Acute changes in neurovascular reactivity after subarachnoid hemorrhage <i>in vivo</i>

Balbi, Matilde; Koide, Masayo; Schwarzmaier, Susanne M.; Wellman, George C.; Plesnila, Nikolaus

doi:10.1177/0271678x15621253

Cited by 26 publications

(38 citation statements)

References 39 publications

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“…Recent ex vivo studies investigating intraparenchymal arterioles in rats after SAH reported an inversion of NVC: arterioles constricted rather than dilated in response to neuronal activity 24 to 96 h after SAH. 30 While our previous study investigating neurovascular reactivity showed that NVC is not impaired within the first few hours after SAH, 11 in the current study, we unequivocally demonstrate in vivo and ex vivo a progression in vascular dysfunction, affecting NVC 24 h after SAH. These findings define a therapeutic time window that could lead to an improvement in the outcome of already promising approaches like NO-based strategies, i.e.…”

Section: Discussionsupporting

confidence: 49%

“…Mice were re-anesthetized 24 h after SAH and the CBF response after NVC was evaluated as previously described. 11,17 Briefly, the left forepaw was stimulated with two subdermal needle electrodes with a diameter of 0.2 mm (Hwato, Suzhou, China) at an intensity of 2 mA for 0.3 ms (Digitimer Ltd, Hertfordshire, England). One stimulation cycle contained 96 stimulations and lasted for 16 s (6 Hz).…”

Section: Forepaw-evoked Nvcmentioning

confidence: 99%

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Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

Balbi

Koide

Wellman

et al. 2017

J Cereb Blood Flow Metab

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Subarachnoid hemorrhage (SAH) induces acute changes in the cerebral microcirculation. Recent findings ex vivo suggest neurovascular coupling (NVC), the process that increases cerebral blood flow upon neuronal activity, is also impaired after SAH. The aim of the current study was to investigate whether this occurs also in vivo. C57BL/6 mice were subjected to either sham surgery or SAH by filament perforation. Twenty-four hours later NVC was tested by forepaw stimulation and CO reactivity by inhalation of 10% CO. Vessel diameter was assessed in vivo by two-photon microscopy. NVC was also investigated ex vivo using brain slices. Cerebral arterioles of sham-operated mice dilated to 130% of baseline upon CO inhalation or forepaw stimulation and cerebral blood flow (CBF) increased. Following SAH, however, CO reactivity was completely lost and the majority of cerebral arterioles showed paradoxical constriction in vivo and ex vivo resulting in a reduced CBF response. As previous results showed intact NVC 3 h after SAH, the current findings indicate that impairment of NVC after cerebral hemorrhage occurs secondarily and is progressive. Since neuronal activity-induced vasoconstriction (inverse NVC) is likely to further aggravate SAH-induced cerebral ischemia and subsequent brain damage, inverse NVC may represent a novel therapeutic target after SAH.

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Section: Discussionsupporting

confidence: 49%

Section: Forepaw-evoked Nvcmentioning

confidence: 99%

Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

Balbi

Koide

Wellman

et al. 2017

J Cereb Blood Flow Metab

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“…In both SAH and CADASIL, dysregulation of brain PA reactivity precedes the onset of neurological deficits. Using well‐established rabbit, rat, and mouse models of SAH, and a transgenic mouse model of CADASIL (TgNotch3 R169C ) in which a human NOTCH3 receptor mutation—the molecular cause of CADASIL—is overexpressed, we have discovered that K V channel activity in PA SMCs is abnormal in both pathological conditions . Although abnormal K V activity could conceivably reflect changes in channel gating properties or recruitment of new K V channel family members, our experimental data demonstrated unchanged τ act , V 0.5 , or k in both disease models.…”

