30 June - 2 July 2014, London UK
A transient increase in cortical neuronal activity is followed by a transient increase in cerebral blood flow. We investigated changes in neurovascular coupling after a minimally injuring transient global cerebral ischemia (GCI) in adult male Wistar rats. We measured the hemodynamic response function (HRF) by taking advantage of the whole-brain discontinuous EEG burst-suppression (BS) state after a chloral-hydrate overdose. We tested the changes in HRF at 48 hours after a 5-minute GCI induced using a variation of the “4-vessel occlusion model”. Simultaneous cortical electroencephalographic (EEG) activity and Laser Doppler (LD) signal were recorded. The rectified EEG was convoluted with a prototype HRF to obtain a synthetic LD signal. Peak HRF latency and HRF width were optimized to attain a maximum correlation between the recorded and the synthetic LD signals within 0.1-0.4 Hz. The HRF was found to depend on the depth of BS anaesthesia. With decreasing bursting frequency there was a progressive increase of HRF latency (time to HRF peak) that could be reasonably described by a linear regression. The slope of the relationship was similar prior to and after GCI. Nevertheless, the Y-intercept was, about double after GCI (F=81, P<0.01). The delayed hemodynamic response after GCI could not be attributed either to cardio-vascular changes (HR remained normal) or to changes in electrical activity patterns (intra-burst EEG was similar to that during aesthetic coma). Our data suggest that the process of neurovascular coupling itself remains delayed for days after a brief global cerebral ischemia.