A transient increase in cortical neuronal activity is followed by a transient increase in cerebral blood flow. This physiological process of neurovascular coupling, measured by its hemodynamic response function (HRF), is used to infer neuronal activity in modern vascular-based brain imaging techniques. Nevertheless, brain pathology may alter the HRF confounding the interpretation of imaging studies. Our aim was to investigate the extent of HRF alterations after a minimally injuring transient global cerebral ischemia (GCI) in adult male Wistar rats (n=11). We introduced a new technique of measuring HRF by taking advantage of the whole-brain discontinuous EEG burst-suppression (BS) state induced by a chloral-hydrate overdose (400 mg/kg BW i.p.). 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 from the left hemisphere. The rectified EEG was convoluted with a prototype HRF to obtain a synthetic LD signal. Two parameters of the prototype HRF (peak response latency and response width) were then programmatically optimized to attain a maximum correlation between the recorded and the synthetic LD signals within the 0.1-0.4 Hz band. 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 (heart rate remained normal) or to changes in electrical activity patterns (intra-burst EEG was similar to that during anaesthetic coma). Our data suggest that the process of neurovascular coupling itself remains delayed for days after a brief global cerebral ischemia.
Physiology 2014 (London, UK) (2014) Proc Physiol Soc 31, PCA063
Poster Communications: Delayed neurovascular coupling after transient global cerebral ischemia in rat
A. Zagrean1, C. Acatrinei1, A. Calin2, D. Zahiu1, A. Paslaru1, A. Stoian1, M. Stancu1, L. Zagrean1, M. Moldovan1,3
1. Physiology and 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.
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