Vascular permeability precedes spontaneous intracerebral hemorrhage in stroke-prone spontaneously hypertensive rats.
نویسندگان
چکیده
BACKGROUND AND PURPOSE Stroke-prone spontaneous hypertensive rats (SHRsp) fed a high-salt diet develop malignant hypertension, blood-brain barrier breakdown, and spontaneous intracerebral hemorrhage (ICH). The precise spatial and temporal relationship between these events has not been well-delineated. METHODS Ten SHRsp male rats, fed a high-salt diet, were imaged weekly using MRI, starting at 12 weeks of age. T1-weighted (with and without Gd), T2-weighted, and T2* sequences were acquired. Permeability maps were calculated. RESULTS Seven SHRsp rats had spontaneous ICH develop before death. Five of the 7 rats had focally increased vascular permeability at the site of the ICH; 3 of these rats had vascular permeability 1 to 2 weeks before spontaneous ICH. CONCLUSIONS Salt-loaded SHRsp rats have increased vascular permeability up to 2 weeks before ICH, predicting hemorrhage both in space and time. These results suggest that hypertensive ICH is preceded by focal vasculopathy detectable by Gd leak.
منابع مشابه
Bone marrow mesenchymal stem cells ameliorate neurological deficits and blood-brain barrier dysfunction after intracerebral hemorrhage in spontaneously hypertensive rats.
Spontaneous intracerebral hemorrhage (ICH) is a common and fatal subtype of stroke, with hypertension the most common cause of this disorder. Bone marrow derived mesenchymal stem cells (BM-MSCs) have been shown to elicit protective properties in stroke models. In the present study, male spontaneously hypertensive rats (SHR) were subjected to ICH by intracerebral injection with autologous blood,...
متن کاملRupture of the internal elastic lamina and vascular fragility in stroke-prone spontaneously hypertensive rats.
We studied a possible relation between stroke and an enhanced susceptibility to rupture of the arterial internal elastic lamina by comparing stroke-prone spontaneously hypertensive rats with spontaneously hypertensive rats, which have a very low incidence of stroke. We quantified interruptions in the internal elastic lamina in certain arteries and studied the effect of beta-aminopropionitrile, ...
متن کاملBrain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.
BACKGROUND AND PURPOSE Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stro...
متن کاملPotassium reduces cerebral hemorrhage and death rate in hypertensive rats, even when blood pressure is not lowered.
In a study of the effects of K+ in stroke prone spontaneously hypertensive rats, adding K+ to normal chow was found to reduce the mortality from 83% to 2%, a 98% reduction. An 86% reduction in mortality occurred even when blood pressure was virtually equal in the two stroke prone spontaneously hypertensive groups being compared. Dietary K+ supplements also reduced mortality in hypertensive Dahl...
متن کاملAnalysis of cerebrovascular sympathetic nerve density in relation to stroke development in spontaneously hypertensive rats.
Previous studies have shown that elevating the K+ levels from 0.75% to 2.11% in the diet of stroke-prone spontaneously hypertensive rats significantly retards the development of stroke and increases their lifespan. On the other hand, stroke-resistant spontaneously hypertensive rats fail to develop stroke even if they are fed the low-K+ version of this diet. Since sympathetic nerves surrounding ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Stroke
دوره 38 12 شماره
صفحات -
تاریخ انتشار 2007