The Effects of Hypertension and Stroke on the Cerebral Vasculature

Dorrance, Anne M.

doi:10.1007/978-3-319-29152-9_5

Cited by 2 publications

(2 citation statements)

References 178 publications

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“…Nevertheless, the range of active CA was more restricted than the range of 100 mm Hg between a CPP of 50 and 150 mm Hg, as often cited. 16 , 17 , 18 Baseline CPP was centered between the LLA and ULA1, indicating that normal physiological CA operates between these limits. From baseline CPP, the capacity of CA to buffer increased CPP is greater than the capacity to buffer decreased CPP.…”

Section: Discussionmentioning

confidence: 94%

“…Lassen’s CA concept does not necessarily represent the pressure‐flow relationship within an individual. 16 , 17 , 18 In healthy individuals, the study of CA is limited by the need for pharmacological blood pressure manipulations with associated confounding effects on cerebrovascular tone and/or indirect effects from alterations of arterial gasses. 19 Only few studies have corrected for the effects of CO 2 .…”

mentioning

confidence: 99%

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Differential Hemodynamic Response of Pial Arterioles Contributes to a Quadriphasic Cerebral Autoregulation Physiology

Klein

Sloovere

Meyfroidt³

et al. 2022

JAHA

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Background Cerebrovascular autoregulation (CA) regulates cerebral vascular tone to maintain near‐constant cerebral blood flow during fluctuations in cerebral perfusion pressure (CPP). Preclinical and clinical research has challenged the classic triphasic pressure‐flow relationship, leaving the normal pressure‐flow relationship unclear. Methods and Results We used in vivo imaging of the hemodynamic response in pial arterioles to study CA in a porcine closed cranial window model during nonpharmacological blood pressure manipulation. Red blood cell flux was determined in 52 pial arterioles during 10 hypotension and 10 hypertension experiments to describe the pressure‐flow relationship. We found a quadriphasic pressure‐flow relationship with 4 distinct physiological phases. Smaller arterioles demonstrated greater vasodilation during low CPP when compared with large arterioles ( P <0.01), whereas vasoconstrictive capacity during high CPP was not significantly different between arterioles ( P >0.9). The upper limit of CA was defined by 2 breakpoints. Increases in CPP lead to a point of maximal vasoconstriction of the smallest pial arterioles (upper limit of autoregulation [ULA] 1). Beyond ULA1, only larger arterioles maintain a limited additional vasoconstrictive capacity, extending the buffer for high CPP. Beyond ULA2, vasoconstrictive capacity is exhausted, and all pial arterioles passively dilate. There was substantial intersubject variability, with ranges of 29.2, 47.3, and 50.9 mm Hg for the lower limit, ULA1, and ULA2, respectively. Conclusions We provide new insights into the quadriphasic physiology of CA, differentiating between truly active CA and an extended capacity to buffer increased CPP with progressive failure of CA. In this experimental model, the limits of CA widely varied between subjects.

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Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

Differential Hemodynamic Response of Pial Arterioles Contributes to a Quadriphasic Cerebral Autoregulation Physiology

Klein

Sloovere

Meyfroidt³

et al. 2022

JAHA

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Uric Acid Treatment After Stroke Prevents Long-Term Middle Cerebral Artery Remodelling and Attenuates Brain Damage in Spontaneously Hypertensive Rats

Jiménez‐Xarrié

Pérez

Dantas

et al. 2018

Transl. Stroke Res.

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Hypertension is the most important modifiable risk factor for stroke and is associated with poorer post-stroke outcomes. The antioxidant uric acid is protective in experimental normotensive ischaemic stroke. However, it is unknown whether this treatment exerts long-term protection in hypertension. We aimed to evaluate the impact of transient intraluminal middle cerebral artery (MCA) occlusion (90 min)/reperfusion (1-15 days) on brain and vascular damage progression in adult male Wistar-Kyoto (WKY; n = 36) and spontaneously hypertensive (SHR; n = 37) rats treated (i.v./120 min post-occlusion) with uric acid (16 mg kg) or vehicle (Locke's buffer). Ischaemic brain damage was assessed longitudinally with magnetic resonance imaging and properties of MCA from both hemispheres were studied 15 days after stroke. Brain lesions in WKY rats were associated with a transitory increase in circulating IL-18 and cerebrovascular oxidative stress that did not culminate in long-term MCA alterations. In SHR rats, more severe brain damage and poorer neurofunctional outcomes were coupled to higher cortical cerebral blood flow at the onset of reperfusion, a transient increase in oxidative stress and long-lasting stroke-induced MCA hypertrophic remodelling. Thus, stroke promotes larger brain and vascular damage in hypertensive rats that persists for long-time. Uric acid administered during early reperfusion attenuated short- and long-term brain injuries in both normotensive and hypertensive rats, an effect that was associated with abolishment of the acute oxidative stress response and prevention of stroke-induced long-lasting MCA remodelling in hypertension. These results suggest that uric acid might be an effective strategy to improve stroke outcomes in hypertensive subjects.

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The Effects of Hypertension and Stroke on the Cerebral Vasculature

Cited by 2 publications

References 178 publications

Differential Hemodynamic Response of Pial Arterioles Contributes to a Quadriphasic Cerebral Autoregulation Physiology

Differential Hemodynamic Response of Pial Arterioles Contributes to a Quadriphasic Cerebral Autoregulation Physiology

Uric Acid Treatment After Stroke Prevents Long-Term Middle Cerebral Artery Remodelling and Attenuates Brain Damage in Spontaneously Hypertensive Rats

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