Because cerebrovascular hemorrhage in newborns is often associated wit
h fluctuations in cerebral blood flow, this study was designed to inve
stigate the effects of pulsatile flow in isolated cerebral arteries fr
om neonatal piglets. Arteries mounted on cannulas were bathed in and p
erfused with a physiologic saline solution. An electronic system produ
ced pulsations, the amplitude and frequency of which were independentl
y controlled. At constant mean transmural pressure (20 mm HE) increasi
ng flow in steps from 0 to 1.6 mL/min under steady flow conditions cau
sed a biphasic response, constriction at low flow, and dilation at hig
h flow. Under pulsatile dow conditions (pulse amplitude 16-24 mm Hg; 2
Hz), the arteries dilated upon flow initiation and continued to dilat
e as mean flow increased. Dilation to pulsatile flow did not depend on
the level of mean how because switching from steady to pulsatile flow
at each flow step also caused dilation. Arteries dilated further upon
increasing either pulse amplitude (12-28 mm Hg; 2 Hz) or frequency (1
6-24 mm Hg; 4 Hz). Inhibiting nitric oxide synthesis with N-omega-nitr
o-L-arginine or perfusing with glutaraldehyde to decrease endothelial
cell deformability significantly reduced dilations to pulsatile Bow an
d to increased amplitude and frequency. These data suggest that the ar
terial response to flow is highly dependent on the mode of flow. Dilat
ion induced by initiating pulsatile how or increasing either pulse amp
litude or frequency appears to be mediated by augmented nitric oxide r
elease as result of shear stress-induced deformation of the endothelia
l cells.