1. ¹Department of Neurology, School of Medicine, Keio University, Tokyo, Japan
2. ²Laboratoire de Biologie et Physiologie Moléculaire du Vaisseau, Paris, France

Correspondence: Dr Minoru Tomita, Department of Neurology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail: mtomita@sc.itc.keio.ac.jp

Received 7 June 2004; Revised 30 September 2004; Accepted 21 October 2004; Published online 23 February 2005.

Abstract

Local cerebral blood volume (CBV) and capillary flow changes in regions of depolarizing neurons during K⁺-induced cortical spreading depression (CSD) in the cerebral cortex of -chloralose-urethane-anesthetized rats were examined employing a transillumination (550 nm) video system. Capillary flow was calculated as the reciprocal of mean transit times of blood in pixels of 40 m 40 m, each of which contains a few capillaries. Potassium microinjection into the cortex evoked repetitive wave-ring spreads of oligemia at a speed of ca. 2.330.48 mm/min. During the spread of CSD, tracer (either saline or carbon black) was injected into the internal carotid artery. Colocated with the oligemic wave, we detected capillary flow stop as evidenced by disappearance of the hemodilution curves. At any location in the region of interest within the cerebral cortex, we observed cyclic changes of capillary flow stop/hyperperfusion in synchrony with oligemia/hyperemia fluctuations. The initial flow stop and oligemia were ascribed to capillary compression by astroglial cell swelling, presumably at the pericapillary endfeet, since the oligemia occurred before larger vessel changes. We conclude that local depolarizing neurons can decrease adjacent capillary flow directly and immediately, most likely via astroglial cell swelling, and that the flow stop triggers upstream arteriolar dilatation for capillary hyperperfusion.