Reductions in focal ischemic infarctions elicited from cerebellar fastigial nucleus do not result from elevations in cerebral blood flow.

To determine whether the neuroprotection elicited from electrical stimulation of the cerebellar fastigial nucleus (FN) is attributable to the elevation in regional cerebral blood flow (rCBF), we compared the effects in spontaneously hypertensive rats of stimulation of the rostral ventrolateral medulla (RVL) or FN on (a) a focal ischemic lesion produced by middle cerebral artery (MCA) occlusion, and (b) the changes in rCBF, measured by laser-Doppler flowmetry for 1.5 h, over regions corresponding to the ischemic core (parietal cortex), penumbra (occipital cortex), and nonischemic area (contralateral parietal cortex). Stimulation of FN for 1 h following MCA occlusion reduced infarction 24 h later by 52%. Stimulation of RVL was ineffective. Changes in the lesion were confined to the penumbra. FN and RVL stimulation comparably and significantly increased rCBF up to 185% in unlesioned animals. Following MCA occlusion, stimulation of FN or RVL and hypercarbia failed to elevate rCBF in the ischemic area but did so in the nonischemic area, even though in the same animals only FN stimulation reduced infarction 24 h later. We conclude that (a) the neuroprotection elicited from FN is not the result of an increase in rCBF but results from another mechanism, possibly reduction of metabolism in penumbra, and (b) the pathways mediating central neurogenic vasodilation and neuroprotection are, in part, distinct.