Role of large arteries in regulation of blood flow to brain stem in cats.

Faraci, Frank M.; Heistad, D D; Mayhan, William G.

doi:10.1113/jphysiol.1987.sp016566

Cited by 103 publications

(65 citation statements)

References 26 publications

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“…Wahl et al 18 also found larger arteries to be pH sensitive but noted that the fluid of lower pH had to penetrate the Virchow-Robin space to attain this effect. In addition, our data showing an approximately 10% decrease in basilar artery diameter with hypocapnia, thus confirming earlier reports, 19 support the contention that the basilar artery is pH sensitive since it has been well demonstrated that the reactivity of cerebral arteries to CO 2 is mediated via changes in extracellular pH. 18 -20 Moreover, the observations of Kapp et al 13 were made in an open preparation, which in itself may have blunted the vascular responses to local pH variations.…”

Section: Discussionsupporting

confidence: 81%

Description of a closed window technique for in vivo study of the feline basilar artery.

Bouma

Levasseur

Muizelaar

et al. 1991

Stroke

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Recent interest in the regulatory functions of large cerebral arteries has led to many studies addressing the specific reactivity of these vessels. Current data originate mainly from in vitro experiments, as in vivo studies of larger intracranial cerebral arteries have been cumbersome so far due to the lack of a suitable animal model. We provide a detailed technical description of a closed transclival window method for in vivo study of the basilar artery in cats. We present our experience with this preparation in 29 animals, which shows that the technique is feasible and allows repeated, accurate, and reproducible measurements of the basilar artery, although possible depressive effects of the anesthesia on vascular reactivity have to be taken into account With hyper-ventilation, the basilar artery constricted by 12.2 ±7.6% of the baseline diameter. The cerebral blood flow response to hypocapnia with this preparation was 2.0±0.4%/torr Paco ; . An exudative clouding of the window occurred in some cats but had no apparent effect on vascular reactivity. We also discuss possible pitfalls in the surgical preparation. (Stroke 1991^2:522-526)

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Section: Discussionsupporting

confidence: 81%

Description of a closed window technique for in vivo study of the feline basilar artery.

Bouma

Levasseur

Muizelaar

et al. 1991

Stroke

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“…10 The cranial window was suffused with artificial CSF (temperature, 37°C to 38°C) at 3 mL/min, and a portion of the dura mater was opened. In CSF sampled from the craniotomies, PCO 2 was 38Ϯ1 mm Hg, PO 2 102Ϯ2 mm Hg, and pH 7.38Ϯ0.01.…”

Section: Methodsmentioning

confidence: 99%

Activation of Protease-Activated Receptor-2 (PAR-2) Elicits Nitric Oxide–Dependent Dilatation of the Basilar Artery In Vivo

Sobey

Cocks

1998

Stroke

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Background and Purpose-Protease-activated receptors (PARs) are a family of G-protein-coupled receptors activated by a tethered ligand amino acid sequence within the amino terminal that is revealed by site-specific proteolysis. In the vascular endothelium, activation of PAR-2 by treatment with trypsin or by using the amino acid ligand sequence (SLIGRL) produces endothelium-dependent relaxation of isolated noncerebral vascular segments. In this study, we first tested whether PAR-2 activation produces cerebral vasodilatation in vivo and then examined whether PAR-2-mediated vasodilatation is dependent on the production of nitric oxide. Methods-Concentration-dependent vasodilator effects of the PAR-2 agonist peptide SLIGRL and trypsin were examined on the basilar artery using a cranial window in anesthetized rats. In addition, the vasodilator effects of SLIGRL, acetylcholine (ACh), and sodium nitroprusside (SNP) were examined in the absence and presence of mol/L) and trypsin (0.01 to 10 U/mL) produced concentration-dependent vasodilator responses. In time-control experiments, SLIGRL (3ϫ10 -6 and 10 -5 mol/L), ACh (10 -6 and 10 -5 mol/L), and SNP (10 -8 and 10 -7 mol/L) elicited reproducible dilatation of the basilar artery. In another group of rats, L-NNA (10 -4 mol/L) markedly inhibited dilator responses to both SLIGRL (13Ϯ3% versus 1Ϯ1% and 39Ϯ7% versus 11Ϯ2%; both PϽ0.05) and ACh (8Ϯ1% versus 0Ϯ0% and 13Ϯ2% versus 3Ϯ1%; both PϽ0.05). By contrast, responses to SNP were significantly augmented after treatment with L-NNA (PϽ0.05 versus control), indicating that inhibitory effects of L-NNA were specific for responses mediated by endogenous nitric oxide. Furthermore, in another group ODQ (10 Ϫ5 mol/L) inhibited responses to SLIGRL to a degree similar to that seen with L-NNA, consistent with a mechanism of PAR-2-mediated vasodilatation that involves activation of guanylate cyclase by nitric oxide. Conclusions-To the best of our knowledge, this study is the first to examine whether PAR-2-mediated vasodilatation is functional in cerebral arteries and is also the first to directly assess the effects of PAR-2 activation on vascular tone in vivo. The results suggest that activation of PAR-2 is an effective and powerful vasodilator mechanism in cerebral arteries in vivo. Cerebral vasodilator responses to PAR-2 activation are mediated by nitric oxide and are likely to be endothelium dependent.

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“…Early canine in situ work showed that the arteries of the neck (i.e., ICA and VA) may provide as much as 50% of cerebrovascular resistance at rest. [11][12][13] These large arteries actively change diameters in response to various stimuli including alterations in arterial blood gas partial pressures, 14 and orthostatic challenges. 15 Both extracranial and pial arteries are innervated by sympathetic neurons originating from the superior cervical ganglion, which may serve to regulate CBF through the release of norepinephrine and neuropeptide Y.…”

Section: Regulation Of Cerebral Blood Flowmentioning

confidence: 99%

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications

Phillips

Chan

Zheng

et al. 2015

J Cereb Blood Flow Metab

343

364

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Neurovascular coupling reflects the close temporal and regional linkage between neural activity and cerebral blood flow. Although providing mechanistic insight, our understanding of neurovascular coupling is largely limited to nonphysiological ex vivo preparations and non-human models using sedatives/anesthetics with confounding cerebrovascular implications. Herein, with particular focus on humans, we review the present mechanistic understanding of neurovascular coupling and highlight current approaches to assess these responses and the application in health and disease. Moreover, we present new guidelines for standardizing the assessment of neurovascular coupling in humans. To improve the reliability of measurement and related interpretation, the utility of new automated software for neurovascular coupling is demonstrated, which provides the capacity for coalescing repetitive trials and time intervals into single contours and extracting numerous metrics (e.g., conductance and pulsatility, critical closing pressure, etc.) according to patterns of interest (e.g., peak/minimum response, time of response, etc.). This versatile software also permits the normalization of neurovascular coupling metrics to dynamic changes in arterial blood gases, potentially influencing the hyperemic response. It is hoped that these guidelines, combined with the newly developed and openly available software, will help to propel the understanding of neurovascular coupling in humans and also lead to improved clinical management of this critical physiological function.

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Role of large arteries in regulation of blood flow to brain stem in cats.

Cited by 103 publications

References 26 publications

Description of a closed window technique for in vivo study of the feline basilar artery.

Description of a closed window technique for in vivo study of the feline basilar artery.

Activation of Protease-Activated Receptor-2 (PAR-2) Elicits Nitric Oxide–Dependent Dilatation of the Basilar Artery In Vivo

Neurovascular coupling in humans: Physiology, methodological advances and clinical implications

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