical signals are in the list of mandatory outcome measures according to the recommendations from the first Stroke Academic Industry Roundtable meeting for the preclinical evaluation of neuroprotective and recovery enhancing drugs [26].…”