Journal articles on the topic 'Cerebral circulation Innervation'
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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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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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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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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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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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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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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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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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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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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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Ivanov, V. S., E. K. E. K. Valeev, V. E. Krylov, and I. A. Ibatullin. "The state of the microcircular bed in patients with severe traumatic brain damage." Kazan medical journal 72, no. 6 (December 15, 1991): 456–59. http://dx.doi.org/10.17816/kazmj89546.
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The course and outcome of severe traumatic brain injury (TBI) is more influenced by the degree and nature of cerebral blood flow disorders. Changes in blood circulation, in turn, depend on the state of the microvasculature, which ensures the transcapillary metabolism between blood and tissues. The most convenient object in the study of the microcirculatory network of the brain in patients is the vessels of the bulbar conjunctiva. This is due, on the one hand, to the fact that the vascular network of the outer and inner shell of the eyeball belongs to those few structures of the body that can be directly observed and photographed, on the other hand, the vessels of the bulboconjunctiva have the same source of blood circulation and innervation as the head brain.
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Edvinsson, L., H. Hara, and R. Uddman. "Retrograde Tracing of Nerve Fibers to the Rat Middle Cerebral Artery with True Blue: Colocalization with Different Peptides." Journal of Cerebral Blood Flow & Metabolism 9, no. 2 (April 1989): 212–18. http://dx.doi.org/10.1038/jcbfm.1989.31.
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The origin of nerve fibers to the rat middle cerebral artery was studied by retrograde tracing with the fluorescent tracer True Blue (TB) in combination with immunocytochemistry to known perivascular peptides. Application of TB to the middle cerebral artery labeled nerve cell bodies in the ipsilateral superior cervical ganglion, the otic ganglion, the sphenopalatine ganglion, the trigeminal ganglion, and the cervical dorsal root ganglion at level C2. A few labeled nerve cell bodies were seen in contralateral ganglia. Judging from the number and intensity of the labeling, the superior cervical ganglion and the trigeminal ganglion and dorsal root ganglion at level C2 contributed most to the innervation. A moderate number of nerve cell bodies were labeled in the sphenopalatine and otic ganglia. The TB-labeled nerve cell bodies were further examined for the presence of neuropeptides. For that purpose antibodies raised against neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) were used. A considerable portion of the TB-labeled nerve cell bodies in the superior cervical ganglion contained NPY. About half of the labeled nerve cell bodies in the sphenopalatine and otic ganglia contained VIP. In the trigeminal ganglion and in the dorsal root ganglion at level C2, one-third of the TB-labeled nerve cell bodies were CGRP-immunoreactive, while only few nerve cell bodies contained SP. The study provides direct evidence for the origin of cerebrovascular peptidergic nerve fibers and demonstrates that not only ipsilateral but also contralateral ganglia contribute to the innervation of the cerebral circulation.
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Dunatov, Sinisa, Igor Antoncic, and Marina Bralic. "Hemodynamic changes in the posterior cerebral circulation triggered by insufficient sympathetic innervation – Cause of primary intracerebral hemorrhage?" Medical Hypotheses 76, no. 5 (May 2011): 668–69. http://dx.doi.org/10.1016/j.mehy.2011.01.027.
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Kasparova, E. A., and N. R. Marchenko. "Neurotrophic Keratitis. Etiology, Pathogenesis, Clinical Manifestations. Review. Part 1." Ophthalmology in Russia 19, no. 1 (April 6, 2022): 38–45. http://dx.doi.org/10.18008/1816-5095-2022-1-38-45.
