The Upper Limit of Autoregulation of Cerebral Blood Flow — On the Pathogenesis of Hypertensive Encepholopathy

Lassen, Niels A.; Agnoli, A.

doi:10.3109/00365517209081099

Cited by 134 publications

(41 citation statements)

References 4 publications

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“…The demonstrated shift to a higher blood pressure level of the brain autoregulation curve with hypertension may be caused by hypertrophy of the arteriolar walls (Folkow, 1971 Our observations during induced hypertension may contribute to the current discussion on the pathogenesis of acute hypertensive encephalopathy (Byrom, 1969;Lassen and Agnoli, 1972 (Symon et al, 1971). The fact that a similar increase in cerebral blood flow was found in one normotensive patient with a mean arterial blood pressure above 120 mm Hg suggests that the phenomenon is not caused by hypertensive vascular disease per se; it seems more likely that an upper limit of autoregulation is present in all persons and that even this upper limit is raised in hypertension.…”

Section: Discussionmentioning

confidence: 86%

“…The traditional concept is that a state of spasm is provoked in the arterioles at a very high blood pressure, resulting in critical hypoperfusion with ischaemia of the brain tissue (Byrom, 1954;Fazekas, 1966;Finnerty, 1972). Alternatively failure of the autoregulation mechanism with forced vasodilatation has been suggested as the initial pathogenetic event leading to this disorder (Byrom, 1969;Lassen and Agnoli, 1972 (Lennox and Gibbs, 1932). If the cerebral metabolic rate of oxygen (CMRo,) is assumed to be constant the cerebral blood flow can be calculated from the cerebral arteriovenous oxygen difference (AVo5) by means of the Fick principle:…”

Section: Introductionmentioning

confidence: 99%

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Autoregulation of Brain Circulation in Severe Arterial Hypertension

Strandgaard

Olesen

SKINH??J

et al. 1974

Survey of Anesthesiology

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132

168

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SummaryCerebral blood flow was studied by the arteriovenous oxygen difference method in patients with severe hypertension and in normotensive controls. The blood pressure was lowered to study the lower limit of autoregulation (the pressure below which cerebral blood flow decreases) and the pressure limit of brain hypoxia. Both limits were shifted upwards in the hypertensive patients, probably as a consequence of hypertrophy of the arteriolar walls. These findings have practical implications for antihypertensive therapy.When the blood pressure was raised some patients showed an upper limit of autoregulation beyond which an increase of cerebral blood flow above the resting value was seen without clinical symptoms. No evidence of vasospasm was found in any patient at high blood pressure. These observations may be of importance for the understanding of the pathogenesis of hypertensive encephalopathy.

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Section: Discussionmentioning

confidence: 86%

Section: Introductionmentioning

confidence: 99%

Autoregulation of Brain Circulation in Severe Arterial Hypertension

Strandgaard

Olesen

SKINH??J

et al. 1974

Survey of Anesthesiology

Self Cite

132

168

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“…These investigators additionally suggested that the severity of such damage may depend not only on the severity of the hypertension but also on the renal autoregulatory or myogenic capacity. The importance of local myogenic mechanisms in protecting against hypertensive injury was formally recognized in the concept proposed in 1972 that hypertensive encephalopathy may develop only when BPs exceed the upper limit of cerebral blood flow autoregulation (94). A great deal of experimental and clinical evidence has since been obtained in support of the concept (86,93).…”

Section: Historical Perspectivesmentioning

confidence: 99%

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Loutzenhiser

Griffin²,

Bidani³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

237

244

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dani. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms. Am J Physiol Regul Integr Comp Physiol 290: R1153-R1167, 2006. doi:10.1152/ajpregu.00402.2005.-When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology. This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned. Evidence is presented suggesting that additional mechanisms exist to maintain ambient levels of RBF and GFR within normal range, despite chronic alterations in BP and severely impaired acute responses to pressure. Finally, the implications of this new perspective on the divergent roles of the myogenic response to pressure vs. the TGF response to changes in distal delivery are considered, and it is proposed that in addition to TGF-induced vasoconstriction, vasodepressor responses to reduced distal delivery may play a critical role in modulating afferent arteriolar reactivity to integrate the regulatory and protective functions of the renal microvasculature. renal microcirculation; afferent arteriole; myogenic; tubuloglomerular feedback ONE OF THE MOST STRIKING CHARACTERISTICS of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered. The dual regulation of both RBF and GFR is achieved by proportionate changes in the preglomerular resistance and is believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and the renal myogenic response. TGF involves a flow-dependent signal that is sensed at the macula densa and alters tone in the adjacent segment of the afferent arteriole via a mechanism that remains controversial but likely involves adenosine and/or ATP (30,80,144). The myo...

