Autoregulation of Brain Circulation in Severe Arterial Hypertension

Strandgaard, Svend; Olesen, Jes; Skinhøj, E; Lassen, Niels A.

doi:10.1136/bmj.1.5852.507

Cited by 804 publications

(165 citation statements)

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“…The pressure range over which autoregulation of cerebral blood flow occurs has been reported to be shifted to higher levels in experimental hypertension in rats and in human essential hypertension in vivo [13, 14]. The principal mechanism thought to underlie autoregulation of blood flow is the pressure-induced myogenic response, whereby an increase in pressure produces a vasoconstrictor response, while a reduction in pressure produces a vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

“…This mechanism is believed to be largely responsible for maintaining cerebral blood flow at a constant level over a wide pressure range [12]. The pressure range over which autoregulation of cerebral blood flow occurs has been reported to be shifted to higher levels in both experimental and human essential hypertension in vivo [13, 14]. This extension of the pressure range is also apparent in isolated cerebral resistance arteries from spontaneously hypertensive rats (SHR) which respond myogenically over a greater pressure range in comparison to vessels isolated from WKY rats [15].…”

Section: Introductionmentioning

confidence: 99%

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Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats

Dunn

Wallis

Gardiner³

1998

J Vasc Res

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In this study, we examined the structural and functional properties of cerebral resistance arteries isolated from normotensive (Di/N), and hypertensive (Di/H), vasopressin-deficient rats. Di/H rats had a significantly higher mean arterial blood pressure (MAP, 159 ± 3 mm Hg) than Di/N rats (125 ± 2 mm Hg). Vessels were set up in a pressure myograph, and the internal diameter and wall thickness were determined at increasing intraluminal pressures under passive (calcium-free) conditions. Arteries were then pressurized to the MAP of the animal, from which they were isolated and fixed with glutaraldehyde, embedded in araldite, sectioned and examined histologically. Under passive conditions, the middle cerebral artery (MCA) from Di/H rats had a smaller internal diameter than the MCA isolated from Di/N rats at all distending pressures. This smaller internal diameter of vessels from hypertensive rats is characteristic of eutrophic inward remodelling, whereby a similar amount of wall material is organized around a smaller lumen, without vascular growth or an alteration in artery distensibility. We have previously shown that similar structural alterations occur in mesenteric resistance arteries isolated from Di/H rats. In the presence of extracellular calcium (1.6 mmol/l), the MCA isolated from Di/H rats had significantly more intrinsic tone than the MCA isolated from Di/N rats in the pressure range of 10–110 mm Hg, although arteries from both strains had a similar myogenic index. The increased intrinsic constriction was a specific enhancement of pressure-induced tone, since responses to the thromboxane mimetic, U46619, were decreased, rather than increased, in the MCA isolated from Di/H rats. Furthermore, it is unlikely that the increased intrinsic tone in arteries isolated from Di/H rats was due to an impaired endothelial function since responses to the endothelium-dependent vasodilator, bradykinin, were enhanced in these vessels compared to arteries isolated from Di/N rats.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats

Dunn

Wallis

Gardiner³

1998

J Vasc Res

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“…The level of arterial pressure that is observed during chronic hypertension is sufficiently high that one might expect passive dilatation and increased cerebral blood flow. Cerebral blood flow, however, is normal in chronically hypertensive patients and experimental models of hypertension (Strandgaard et al, 1973;Jones et al, 1976;Hoffman et al, 1982;Sadoshima et al, 1983).…”

mentioning

confidence: 99%

Effects of chronic hypertension and sympathetic nerves on the cerebral microvasculature of stroke-prone spontaneously hypertensive rats.