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Neurotrophic keratitis (also called neurotrophic keratopathy) (NTK) is a degenerative disease of the cornea, accompanied with neurogenic inflammation. It caused by a sensitive innervation loss of the trigeminal nerve and characterized by reduced sensitivity of the cornea and a retardation of its healing process. NTC-causing damage to the trigeminal nerve can occur at different levels-from the nucleus to the terminals located in the cornea, and can be caused by ocular and systemic diseases both. The most common causes include herpetic keratitis, diabetes, chemical burns and iatrogenic injuries during ophthalmic operations, intracranial neoplasms, disorders of cerebral circulation and neurosurgical interventions. Corneal changes include epitheliopathy (grade I), persistent erosion (grade II), ulcer and its complications (grade III). The determining diagnostic sign of NTK is a decrease or loss of corneal sensitivity. The morphological characteristics of the corneal nerves can be studied using confocal microscopy.
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Hanley, D. F., D. A. Wilson, M. A. Conway, R. J. Traystman, J. A. Bevan, and J. E. Brayden. "Neural mechanisms regulating neurohypophysial resistance arteries." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 5 (November 1, 1992): H1605—H1615. http://dx.doi.org/10.1152/ajpheart.1992.263.5.h1605.
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We defined the extent of vasoactive intestinal polypeptide (VIP) and noradrenergic influences on isolated 100- to 200-microns-diameter vessels from the resistance arterial circulation of the neurohypophysis. A dual extracranial (inferior hypophysial) and intracranial (superior hypophysial) arterial supply to the neurohypophysis was confirmed. The inferior hypophysial artery demonstrates noradrenergic and VIP-like perivascular nerves, whereas the superior hypophysial artery shows primarily VIP-like innervation. Pharmacological sensitivity of the inferior hypophysial to VIP [mean effective dose (ED50) = 10(-8.2) M] and to norepinephrine (ED50 = 10(-5.7) M) was demonstrated. The superior hypophysial reacted only to VIP (ED50 = 10(-8.6) M). The physiological relevance of these findings was tested with transmural nerve stimulation. Frequency-dependent vasodilation of both inferior and superior hypophysial arteries was demonstrated. This dilation could not be blocked with atropine or propranolol. Frequency-dependent vasoconstriction was identified in extracranial vessels including the inferior hypophysial artery. This constriction is only partially blocked by prazosin, phentolamine, and guanethidine. When neurohypophysial resistance vessels are compared with larger circle of Willis arteries and similar-size pial vessels of other cerebral regions, they appear to have regionally unique neural mechanisms for regulating blood flow. Specifically whether controlled by periarterial nerves or other tissue influences, the inferior hypophysial artery appears to meet anatomic, pharmacological, and physiological definitions of neural control for both dilator and constrictor activities of flow to the neurohypophysis.
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Valle, J., A. L. Garcia-Villalon, E. Nava-Hernandez, J. L. Garcia, L. Santamaria, B. Gomez, and G. Dieguez. "In vitro reactivity of dog cavernous carotid artery to stretch and adrenergic stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 6 (December 1, 1989): R1335—R1344. http://dx.doi.org/10.1152/ajpregu.1989.257.6.r1335.
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The reactivity of the dog cavernous carotid artery to stretch, field electrical stimulation, and norepinephrine was studied using arterial segments under isometric conditions. Light microscopy revealed that this artery is of muscular type and its external surface is covered by venous endothelium, and fluorescence microscopy showed a dense adrenergic innervation. On stretch, arteries exhibited an immediate, transient contraction (phasic response) and a late, maintained contraction (tonic response) that were unaffected by tetrodotoxin (10(-6) M) or endothelium removal but were reduced by the inhibitors of cyclooxygenase indomethacin (10(-6) M), acetylsalicylic acid (3 x 10(-5) M), or meclofenamate (10(-5) M). Electrical stimulation (0.5-4 Hz) contracted the arteries in a frequency-dependent manner, and the response was reduced by tetrodotoxin, phentolamine, (10(-6) M), or the inhibitors of cyclooxygenase used but was unaffected by endothelium removal. Norepinephrine (10(-9)-3 x 10(-4) M) caused dose-dependent contraction that was blocked by phentolamine and by the inhibitors of cyclooxygenase but was not modified by endothelium removal. The results indicate that the dog cavernous carotid artery develops myogenic tone on stretch and contracts on adrenergic stimulation. They also suggest that in these responses prostaglandins but not the endothelium are involved. Therefore, the cavernous carotid artery, because of its location and reactivity, could be of relevance in regulating blood flow or pressure within the cerebral circulation when arterial pressure or adrenergic activity increases.
