Contribution of cerebral edema to the neuronal salvage elicited by stimulation of cerebellar fastigial nucleus after occlusion of the middle cerebral artery in rat.

To the Editor: Electrical stimulation of the cerebellar fastigial nucleus (FN) in rat reduces, by over 40%, the vol­ ume of the focal ischemic infarction produced by occlusion of the middle cerebral artery (MCA) (Berger et aI. , 1990; Reis et aI. , 1991; Zhang and Iadecola, 1992; Yamamoto et aI. , 1993). The mech­ anism of the effect is unknown. While the salvage has been attributed to neuronal protection, Drs. Swanson and Sharp have raised the question of whether the reduction in lesion volume results rather from a reduction of edema (Katzman et aI. , 1977), a mechanism that might be overlooked when lesion volume is computed in only the affected hemisphere by delineating lesion boundaries, mea­ suring the lesion area in serial thionine stained sec­ tions, and then computing the lesion volume. We have therefore investigated whether the de­ crease in the volume of a focal ischemic infarction produced by electrical stimulation of the FN is sec­ ondary to a reduction of the edema invariably asso­ ciated with focal ischemia (Katzman et aI. , 1977; Ames and Nesbett, 1983; Gotoh et aI., 1985; Klatzo, 1985) and maximal within the ischemic core (Symon et aI. , 1979; Young et aI. , 1987; Dickinson and Betz, 1992; Menzies et aI. , 1993) by comparing the contribution of edema to lesion volume in brains of rats in which the MCA was occluded with or without FN stimulation (Reis et aI. , 1991; Ya­ mamoto et aI. , 1993). (The detailed methods are de­ scribed in these publications. ) The contribution of edema to the lesion volume can be estimated by several methods: By directly comparing wet and dry weights of lesioned and in­ tact hemispheres (Lin et aI. , 1993), by measuring the infarct area limited to the gray matter as sug­ gested by Swanson et aI. (1990; Lin et aI., 1993), and by computing the ratio of the volume of the infarcted to the intact hemispheres, the method used here and validated in many other studies (Ka­ plan et aI. , 1991; Kawamura et aI. , 1991a,b; Mayer and Pulsinelli, 1992). The rationale for the latter method is that the accumulation of water, usually 8-14% within the infarction (Hatashita et aI., 1988; Mayer and Pulsinelli, 1992; Lin et aI. , 1993), pro-