SUMMARY Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 ± 6.2 and 58.9 ± 4.6 ml/100 g/min (mean ± SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 ± 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74 % and further to 58 % of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 ± 4.9 and CeBF to 53.9 ± 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation. The present results suggest that autoregulatory function of the cerebellum may be modulated to some degree by the supratentorial brain but a more likely explanation for the results in the present work is the loss of perfusion pressure in cerebellar vessels.
SUMMARY The upper limit of cerebral autoregulation was studied in pre-or early established hypertension in spontaneously hypertensive rats (SHR). Cerebral blood flow (CBF) was measured with the hydrogen clearance method, and wall/lumen ratio of cerebral arteries was morphometrically measured with the freeze-substitution technique. To test autoregulation, phenylephrine was intravenously infused to cause stepwise increments of blood pressure. Unilateral superior cervical ganglionectomy was carried out to examine the effects of sympathetic denervation on CBF autoregulation and thickness of vascular wall.Resting blood pressure at 4 weeks, 3 months and 6 months of age were 89 ± 3 mm Hg (mean ± SEM), 140 ± 6 and 165 ± 6, respectively. Baseline CBF was slightly diminished with age; 50.6 ± 9.2 ml/100 g/min at 4 weeks, 49.8 ± 8.1 at 3 months and 44.1 ± 5.6 at 6 months. The upper limit of autoregulation was markedly raised with age; 118 ± 5 mm Hg at 4 weeks, 180 ± 7 at 3 months and 208 ± 10 at 6 months. Acute sympathetic denervation lowered the upper limits to 105 ± 2, 162 ± 4 and 185 ± 7 mm Hg, respectively. On the other hand, in chronic denervation which was made at 4 weeks of age, the upper limit of autoregulation in the denervated hemisphere was slightly lower than that in innervated hemisphere at 2 months (165 ± 5 and 178 ± 6 mm Hg), and at 5 months (202 ± 8 and 215 ± 8 mm Hg) after ganglionectomy.Wall to lumen ratio was increased with the elevation of basal blood pressure; 0.131 ± 0.008 at 4 weeks, 0.170 ± 0.005 at 3 months and 0.223 ± 0.007 at 6 months. Chronic denervation reduced such increased ratio to 0.128 ± 0.004 at 2 months and 0.196 ± 0.007 at 5 months after ganglionectomy.We conclude that during development of hypertension, the upward shift of CBF autoregulation is closely related to an elevation of basal blood pressure, which is also correlated to the thickness of vessel wall. By means of tonic and trophic effects, sympathetic innervation appears to play an important role in regulation of CBF in response to acute elevations of systemic blood pressure.Stroke Vol 16, No 3, 1985 IN CHRONIC HYPERTENSION, the upper as well as lower limits of cerebral autoregulation are raised as tested by acute elevations of basal blood pressure. Although the mechanisms are not fully understood, results obtained from observations in both humans and experimental animals indicate that hypertensive vascular alterations are primarily responsible for these shifts of autoregulation. 1 -2 Therefore long-term antihypertensive treatment lowers the limits of autoregulation towards those seen in normotensives, 2 which supports the concept that structural adaptations of cerebral vessels to high blood pressure are reversible.The present study was designed to investigate the changes of autoregulatory capacity in early, middle and late phases of sustained hypertension in spontaneously hypertensive rats (SHR). Recent findings of Nordborg and Johansson have shown that the muscularis media/radius ratio of cerebral arteries in early or prehype...
Autoregulation of cerebral blood flow (CBF) to the controlled hemorrhagic hypotension was studied in young adult spontaneously hypertensive rats (SHR, 3.4 months of age) and aged SHR (20.3 months). There were no differences in average values for mean arterial pressure and baseline CBF between two groups of rats. During hypotension, however, CBF was more reduced in aged SHR than in young SHR, indicating that the lower limit of cerebral autoregulation is shifted to a higher level in aged SHR. Such upward shift of the autoregulation is likely due to a long-lasting hypertension which may lead to the diminished vasodilatory response of the brain to hypotension.
Serial magnetic resonance (MR) imagings of two autopsied patients with Creutzfeldt-Jakob disease (CJD) are presented. Both patients showed a dramatic progression of brain atrophy. The initial MR imagings were, however, interpreted as normal except for localized mild cortical atrophy in one patient. When a normal MR image is obtained in a demented middle-aged or aged patient, CJD may still need to be ruled out: follow up MR imaging may be useful.
Participation of the autonomic nervous system in cerebellar autoregulation during supratentorial cerebral ischemia induced by bilateral carotid ligation was studied using 23 spontaneously hypertensive rats. Cerebral and cerebellar blood flows measured by a hydrogen clearance method were evaluated under stepwise hemorrhagic hypotension before and 30 minutes after ligation and after a 30-minute recirculation period following 1 hour of ligation. a-Adrenergic blockade with phenoxybenzamine, (3-adrenergic blockade with propranolol, and muscarinic cholinerglc blockade with atropine were selectively administered before ligation for inhibition of sympathetic and parasympathetic tone. Cerebral blood flow autoregulation was severely impaired during and after cerebral ischemia in each treatment group. During cerebral ischemia, cerebellar blood flow autoregulation was also significantly impaired in both the propranolol and atropine groups although it was better preserved in the phenoxybenzamine group. After recirculation, cerebellar blood flow autoregulation recovered almost to the normal range in the phenoxybenzamine and atropine groups but remained impaired in the propranolol group. Our results suggest that impaired cerebellar blood flow autoregulation in supratentorial cerebral ischemia is partly modulated by the a-adrenoceptor system, which is activated by hypertensive stimuli and cerebral ischemia, leading to vasoconstriction in the cerebellum. O ur previous study demonstrated that in experimental ischemia induced in the cerebrum, autoregulation is impaired not only in the cerebrum but also in the nonischemic cerebellum.' The precise mechanism of decreased flow in the cerebellum is under dispute. Neuronal factors seem to be involved since many recent reports indicate the importance of either innervation to or function of neuropeptides in cerebral blood vessels.Sympathetic nerves are known to constrict cerebral blood vessels in response to changes in perfusion pressure. 2 3 It is pertinent to note that cerebral ischemia activates the noradrenergic system of the brain, with large amounts of catecholamines being released in the ischemic site <5 as well as from nonischemic nerve terminals, 6 which in turn affect vasoreactivity to various stimuli such as autoregulation and CO 2 response.To examine whether sympathetic nerves or catecholamines relate to the impairment of autoregulation in remote areas of the brain, we tested autoregulation in the cerebellum during cerebral ischemia in spontaneously hypertensive rats treated with adrenergic or muscarinic cholinergic blockade.From the Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka City, Japan.Address for correspondence: Osamu Shiokawa, MD, Stroke Care Division, Kyushu Rosai Hospital, 1-3-1 Takamatsu, Kuzuhara, Kokura-Minami-Ku, Kitakyushu-City, 800-02 Japan.Received April 29, 1987; accepted November 12, 1987. Materials and Methods Preparation of RatsFemale spontaneously hypertensive rats (SHR) aged 6-7 months were anesthetized with 100 m...
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