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Hosseini, Mersedeh Bahr, and Jeffrey L. Saver. "Mechanisms of action of acute and subacute sphenopalatine ganglion stimulation for ischemic stroke." International Journal of Stroke 15, no. 8 (April 23, 2020): 839–48. http://dx.doi.org/10.1177/1747493020920739.
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Background Sphenopalatine ganglion stimulation (SPG-Stim) for ischemic stroke, starting 8–24 h after onset and continuing through five days in a pooled analysis of two recent, randomized, sham-controlled trials, improved outcome of acute ischemic stroke patients with confirmed cortical involvement. As a neuromodulatory therapy, SPG-Stim differs substantially from existing pharmacologic (lytic and antiplatelets) and device (endovascular thrombectomy) acute ischemic stroke treatments. Aim Focused review of SPG anatomy, physiology, and neurovascular and neurobiologic mechanisms of action mediating benefit of SPG-Stim in acute ischemic stroke. Summary of review Located posterior to the maxillary sinus, the SPG is the main source of parasympathetic innervation to the anterior circulation. Preclinical and human studies delineate four distinct mechanisms of action by which the SPG-Stim may confer benefit in acute ischemic stroke: (1) collateral vasodilation and enhanced cerebral blood flow, mediated by release of neurotransmitters with vasodilatory effects, nitric oxide, and acetylcholine, (2) stimulation frequency- and intensity-dependent stabilization of the blood–brain barrier, reducing edema (3) direct acute neuroprotection from activation of the central cholinergic system with resulting anti-inflammatory, anti-apoptotic, and anti-excitatory effects; and (4) neuroplasticity enhancement from enhanced central cholinergic and adrenergic neuromodulation of cortical networks and nitrous oxide release stimulating neurogenesis. Conclusion The benefit of SPG-Stim in acute ischemic stroke is likely conferred not only by potent collateral augmentation, but also blood–barrier stabilization, direct neuroprotection, and neuroplasticity enhancement. Further studies clarifying the relative contribution of these mechanisms and the stimulation protocols that maximize each may help optimize SPG-Stim as a therapy for acute ischemic stroke.
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Romanchuk, P., and A. Volobuev. "Modern Tools and Methods of Epigenetic Protection of Healthy Aging and Longevity of the Homo sapiens." Bulletin of Science and Practice 6, no. 1 (January 15, 2020): 43–70. http://dx.doi.org/10.33619/2414-2948/50/06.
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The human brain is the main tool and the most valuable resource on our planet. New epigenetics Homo sapiens and H. sapiens brain manage the interaction of genetic and epigenetic programs of aging and healthy longevity. Epigenetic clocks are mathematical models and artificial intelligence that predict the biological age of a person using DNA methylation data and are the most accurate biomarkers of the aging process. Genetic and epigenetic factors that limit a person’s life expectancy are relevant in biogerontological, biophysical and neurophysiological studies, especially from the point of view of the medical economy. Cerebrovascular aging can be considered from several points of view, including changes in vascular density (number of capillaries and arterioles), vascular plasticity (dynamic regulation of vascular density or structure) and vascular reactivity (adaptation of vessels to acute metabolic changes in tissues). The main control mechanisms in the cerebral circulation are unique in comparison with other vascular channels and include, but are not limited to such features as the blood-brain barrier, perivascular innervation, intracellular communication between neurons, perivascular glial cells and smooth muscle cells, high tissue metabolism, lack of anoxic tolerance and the presence of collateral arteries. Multidisciplinary and multimodal interaction in the triad brain-eyes-vessels makes it possible to identify early biomarkers of both general accelerated and pathological aging, and to diagnose neurodegeneration in a timely manner, and to carry out effective neurorehabilitation of cognitive impairment. Biochipping, neural and brain chips, the next (new) generation sequencing technology will allow the study of the expression of thousands of genes that will be used as biomarkers. Combined and hybrid methods of neuroimaging in collaboration with artificial intelligence technologies are modern tools for the diagnosis and prevention of cognitive impairment and healthy aging of the H. sapiens brain.
