Transient global cerebral ischemia impairs neurovascular coupling in rat

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

A XXVII - a Conferinta Nationala de Fiziologie a Societatii Romane de Fiziologie
5 - 7 iunie 2014, Bucuresti

Abstract published in Fiziologia - Physiology, 2014, Supp 1


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.