Experimental Physiology Exp Physiol 00.00 (2012) pp 1–9 1 Research Paper Research Paper Blood flow in internal carotid and vertebral arteries during orthostatic stress Kohei Sato 1 , James P. Fisher 2 , Thomas Seifert 3 , Morten Overgaard 3 , Niels H. Secher 3 and Shigehiko Ogoh 1,4 1 Research Institute of Physical Fitness, Japan Women’s College of Physical Education, Tokyo, Japan 2 School of Sport and Exercise Sciences, University of Birmingham, Birmingham, UK 3 Department of Anaesthesia, The Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark 4 Department of Biomedical Engineering, Toyo University, Saitama, Japan It remains unclear whether orthostatic stress evokes regional differences in cerebral blood flow. The present study compared blood flow in the internal carotid (ICA) and vertebral arteries (VA) during orthostatic stress (60 deg head-up tilt; HUT) in six healthy young men. The ICA and VA blood flow were measured using Doppler ultrasonography. Dynamic cerebral autoregulation was also determined during supine (Supine) and HUT conditions, from the rate of regulation (RoR) in cerebrovascular conductance of the ICA and VA during acute hypotension induced by the release of bilateral thigh-cuffs. The HUT decreased ICA blood flow by -9.4 ± 1.7% (P < 0.01 versus Supine), leaving ICA conductance unchanged. In contrast, there was no significant difference in VA blood flow between Supine and HUT, and VA conductance increased (+12.9 ± 0.8%, P < 0.01). In addition, dynamic cerebral autoregulation in both the ICA and VA was attenuated during HUT, and the magnitude of the attenuation in RoR was greater in the VA [0.25 ± 0.03 s -1 Supine versus 0.16 ± 0.02 s -1 HUT (-33.9 ± 5.8%); P < 0.05] compared with the ICA [0.23 ± 0.02 s -1 Supine versus 0.20 ± 0.03 s -1 HUT (-10.6 ± 13.4%); P > 0.05]. These data indicate that orthostatic stress evokes regional differences in cerebral blood flow and possible differences in dynamic cerebral autoregulation between two main brain vascular areas in response to an acute change in blood pressure during orthostatic stress. (Received 24 January 2012; accepted after revision 6 June 2012; first published online 11 June 2012) Corresponding author K. Sato: Research Instituteof Physical Fitness, Japan Women’s College of Physical Education, Kita-Karasuyama, Setagaya-ku, Tokyo 157-8565, Japan. Email: ksato@jwcpe.ac.jp In humans, cerebral blood flow (CBF) is greater when supine compared with when seated or in an upright position (Alperin et al. 2005). Likewise, CBF velocity, measured in the middle cerebral artery (MCA) by transcranial Doppler (TCD), is reduced by ∼15–20% during simulation of orthostatic stress using head-up tilt (HUT) or lower body negative pressure (Levine et al. 1994; Immink et al. 2006; Zhang & Levine, 2007) and this cannot be explained by the concomitant reduction in the arterial carbon dioxide tension (P aCO 2 ; Immink et al. 2009). An important question regarding the reduction in CBF during orthostatic stress concerns whether it is a general phenomenon or whether it affects only the anterior part of the circle of Willis (the internal carotid system) as evaluated by mean blood flow velocity in the MCA (MCA V mean ; Madsen & Secher, 1999; Van Lieshout et al. 2003; Panerai, 2009). Sparse information is available on blood flow in the posterior part of the cerebral circulation (the vertebro-basilar system) during orthostatic stress (Haubrich et al. 2004; Sorond et al. 2005; Deegan et al. 2010). The vertebral artery (VA) and offshoots from the VA, including the anterior spinal and the posterior inferior cerebellar arteries, supply blood to the medulla oblongata, which is the location of important cardiac, vasomotor and respiratory control centres (Tatu et al. 1996). Many of the manifestations associated with development of presyncopal symptoms are likely to result from hypoperfusion in the vertebro-basilar system (Shin et al. 1999). Therefore, it is hypothesized that hypoperfusion of the medulla oblongata rather than the cerebral cortex during orthostatic stress could impair cardiac, vasomotor C  2012 The Authors. Experimental Physiology C  2012 The Physiological Society DOI: 10.1113/expphysiol.2012.064774