The effect of acute arterial hypertension on the blood-brain barrier to protein tracers

Johansson, Barbro; Li, Choh-Luh; Olsson, Yngve; Klatzo, Igor

doi:10.1007/bf00687666

Cited by 210 publications

(59 citation statements)

References 28 publications

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“…50 -53 Alternatively, autoregulation can be diminished or lost under pathologic conditions such as traumatic brain injury and stroke. 54,55 The loss of autoregulation decreases CVR, a result that produces hyperperfusion, BBB disruption, and vasogenic edema formation, 5,[51][52][53]56 the underlying cause of the neurologic symptoms of hypertensive encephalopathy and eclampsia. 5,56 One of the most pronounced cardiovascular adaptations that occurs during pregnancy is that maternal cardiac output and plasma volume increase by 40% to 50% by midgestation.…”

Section: Cerebral Hemodynamics During Pregnancy and Eclampsiamentioning

confidence: 99%

Cerebrovascular Function in Pregnancy and Eclampsia

2007

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Section: Cerebral Hemodynamics During Pregnancy and Eclampsiamentioning

confidence: 99%

Cerebrovascular Function in Pregnancy and Eclampsia

2007

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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). Because of the significant involvement of the cerebrovasculature in mediating these symptoms, investigating how pregnancy and hypertension during pregnancy affect the cerebral circulation seems critical to understanding and treating eclampsia.…”

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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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“…15 ' 16 It may explain why Grubb and coworkers" could raise the mean blood pressure in rhesus monkeys to about 180 mm Hg without any rise in the blood volume of subcortical brain tissue; on the contrary, a continuous decrease in subcortical cerebral blood volume was found during rising blood pressure, as expected when autoregulation is effective.…”

Section: Discussionmentioning

confidence: 97%