Cerebral vasodilation during hypercapnia. Role of glibenclamide-sensitive potassium channels and nitric oxide.

Faraci, Frank M.; Breese, Keith; Heistad, D D

doi:10.1161/01.str.25.8.1679

Cited by 106 publications

(82 citation statements)

References 36 publications

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“…When the dependent variables were considered separately with a Bonferroni adjusted alpha level of 0.001, statistically significant group differences were identified for pCO 2 49.52, P Ͻ .0005; partial eta squared ϭ 0.70]. There was, however, no statistically significant group difference in measures of ABG percent O 2 saturation [F (2,41) ϭ 0.15, P ϭ .858; partial eta squared ϭ 0.007].…”

Section: Discussionmentioning

confidence: 99%

“…Regression analysis revealed a significant positive linear relationship between cerebral perfusion and pCO 2 [␤ ϭ 4.02, t ϭ 11.03; P Ͻ .0005], such that rates of cerebral perfusion changed by 4.0 mL/100 g/min for each 1-mm Hg change in pCO 2 (Fig 5). A statistically significant proportion of the variance (73%) associated with cerebral perfusion was explained by pCO 2 …”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] The precise vasodilatory mechanism of CO 2 in humans is still being refined. 5,6,30,31 Animal studies have shown hypercapnia activates K ATP channels in vascular smooth muscle, causing vasodilation.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

“…[1][2][3][4][5][6] Gas mixtures with elevated concentrations of carbon dioxide (CO 2 ) are commonly used in both the research and clinical settings to evaluate cerebrovascular reserve, most frequently in patients with stenotic or occlusive cerebrovascular disease before extracranial-to-intracranial bypass. 2,7,8 Even small increases in the partial pressure of CO 2 (pCO 2 ) on the order of 5 to 6 mm Hg are capable of generating appreciable changes on perfusion imaging. 3,4,[7][8][9][10][11][12][13] Techniques such as transcranial Doppler, nuclear medicine positronemission tomography (PET) and single-photon emission CT, angiography, phase-contrast MR imaging, and arterial spinlabeled (ASL) MR perfusion have been used to evaluate the experimental hypercapnic effect on cerebral perfusion.…”

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confidence: 99%

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Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

Pollock¹,

Deibler²,

Whitlow³

et al. 2008

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:The incidence of cerebral hyperperfusion and hypoperfusion, respectively, resulting from hypercapnia and hypocapnia in hospitalized patients is unknown but is likely underrecognized by radiologists and clinicians without routine performance of quantitative perfusion imaging. Our purpose was to report the clinical and perfusion imaging findings in a series of patients confirmed to have hypercapnic cerebral hyperperfusion and hypocapnic hypoperfusion.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

Pollock¹,

Deibler²,

Whitlow³

et al. 2008

AJNR Am J Neuroradiol

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Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

270

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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Regulation of the Cerebral Circulation by Arterial Carbon Dioxide

Hoiland

Fisher

Ainslie

2019

Comprehensive Physiology

172

189

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Intact, coordinated, and precisely regulated cerebrovascular responses are required for the maintenance of cerebral metabolic homeostasis, adequate perfusion, oxygen delivery, and acid‐base balance during deviations from homeostasis. Increases and decreases in the partial pressure of arterial carbon dioxide (PaCO 2 ) lead to robust and rapid increases and decreases in cerebral blood flow (CBF). In awake and healthy humans, PaCO 2 is the most potent regulator of CBF, and even small fluctuations can result in large changes in CBF. Alterations in the responsiveness of the cerebral vasculature can be detected with carefully controlled stimulus‐response paradigms and hold relevance for cerebrovascular risk in steno‐occlusive disease. As changes in PaCO 2 do not typically occur in isolation, the integrative influence of physiological factors such as intracranial pressure, arterial oxygen content, cerebral perfusion pressure, and sympathetic nervous activity must be considered. Further, age and sex, as well as vascular pathologies are also important to consider. Following a brief summary of key historical events in the development of our understanding of cerebrovascular physiology and an overview of the measurement techniques to index CBF this review provides an in‐depth description of CBF regulation in response to alterations in PaCO 2 . Cerebrovascular reactivity and regional flow distribution are described, with further consideration of how differences in reactivity of parallel networks can lead to the “steal” phenomenon. Factors that influence cerebrovascular reactivity are discussed and the mechanisms and regulatory pathways mediating the exquisite sensitivity of the cerebral vasculature to changes in PaCO 2 are outlined. Finally, topical avenues for future research are proposed. © 2019 American Physiological Society. Compr Physiol 9:1101‐1154, 2019.

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Cerebral vasodilation during hypercapnia. Role of glibenclamide-sensitive potassium channels and nitric oxide.

Abstract: Thus, activation of glibenclamide-sensitive potassium channels may contribute to dilatation of cerebral arterioles during hypercapnia. Cerebral vasodilatation during hypercapnia is dependent in large part on production of nitric oxide.

Cited by 106 publications

References 36 publications

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Regulation of the Cerebral Circulation by Arterial Carbon Dioxide

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