Werber¹,

Heistad²

1984

Circulation Research

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SUMMARY. The purpose of this study was to examine hemodynamic mechanisms which protect cerebral vessels against chronic hypertension, and contribute to protective effects of sympathetic nerves in the cerebral circulation. We studied stroke-prone spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. At 3-4 weeks of age, all rats underwent removal of one superior cervical sympathetic ganglion. Approximately 1 year later, we cut the superior cervical sympathetic nerve contralateral to the chronic ganglionectomy and exposed pial arterioles on the cerebral cortex ipsilateral or contralateral to the chronic ganglionectomy. We measured aortic, pial arteriolar, and venous pressures with a servo-null technique, and cerebral blood flow with microspheres. Large artery resistance and small vessel resistance were calculated. During control conditions, pressure in pial arterioles was higher in stroke-prone spontaneously hypertensive rats (83 ± 6 mm Hg) (mean ± SE) than in Wistar-Kyoto rats (60 ± 3 mm Hg, P < 0.05), even though large artery resistance was almost two-fold greater in stroke-prone spontaneously hypertensive rats than in Wistar-Kyoto rats (P < 0.05). During maximal dilation produced by seizures, large artery resistance was almost three-fold higher in stroke-prone spontaneously hypertensive rats than in Wistar-Kyoto rats (P < 0.05). Small vessel resistance also was increased in stroke-prone spontaneously hypertensive rats. During seizures in stroke-prone spontaneously hypertensive rats, large artery resistance was 29% lower in chronically denervated vessels than in acutely denervated vessels (P < 0.05). Three stroke-prone spontaneously hypertensive rats had pial vessels with a "sausage string' appearance. Diameter of pial arterioles in the animals with "sausage string" vessels was greater than in stroke-prone spontaneously hypertensive rats with normal vessels (80 ± 1 1 vs. 56 ± 4 ^m, respectively, P < 0.05). We conclude that: first, increases in large artery resistance in stroke-prone spontaneously hypertensive rats attenuate increases in cerebral microcirculatory pressure during chronic hypertension; second, structural changes in cerebral vessels account, in part, for this increased resistance; third, chronic sympathectomy reduces the structural component of resistance of large cerebral arteries in stroke-prone spontaneously hypertensive rats; and, fourth, preliminary evidence suggests that stroke-prone spontaneously hypertensive rats with "sausage string" pial arterioles may have dilation of large cerebral arteries. (CircRes 55: 286-294, 1984)

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“…The mechanism behind the brain edema development is controversial. The failure of auto‐regulation caused by severe hypertension or direct toxic insult to endothelium is the most popular theory for pathophysiology (Bartynski, 2008b; Dinsdale, 1983; Schwartz et al., 1995; Strandgaard, Olesen, Skinhoj, & Lassen, 1973). One of the unsettled questions about PRES is the correlation between the brain lesion distribution patterns and blood pressure (BP).…”

Section: Introductionmentioning

confidence: 99%

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

et al. 2018

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ObjectiveThe effect of blood pressure (BP) on the lesion distribution of posterior reversible encephalopathy syndrome (PRES) is controversial. The aim of this study was to identify the relationship between brain lesion distribution patterns and BP.MethodsSixty‐five patients with PRES were selected from the database. Data regarding brain MRI findings, clinical symptoms, medical conditions, and BP at the presymptomatic period (24 hr before the symptom onset) and at the symptom onset were collected. The brain lesion distribution degree was numerically calculated (lesion scoring point [LSP]) and compared with BP and medical conditions.ResultsMean onset‐MAP was higher than mean pre‐MAP. Pre‐MAP correlated with onset‐MAP. The LSP was significantly correlated with pre‐MAP (p = 0.009, correlation coefficient [cc] = 0.323), whereas no significant correlation was found between LSP and onset‐MAP (p = 0.159, cc = 0.177). Similarly, when patients were grouped by mean MAP values, LSP was significantly higher in the patients with high MAP at the presymptomatic period (p = 0.004), whereas no difference was found in the LSP value between patients with low MAP and high MAP at the symptom onset (p = 0.272).ConclusionThe patient with PRES who has relatively higher BP in the presymptomatic period would be more likely to have wider lesion distribution than the patient with lower BP. BP elevation during presymptomatic period may be a heralding sign of impending PRES and a factor affecting the severity of PRES although BP was not investigated at earlier time points.

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Autoregulation of Brain Circulation in Severe Arterial Hypertension

Cited by 804 publications

References 12 publications

Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats

Remodelling and Enhanced Myogenic Tone in Cerebral Resistance Arteries Isolated from Genetically Hypertensive Brattleboro Rats

Effects of chronic hypertension and sympathetic nerves on the cerebral microvasculature of stroke-prone spontaneously hypertensive rats.

The effect of presymptomatic hypertension in posterior reversible encephalopathy syndrome

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