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Relevant bibliographies by topics / Cerebral circulation Innervation

Academic literature on the topic 'Cerebral circulation Innervation'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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Journal articles on the topic "Cerebral circulation Innervation"

1

EDVINSSON, LARS. "Innervation of the Cerebral Circulation." Annals of the New York Academy of Sciences 519, no. 1 The Terminal (December 1987): 334–48. http://dx.doi.org/10.1111/j.1749-6632.1987.tb36308.x.

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2

Edvinsson, L., I. Jansen, R. Uddman, and S. Gulbenkian. "Innervation of the human cerebral circulation." Journal of the Autonomic Nervous System 49 (September 1994): 91–96. http://dx.doi.org/10.1016/0165-1838(94)90094-9.

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3

Hara, H., I. Jansen, R. Ekman, E. Hamel, E. T. MacKenzie, R. Uddman, and L. Edvinsson. "Acetylcholine and Vasoactive Intestinal Peptide in Cerebral Blood Vessels: Effect of Extirpation of the Sphenopalatine Ganglion." Journal of Cerebral Blood Flow & Metabolism 9, no. 2 (April 1989): 204–11. http://dx.doi.org/10.1038/jcbfm.1989.30.

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The innervation of cerebral blood vessels by nerve fibers containing acetylcholinesterase (AChE) and vasoactive intestinal peptide (VIP) and the vasomotor effects of the two neurotransmitters have been analyzed in the rat following the uni- or bilateral removal of the sphenopalatine ganglion (SPG), which is thought to be the major origin of this innervation. Histochemistry of AChE-positive nerve fibers and the immunoreactivity toward VIP revealed only a 30% reduction in the innervation pattern of the rostral part of the cerebral circulation following the operation. At ∼4 weeks postoperatively, the original nerve network was restored. Quantitative measurements of cholineacetyltransferase activity and VIP revealed similar reductions in the levels of collected large cerebral arteries at the base of the brain and in small pial vessels overlying the cerebral cortex at the various postoperative times following uni- or bilateral removal of the SPG. The two techniques thus complemented each other. Vasomotor reactivity to acetylcholine (ACh) and VIP was examined in proximal segments of the middle cerebral artery at the various postoperative times. Generally, the removal of the SPG had no effect on the responses to ACh or VIP. The evidence indicates that only approximately one-third of the cholinergic/VIP innervation of the rostral part of the cerebral circulation originates in the SPG.

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4

Edvinsson, L., and PJ Goadsby. "Neuropeptides in the Cerebral Circulation: Relevance to Headache." Cephalalgia 15, no. 4 (August 1995): 272–76. http://dx.doi.org/10.1046/j.1468-2982.1995.1504272.x.

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The article briefly describes the innervation of the human cerebral circulation by nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gent-related peptide (CGRP). The neuropeptides in human cerebral arteries were characterized by radioimmunoassay in combination with HPLC. These neuropeptides mediate contraction (NPY) and dilatation (VIP, SP, CGRP). In conjunction with spontaneous attacks of migraine or cluster headache, release of CGRP is seen. With the associated symptoms of nasal congestion and rhinorrhea, VIP is released. Successful treatment may abort the peptide release in parallel with disappearance of headache.

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5

Sheth, Raj D., and John B. Bodensteiner. "Hypertensive Encephalopathy and Sympathetic Innervation of the Cerebral Circulation: A Comment." Journal of Child Neurology 11, no. 4 (July 1996): 347. http://dx.doi.org/10.1177/088307389601100417.

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6

Edvinsson, Lars, Rolf Uddman, and Roar Juul. "Peptidergic innervation of the cerebral circulation. Role in subarachnoid hemorrhage in man." Neurosurgical Review 13, no. 4 (1990): 265–72. http://dx.doi.org/10.1007/bf00346363.

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7

Hara, Hideaki, and Lars Edvinsson. "Perivascular innervation of the cerebral circulation: Involvement in the pathophysiology of subarachnoid hemorrhage." Neurosurgical Review 10, no. 3 (September 1987): 171–79. http://dx.doi.org/10.1007/bf01782043.

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8

Imai, H., T. Okuno, J. Y. Wu, and T. J.-F. Lee. "GAB Aergic Innervation in Cerebral Blood Vessels: An Immunohistochemical Demonstration of L-Glutamic Acid Decarboxylase and GABA Transaminase." Journal of Cerebral Blood Flow & Metabolism 11, no. 1 (January 1991): 129–34. http://dx.doi.org/10.1038/jcbfm.1991.15.

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The presence of GAB Aergic innervation in cerebral arteries of several species was investigated by an immunohistochemical method using antibodies against glutamic acid decarboxylase (GAD) and GABA transaminase (GABA-T). Both GAD and GABA-T immunoreactivities were found to be associated with large bundles and single fibers in the adventitial layer of arteries examined. The density and distribution pattern of both GAD-and GABA-T-immunoreactive fibers were found to be comparable at most regions examined. Both fibers were found to be most dense in the anterior cerebral artery and its adjacent part of the circle of Willis. Several peripheral arteries were found to receive very sparse or no GAD-and GABA-T-immunoreactive fibers. Superior cervical ganglionectomy did not appreciably affect the distribution of both fibers. Cold-storage denervation, however, resulted in a drastic decrease in both fibers. At ultrastructural levels, both GAD- and GABA-T-immunoreactive nerve profiles were found to be very close to the smooth muscle cells. These results demonstrate the presence of a potentially functional GAB Aergic innervation in cerebral circulation. On few occasions, GAD immunoreactivities were also found in some endothelial cells, suggesting that a nonneuronal GABA system may also be present in cerebral arteries.

