17-19 Oct, 2013
Modern functional brain imaging techniques rely on the constancy of the neurovascular coupling process, measured by its hemodynamic response function (HRF). Nevertheless, brain pathology may alter the HRF confounding the interpretation of imaging studies. We have recently proposed a method to investigate HRF by taking advantage of the discontinuous burst-suppression (BS) EEG pattern induced by chloral-hydrate anesthesia. BS also occurs during reperfusion following global ischemia (GCI). The aim of this study was to investigate in rats whether the HRF is altered during early reperfusion after a minimally injuring GCI. In 6 male Wistar rats (control), BS patterns were induced by an overdose of chloral-hydrate. In other 5 rats, BS was induced by a 5-minute GCI using a variation of the 4-vessel occlusion model. Simultaneous electroencephalo-graphic (EEG) activity and Laser Doppler (LD) signal were recorded from the left hemisphere. During recovery following GCI, 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 (R2=0.21; slope F=13, P<0.01). The HRF latency also seemed to increase at lower bursting frequencies in control rats, with a similar slope. The Y-intercept was, however, about half than 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 anesthetic coma). Our data suggest that the process of neurovascular coupling itself is altered following GCI in rat.