Journal of Nippon Medical School
Online ISSN : 1884-0108
Print ISSN : 0048-0444
ISSN-L : 0048-0444
White matter changes of corpus callosum in normotensive and hypertensive rats following bilateral carotid artery stenosis
Yutaka NishiyamaYasuo Katayama
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1998 Volume 65 Issue 6 Pages 450-458


The pathological mechanism responsible for cerebral white matter lesions, frequently observed in elderly individuals, is supposed to be chronic cerebral hypoperfusion. Vascular risk factors such as hypertension and carotid artery stenosis are usually involved in these lesions. The objective of this study was to elucidate the role of hypertension in white matter changes using a bilateral carotid artery stenosis model.
To induce cerebral hypoperfusion, chronic stenosis was produced by placing a 3 mm long polyethylene cuff around the bilateral carotid arteries of normotensive Wistar rats (Wistar) and spontaneously hypertensive rats (SHR). Two different diameters of tube, PE-50 (inside diameter 0.58 mm) and PE-60 (inside 0.76 mm). were used to induce different degrees of stenosis. The rats were divided into three groups, sham group, PE-50 group, and PE-60 group (each group included 15 Wistar and 15 SHR).
At 1, 2, and 4 weeks after the operation, pathological changes in white matter were observed in the corpus callosum, and the degree of lesions was assessed using the Vacuole Index. PaO2, PaCO2, pH and mean arterial blood pressure (MABP) were measured prior to and immediately after carotid stenosis.
MABP in SHR was significantly higher than in Wistar in all groups (p<0.05). Other physiological data did not differ significantly between Wistar and SHR. There was no difference in white matter changes between the Wistar sham and SHR sham groups at any time point. There was only a small degree of white matter lesions in the Wistar PE-50 and -60 groups after 4 weeks stenosis, and they did not differ significantly from the sham. In both the SHR PE-50 and -60 groups, however, white matter lesions were slightly apparent at 1 week, and were clearly visible at 4 weeks. The degree of lesions in the SHR PE-50 was significantly higher at 1 week than in the sham (p<0.01), and both the sham and the Wistar PE-50 at 2 and 4 weeks (p<0.01), and the SHR PE-60 at 4 weeks (p<0.01). The SHR PE-60 also had significantly more lesions than the sham at 2 weeks (p<0.05), and both the sham and the Wistar PE-60 at 4 weeks (p<0.01). These findings indicate that both hypertension and chronic hypoperfusion play important roles in the development of white matter lesions. (J Nippon Med Sch 1998; 65: 450-458)

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