Background and Purpose-Hypertension is a major risk factor for ischemic and
hemorrhagic stroke and may also cause more chronic and subtle brain injury
. Progressive brain changes in a rat model of renal hypertension have been
assessed to better understand the pathogenesis of hypertensive brain damage
.
Methods-Young adult rats were made hypertensive by partial occlusion of bot
h renal arteries. MR images of brain were obtained weekly, and histopatholo
gical outcome was assessed. A separate group of rats was used to measure br
ain specific gravity and Evans blue dye content as an indicator of extravas
ation.
Results-Rats developed maximal mean systolic blood pressures of 173 to >300
mm Hg, reaching a plateau in 6 to 8 weeks. Rats whose mean systolic pressu
re never exceeded 210 mm Hg never had brain lesions, while rats whose mean
systolic pressure exceeded 276 mm Hg consistently developed brain lesions,
Brain T2 values increased with increasing blood pressure. Lesions seen on M
RI corresponded to those seen histologically. MRI also demonstrated transie
nt brain expansion, probably due to diffusely increased water content, and
rarely demonstrated focal cortical edema, which had no histological correla
te. These transient phenomena, as well as hemorrhagic and ischemic infarcts
, occurred mainly during the phase of climbing blood pressure and early sta
ges of stable hypertension
Conclusions-Serial MRI reveals aspects of hypertensive brain disease that c
annot be studied by histological examination alone. The observed phenomena
are likely related to loss of autoregulation and/or blood-brain barrier int
egrity. Breach of blood vessel integrity is less likely once the vessels be
come accustomed to high pressures.