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“…This syndrome is characterized by an acute rise in blood pressure that overcomes cerebral artery myogenic tone, causing forced dilatation, autoregulatory breakthrough, and hyperperfusion (21). As a consequence, blood-brain barrier disruption occurs, followed by cerebral edema formation (18).…”

mentioning

confidence: 99%

Pregnancy prevents hypertensive remodeling and decreases myogenic reactivity in posterior cerebral arteries from Dahl salt-sensitive rats: a role in eclampsia?

Aukes¹,

Vitullo²,

Zeeman³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Aukes AM, Vitullo L, Zeeman GG, Cipolla MJ. Pregnancy prevents hypertensive remodeling and decreases myogenic reactivity in posterior cerebral arteries from Dahl salt-sensitive rats: a role in eclampsia? Am J Physiol Heart Circ Physiol 292: H1071-H1076, 2007. First published October 20, 2006; doi:10.1152 doi:10. /ajpheart.00980.2006ous studies have demonstrated that pregnancy prevents protective hypertension-induced remodeling of cerebral arteries using nitric oxide synthase (NOS) inhibition to raise mean arterial pressure (MAP). In the present study, we investigated whether this effect of pregnancy was specific to NOS inhibition by using the Dahl saltsensitive (SS) rat as a model of hypertension. Nonpregnant (n ϭ 16) and late-pregnant (n ϭ 17) Dahl SS rats were fed either a high-salt diet (8% NaCl) to raise blood pressure or a low-salt diet (Ͻ0.7% NaCl). Third-order posterior cerebral arteries were isolated and pressurized in an arteriograph chamber to measure active responses to pressure and passive remodeling. Several vessels from each group were stained for protein gene product 9.5 to determine perivascular nerve density. Blood pressure was elevated in both groups on high salt. The elevated MAP was associated with significantly smaller active and passive diameters (P Ͻ 0.05) and inward remodeling in the nonpregnant hypertensive group only. Whereas no structural changes were observed in the late-pregnant hypertensive animals, both latepregnant groups had diminished myogenic reactivity (P Ͻ 0.05). Nerve density in both the late-pregnant groups was significantly greater when compared with the nonpregnant groups, suggesting that pregnancy has a trophic influence on perivascular innervation of the posterior cerebral artery. However, hypertension lowered the nerve density in both nonpregnant and late-pregnant animals. It therefore appears that pregnancy has an overall effect to prevent hypertensioninduced remodeling regardless of the mode of hypertension. This effect may predispose the brain to autoregulatory breakthrough, hyperperfusion, and eclampsia when MAP is elevated. gestation; hypertension; brain HYPERTENSION IS ONE OF THE most common complications of pregnancy and is a life-threatening disease for both mother and fetus (27). Several organs are affected by pregnancy-induced hypertension, including the brain manifesting itself as eclampsia with classical neurological features such as headache, nausea, cortical blindness, loss of consciousness, and seizures (35). Eclampsia is one of the leading causes of maternal death (12, 23), yet little is known about how hypertension in pregnancy affects the cerebral circulation and causes the symptoms of eclampsia.The primary explanation for the pathogenesis of eclampsia is that it is thought to be a form of hypertensive encephalopathy (11,22,36,37). This syndrome is characterized by an acute rise in blood pressure that overcomes cerebral artery myogenic tone, causing forced dilatation, autoregulatory breakthrough, and hyperperfusion (21). As a consequence, blood-brain ...

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The Upper Limit of Autoregulation of Cerebral Blood Flow — On the Pathogenesis of Hypertensive Encepholopathy

Cited by 134 publications

References 4 publications

Autoregulation of Brain Circulation in Severe Arterial Hypertension

Autoregulation of Brain Circulation in Severe Arterial Hypertension

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Pregnancy prevents hypertensive remodeling and decreases myogenic reactivity in posterior cerebral arteries from Dahl salt-sensitive rats: a role in eclampsia?

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