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Published on: August 9, 2024
Haemodynamic correlates of penumbral depolarization following focal cerebral ischaemia
H Nallet1, E T MacKenzie, S Roussel
1University of Caen, CNRS-UMR 6551, Cyceron, Boulevard Henri Becquerel, BP 5229, 14074 Cedex, Caen, France. nallet@cyceron.fr
Transient ischaemic depolarizations (IDs) are thought to play a key role in the pathogenesis of focal cerebral ischaemia. Most transient IDs are akin to spreading depression (SD), although a negative DC shift is not observed in half the cases. The other IDs may represent transient anoxic depolarizations. Using cortical DC and blood flow recordings, following middle cerebral artery occlusion in rats, we show here that: (i) these later depolarizations do indeed represent transient anoxic depolarizations; (ii) SD-like IDs, DC and haemodynamic parameters are similar to those of SDs when blood flow remains close to base line and; (iii) when blood flow decreases, the hyperaemia associated with SD-like IDs is largely reduced and there is an increasing proportion of cortical sites which fail to display a DC shift. These data demonstrate the coexistence of two mechanisms of IDs, and yield new information as to the flow-dependence of DC and haemodynamic correlates of SD-like IDs, the pathophysiological significance of which remains to be determined.
Transient ischaemic depolarizations (IDs) are thought to play a key role in the pathogenesis of focal cerebral ischaemia. Most transient IDs are akin to spreading depression (SD), although a negative DC shift is not observed in half the cases. The other IDs may represent transient anoxic depolarizations. Using cortical DC and blood flow recordings, following middle cerebral artery occlusion in rats, we show here that: (i) these later depolarizations do indeed represent transient anoxic depolarizations; (ii) SD-like IDs, DC and haemodynamic parameters are similar to those of SDs when blood flow remains close to base line and; (iii) when blood flow decreases, the hyperaemia associated with SD-like IDs is largely reduced and there is an increasing proportion of cortical sites which fail to display a DC shift. These data demonstrate the coexistence of two mechanisms of IDs, and yield new information as to the flow-dependence of DC and haemodynamic correlates of SD-like IDs, the pathophysiological significance of which remains to be determined.

