Hypertension-induced vascular remodeling contributes to reduced cerebral perfusion and the development of spontaneous stroke in aged SHRSP rats.
Stroke in spontaneously-hypertensive, stroke-prone (SHRSP) rats is of particular interest because the pathogenesis is believed to be similar to that in the clinical setting. In this study, we employed multi-modal MRI-ASL, DWI, T(2), GRE, T(1) (pre/post contrast)-to investigate the natural history of spontaneous cerebral infarction and the specific role of cerebral perfusion in disease development. Twelve female SHRSP rats (age: approximately 1 year) were imaged within 1 to 3 days of symptom onset. The distribution of ischemic lesions was the following: 28.1% visual, 21.9% striatal, 18.8% motorsensory, 12.5% thalamic, 12.5% auditory, 3.1% frontal/prelimbic, and 3.1% multiple areas. Ischemic lesions had significantly reduced blood flow in comparison with healthy tissue. Ischemic lesions were characterized by hyperplastic, thrombosed, and compressed vessels. These findings suggest that ischemic lesion development is related to hypertension-induced vascular remodeling and persistent hypoperfusion. This model should be useful for studying the relationship between chronic hypertension and subsequent stroke, both in terms of primary and secondary prevention.
Henning
Erica C
EC
Section on Stroke Diagnostics and Therapeutics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room B1D733, 10 Center Drive, MSC 1063, Bethesda, MD 20892, USA. henninge@ninds.nih.gov
Warach
Steven
S
Spatz
Maria
M
D000818:Animals; D001812:Blood-Brain Barrier / Q000473:pathology / Q000503:physiopathology; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D008279:Magnetic Resonance Imaging / Q000379:methods; D051381:Rats; D011918:Rats, Inbred SHR; D012039:Regional Blood Flow / Q000502:physiology*; D013113:Spin Labels; D020521:Stroke / Q000209:etiology / Q000473:pathology / Q000503:physiopathology
D013113:Spin Labels