Delayed hemodynamic response at 48 hours following global cerebral ischemia in rat

Camelia Acatrinei(1), Alexandru Calin(2,3), Alexandru-Catalin Paslaru(1), Denise Zahiu(1), Stefan Mirica(1), Mihai Stancu(1), Alexandru Stoian(1), Ana-Maria Zagrean(1), Leon Zagrean(1) and Mihai Moldovan(1,4) 1Division of Physiology and Fundamental Neuroscience, "Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania; 2Department of Pharmacology, University of Oxford, Oxford, United Kingdom 3Department of Experimental Psychology, University of Oxford, Oxford, United Kingdom 4Neuroscience and Pharmacology, Panum, University of Copenhagen, Copenhagen, Denmark

NEURONUS 2014 IBRO & IRUN Neuroscience Forum, Kraków, Poland
25-27 April, 2014


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.