Section: Impact Of Pathological Increases (Cadasil) or Decreases (Sahmentioning

confidence: 79%

The yin and yang of K_V channels in cerebral small vessel pathologies

et al. 2018

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Cerebral SVDs encompass a group of genetic and sporadic pathological processes leading to brain lesions, cognitive decline, and stroke. There is no specific treatment for SVDs, which progress silently for years before becoming clinically symptomatic. Here, we examine parallels in the functional defects of PAs in CADASIL, a monogenic form of SVD, and in response to SAH, a common type of hemorrhagic stroke that also targets the brain microvasculature. Both animal models exhibit dysregulation of the voltage‐gated potassium channel, KV1, in arteriolar myocytes, an impairment that compromises responses to vasoactive stimuli and impacts CBF autoregulation and local dilatory responses to neuronal activity (NVC). However, the extent to which this channelopathy‐like defect ultimately contributes to these pathologies is unknown. Combining experimental data with computational modeling, we describe the role of KV1 channels in the regulation of myocyte membrane potential at rest and during the modest increase in extracellular potassium associated with NVC. We conclude that PA resting membrane potential and myogenic tone depend strongly on KV1.2/1.5 channel density, and that reciprocal changes in KV channel density in CADASIL and SAH produce opposite effects on extracellular potassium‐mediated dilation during NVC.

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“…The vasoconstriction observed after SAH is thought to be caused by elevated potassium concentrations outside ( [39]. Such an inversion of neurovascular coupling has also been demonstrated in vivo [40,41].…”

Section: Pathophysiology Of Subarachnoid Hemorrhagementioning

confidence: 89%

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

Albanna¹,

Lüke²,

Alpdogan³

et al. 2018

New Front Ophthalmol

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Purpose: The isolated and superfused retina from vertebrates is routinely used for neurophysiological measurements of basic retinal signal generation and transduction. Such an ex vivo isolated neural network moreover represents a useful model system for the investigation of drugs and toxins and may also be helpful to elucidate molecular mechanisms of CNS diseases. The present overview aims to bring observations to the reader's attention, which, in part, have been made more than 50 years ago and were sparsely followed up upon in subsequent research, but may support the idea that the isolated bovine retina represents a useful system to investigate the physiology and pathophysiology of energy supply to neuronal tissue. Material and methods:Parallel recording of ERGs and pyridine nucleotide oxidation in the isolated and superfused vertebrate retina. The review will focus on topics, which discuss the connection between retinal electrophysiology and underlying energy metabolism.Results: Previous and present reports about (i) transretinal signaling cascades, (ii) the involvement of the pharmacoresistant Cav2.3 / R-type calcium channel in transretinal signaling and (iii) data about the retinal oxygen demands and concentration in different layers are collected, which elucidate that the retina may be used as a cerebral surrogate model in different research areas. Retinal tolerance to ischemia is several times larger than the tolerance in the remaining brain. Conclusions:The retinal energy supply through retinal vessels is regulated and controlled by neurovascular coupling. Classical retinal recording techniques and special retinal abilities in electrical-vascular coupling will be set in perspective with novel recording techniques, currently brought into clinical application for the detection of impaired neurovascular coupling after aneurysmal subarachnoid hemorrhage in the brain. The present review elucidates that important pathophysiological aspects related to the upregulation of pharmacoresistant Cav2.3 / R-type calcium channels during SAH may be investigated in the isolated vertebrate retina. Ischemic tolerance in the vertebrate retinaThe oxygen consumption of the vertebrate retina on a per gram basis has been described as higher than that of the brain [1,2]. Oxygen cannot be "stored" in tissue so that a constant and adequate supply must be guaranteed to preserve function. Metabolic dysfunction regarding to impaired vascular supply is directly reflected by retinal oxygen saturation which can be detected noninvasively by dual wavelength fundus photography [3]. Normally, the oxygen saturation in retinal vessels differs along vascular segments and is higher in the macular region than retinal periphery [4]. Many retinal diseases are caused by a dysfunction of the vascular network. Interestingly, the venous oxygen saturation in diabetic retinopathy was higher in venules draining the macular surroundings than retinal periphery that reflect specific metabolic conditions [5,6].Since a relatively unobstructed light path...

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Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Cited by 26 publications

References 39 publications

Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

The yin and yang of K_V channels in cerebral small vessel pathologies

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

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Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo

Cited by 26 publications

References 39 publications

Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

Inversion of neurovascular coupling after subarachnoid hemorrhage in vivo

The yin and yang of KV channels in cerebral small vessel pathologies

Selected aspects of retinal signaling and energy metabolism and its perspective as a cerebral surrogate model

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The yin and yang of K_V channels in cerebral small vessel pathologies