Vasomotion appears to be an intrinsic property of the cerebral vasculature since it can be observed in vessels maintained ex vivo (Ngai & Winn, 1995). In cerebral vessels rhythmic contractions may be facilitated by the addition of constrictor agents (Fujii et al. 1990; Ngai & Winn, 1995). Vasomotion in feeder arterioles in the cerebral circulation has been found to lead to synchronised oscillations in the velocity of red blood cells flowing downstream in the capillary network (Biswal & Hudetz, 1996). It has been suggested that the activity pattern of vasomotion might be able to influence microcirculatory haemodynamics (Ursino et al. 1996). If vasomotion were to cease locally the abolition of the transient increases in vascular resistance at points of periodic constriction would offer a low resistance path. Thus during periods of increased neuronal activity a temporary cessation of vasomotion might serve to divert blood to the metabolically active area and contribute to the flow-metabolism coupling process. Studies of the coupling process in the deep vessels, which constitute the majority of the cerebral vasculature, have been hampered by their inaccessibility. Direct observations of intra-parenchymal vessels in situ can, however, be made in brain slices and the responses of individual preterminal arterioles observed during localised increases in synaptic activity evoked by electrical stimulation.

Coronal slices of hippocampus, 400 µm thick, were prepared from 150-240 g male Wistar rats anaesthetised with 20 % urethane (0.7 ml (100 g body weight)^-1 I.P.). Slices were maintained at 35 °C in a chamber mounted on the stage of a Zeiss Axioskop 2 microscope as described previously (Lovick et al. 1999). A bipolar stimulating electrode was positioned to stimulate the Schaffer collateral fibre bundle and the evoked field potential recorded from an electrode in CA1. The intensity was adjusted to give 90 % maximal response amplitude. Images of arterioles (inside diameter 6-12 µm, internal/ external diameter ▓le│ 0.6) located 30-150 µm below the surface of the slice in CA1 proximal to the recording site were captured using a CCD camera and a computer running Openlab 2 image analysis software (Improvision Ltd). On addition of the thromboxane A₂ agonist U46619 (75-100 nM) to the superfusate to increase vasoconstrictor tone, rhythmic contractions (vasomotion, 0.6-7.1 min^-1, mean 3.0 ± 0.6 S.E.M.) developed in the smooth muscle cells of the vessel wall. During stimulation of the Schaffer collaterals (0.1 ms pulses, 2.5 Hz for 2 min) vasomotion either ceased (n = 4) or was significantly reduced in frequency (n = 3) from 4.9 ± 1.2 to 0.9 ± 0.3 min^-1 (P < 0.05, paired t test). In the three vessels with residual vasomotion, the amplitude of the contractions was reduced by 12-66 %. The response to a second period of stimulation did not differ significantly from the first. When tetrodotoxin (TTX, 1 µM, n = 4) was added to the bath to block synaptic activity, the basal rhythmic contractile activity of the vessels continued. In contrast, the field potential was abolished together with the stimulus-evoked decrease in the frequency of vasomotion. The results suggest that increases in synaptic activity can evoke relaxation of intraparenchymal arterioles in hippocampal slices. We suggest that the observed reduction in vasomotion may contribute to the mechanism of flow-metabolism coupling.This work was supported by the British Heart Foundation.

Biswal, B.B. & Hudetz, A.G. (1996). Microvasc. Res. 52, 1-12.

Fujii, K., Heistad, D.D. & Faraci, F.M. (1990). Am. J. Physiol. 258, H1829-1834.

Lovick, T.A., Brown, L.A. & Key, B.J. (1999). Neuroscience 92, 47-60.

Ngai, A.C. & Winn, H.R. (1995). Circ. Res. 77, 832-840.

Ursino, M., Cavalcanti, S., Bertuglia, S. & Colantuoni, A. (1996). Microvasc. Res. 51, 229-249.