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9

May, Arne, and Peter J. Goadsby. "The Trigeminovascular System in Humans: Pathophysiologic Implications for Primary Headache Syndromes of the Neural Influences on the Cerebral Circulation." Journal of Cerebral Blood Flow & Metabolism 19, no. 2 (February 1999): 115–27. http://dx.doi.org/10.1097/00004647-199902000-00001.

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Primary headache syndromes, such as cluster headache and migraine, are widely described as vascular headaches, although considerable clinical evidence suggests that both are primarily driven from the brain. The shared anatomical and physiologic substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than as a response to first-division nociceptive pain impulses. In a positron emission tomography study in cluster headache, however, activation in the region of the major basal arteries was observed. This is likely to result from vasodilation of these vessels during the acute pain attack as opposed to the rest state in cluster headache, and represents the first convincing activation of neural vasodilator mechanisms in humans. The observation of vasodilation was also made in an experimental trigeminal pain study, which concluded that the observed dilation of these vessels in trigeminal pain is not inherent to a specific headache syndrome, but rather is a feature of the trigeminal neural innervation of the cranial circulation. Clinical and animal data suggest that the observed vasodilation is, in part, an effect of a trigeminoparasympathetic reflex. The data presented here review these developments in the physiology of the trigeminovascular system, which demand renewed consideration of the neural influences at work in many primary headaches and, thus, further consideration of the physiology of the neural innervation of the cranial circulation. We take the view that the known physiologic and pathophysiologic mechanisms of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to emphasize the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Moreover, the syndromes can be understood only by a detailed study of the cerebrovascular physiologic mechanisms that underpin their expression.

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10

Omar, Nisreen Mansour, and Janice M. Marshall. "Age-related changes in the sympathetic innervation of cerebral vessels and in carotid vascular responses to norepinephrine in the rat: in vitro and in vivo studies." Journal of Applied Physiology 109, no. 2 (August 2010): 314–22. http://dx.doi.org/10.1152/japplphysiol.01251.2009.

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We hypothesized that the density of sympathetic noradrenergic innervation of cerebral arteries and vasoconstrictor responses evoked in carotid circulation by norepinephrine (NE) increase with maturation and age. In rats of 4–5, 10–12, and 42–44 wk of age (juvenile, mature, middle aged), glyoxylic acid applied to stretch preparations showed the density of noradrenergic nerves in basilar and middle cerebral arteries was greater in mature than juvenile or middle-aged rats. In anesthetized rats, infusion of NE (2.5 μg/kg iv) increased mean arterial pressure (ABP) to ∼180 mmHg in mature and middle-aged but to only ∼150 mmHg in juveniles rats. Concomitantly, carotid blood flow (CBF) decreased in mature and middle-aged rats but remained constant in juveniles because carotid vascular conductance (CVC) decreased more in mature and middle-aged than juvenile rats. We also hypothesized that nitric oxide (NO) blunts cerebral vasoconstrictor responses to NE. Inhibition of NO synthase with l-NAME (10 mg/kg iv) induced similar increases in baseline ABP in each group, but larger decreases in CVC and CBF in mature and middle-aged than juvenile rats. Thereafter, the NE-evoked increase in ABP was similar in juvenile and mature but accentuated in middle-aged rats. Concomitantly, NE decreased CVC in juvenile and mature, but not middle-aged rats; in them, CBF increased. Thus, in juvenile rats, sparse noradrenergic innervation of cerebral arteries is associated with weak NE-evoked pressor responses and weak carotid vasoconstriction that allows autoregulation of CBF. Cerebral artery innervation density increases with maturation but lessens by middle age. Meanwhile, NE-evoked pressor responses and carotid vasoconstriction are stronger in mature and middle-aged rats, such that CBF falls despite the evoked increase in ABP. We propose that in juvenile and mature rats, NO does not modulate NE-evoked pressor responses, cerebral vasoconstriction, or CBF autoregulation, but by middle age, NO limits pressor responses and prevents breakthrough of CBF in the upper part of the autoregulatory range.

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Dissertations / Theses on the topic "Cerebral circulation Innervation"

1

Helps, Stephen. "Cerebral blood flow in rats after treatment with the primary sensory neurotoxin capsaicin." Title page, contents and summary only, 1987. http://web4.library.adelaide.edu.au/theses/09SM/09smh484.pdf.

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2

Helps, Stephen. "Cerebral blood flow in rats after treatment with the primary sensory neurotoxin capsaicin." Thesis, 1987. http://hdl.handle.net/2440/110498.

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Books on the topic "Cerebral circulation Innervation"

1

NATO Advanced Research Workshop on Regulatory Mechanisms of Neuron to Vessel Communication in the Brain. Regulatory mechanisms of neuron to vessel communication in the brain. Berlin: Springer-Verlag, 1989.

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Book chapters on the topic "Cerebral circulation Innervation"

1

Bevan, John A., and Christer Owman. "Cerebral Circulation." In Nonadrenergic Innervation of Blood Vessels, 37–62. CRC Press, 2019. http://dx.doi.org/10.1201/9780429277597-2.

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