Impaired Vascular Reactivity of Isolated Rat Middle Cerebral Artery after Cortical Spreading Depression <i>in Vivo</i>

Seitz, Iris A.; Dirnagl, Ulrich; Lindauer, Ute

doi:10.1097/00004647-200405000-00006

Cited by 20 publications

(21 citation statements)

References 36 publications

(43 reference statements)

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“…Most previous studies support a biphasic hemodynamic change in SD, with a large hyperperfusion shortly after the DC shift followed by a long-lasting hypoperfusion (Goadsby, 1992;Lacombe et al, 1992;Seitz et al, 2004). Some studies also reported that, before the hyperemic phase, there is a transient hypoperfusion (Dreier et al, 2001;Ayata et al, 2004;Tomita et al, 2005).…”

Section: Discussionmentioning

confidence: 77%

High-ResolutionIn VivoImaging of the Neurovascular Unit during Spreading Depression

Chuquet¹,

Hollender²,

Nimchinsky³

2007

J. Neurosci.

193

180

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Section: Discussionmentioning

confidence: 77%

High-ResolutionIn VivoImaging of the Neurovascular Unit during Spreading Depression

Chuquet¹,

Hollender²,

Nimchinsky³

2007

J. Neurosci.

193

180

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“…Other experimental studies have shown that CSD is followed by long-lasting hypoperfusion and impaired cerebrovascular reactivity (6). Regulation impairment is confined to the area of the oligoaemia, suggesting that blood flow variations are caused by changes in local metabolism.…”

Section: Introductionmentioning

confidence: 92%

Increased Cerebral Vasomotor Reactivity in Migraine With Aura: An Autoregulation Disorder? A Transcranial Doppler and Near-Infrared Spectroscopy Study

et al. 2008

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Migraine with aura (MA) is associated with changes in cerebral blood flow (CBF), whereas the role of cerebral autoregulation is uncertain. This study aimed to evaluate basal CBF, cerebral blood volume (CBV) and vasomotor reactivity (VMR) in MA patients. Twenty-one controls and 16 MA patients (eight with side predominance) underwent simultaneous examination of flow velocity in the middle cerebral arteries by transcranial Doppler (TCD) and of near-infrared spectroscopy (NIRS) parameters [oxygen haemoglobin saturation: oxygen%, and total haemoglobin content (THC)] at rest and after hypercapnia. Cerebral VMR, THC and oxygen% increases were significantly greater on the predominant compared with the non-predominant migraine side, with both sides of patients without side predominance and with controls. These findings suggest altered autoregulation in MA patients, possibly secondary to impaired cerebrovascular autonomic control. Simultaneous TCD and NIRS investigation could represent a non-invasive approach to evaluate cerebral haemodynamics at the cortical and subcortical level.

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“…Because solutions were applied locally onto the pial arterioles, diminished reactivity was likely due to changes within the vessels, rather than the parenchyma. Indeed, isolated vessels harvested after they were exposed to an SD in situ showed much diminished reactivity to pH and [K ϩ ] o changes (415). Even the response to the direct vasodilator papaverine appeared to be diminished after an SD in one study (130), although responses to acetylcholine, CGRP, NMDA, K ATP channel opener aprikalim, and adenylate cyclase activator forskolin were reportedly preserved after SD in rabbits (46, 80), suggesting that the vasomotor paralysis may not apply to all species or mediators.…”

Section: Impaired Cerebrovascular Reactivity After Spreading Deprmentioning

confidence: 99%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

472

600

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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leão, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

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Impaired Vascular Reactivity of Isolated Rat Middle Cerebral Artery after Cortical Spreading Depression in Vivo

Cited by 20 publications

References 36 publications

High-ResolutionIn VivoImaging of the Neurovascular Unit during Spreading Depression

High-ResolutionIn VivoImaging of the Neurovascular Unit during Spreading Depression

Increased Cerebral Vasomotor Reactivity in Migraine With Aura: An Autoregulation Disorder? A Transcranial Doppler and Near-Infrared Spectroscopy Study

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

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