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Yokote, Hideyoshi, Toru Itakura, Kunio Nakai, Ichiro Kamei, Harumichi Imai, and Norihiko Komai. "A role of the central catecholamine neuron in cerebral circulation." Journal of Neurosurgery 65, no. 3 (September 1986): 370–75. http://dx.doi.org/10.3171/jns.1986.65.3.0370.
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✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.
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Nozaki, Kazuhiko, Michael A. Moskowitz, Kenneth I. Maynard, Naoki Koketsu, Ted M. Dawson, David S. Bredt, and Solomon H. Snyder. "Possible Origins and Distribution of Immunoreactive Nitric Oxide Synthase-Containing Nerve Fibers in Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 13, no. 1 (January 1993): 70–79. http://dx.doi.org/10.1038/jcbfm.1993.9.
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The distribution of perivascular nerve fibers expressing nitric oxide synthase (NOS)-immunoreactivity was examined in Sprague–Dawley and Long–Evans rats using affinity-purified rabbit antisera raised against NOS from rat cerebellum. NOS immunoreactivity was expressed within the endothelium and adventitial nerve fibers in both rat strains. Labeled axons were abundant and dense in the proximal anterior and middle cerebral arteries, but were less numerous in the caudal circle of Willis and in small pial arteries. The sphenopalatine ganglia were the major source of positive fibers in these vessels. Sectioning postganglionic parasympathetic fibers from both sphenopalatine ganglia reduced the density of NOS-immunoreactive (IR) nerve fibers by >75% in the rostral circle of Willis. Moreover, NOS-IR was present in 70–80% of sphenopalatine ganglion cells. Twenty percent of these neurons also contained vasoactive intestinal polypeptide (VlP)-immunoreactivity. By contrast, the superior cervical ganglia did not contain NOS-IR cells. In the trigeminal ganglion, NO-IR neurons were found chiefly within the ophthalmic division; ∼10–15% of neurons were positively labeled. Colocalization with calcitonin gene-related peptide (CGRP) was not observed. Sectioning the major trigeminal branch innervating the circle of Willis decreased positive fibers by ≤25% in the ipsilateral vessels. In the nodose ganglion, 20–30% of neurons contained NOS-immunoreactivity, whereas less than 1% were in the C2 and C3 dorsal root ganglia. Three human circles of Willis obtained at autopsy showed sparse immunoreactive fibers, chiefly within vessels of the posterior circulation. Postmortem delay accounted for some of the reduced density. Our findings indicate that nerve fibers innervating cerebral arteries may serve as a nonendothelial source of the vasodilator nitric oxide (NO). The coexistence of NOS and VIP within sphenopalatine ganglion cells raises the possibility that two vasodilatory agents, one, a highly diffusable short-lived, low-molecular-weight molecule, and the other, a polar 28 amino acid-containing peptide, may serve as coneuromediators within the cerebral circulation.
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Iliff, Jeffrey J., Ruikang Wang, Darryl C. Zeldin, and Nabil J. Alkayed. "Epoxyeicosanoids as mediators of neurogenic vasodilation in cerebral vessels." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (May 2009): H1352—H1363. http://dx.doi.org/10.1152/ajpheart.00950.2008.
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Epoxyeicosatrienoic acids (EETs) are potent vasodilators produced from arachidonic acid by cytochrome P-450 (CYP) epoxygenases and metabolized to vicinal diols by soluble epoxide hydrolase (sEH). In the brain, EETs are produced by astrocytes and the vascular endothelium and are involved in the control of cerebral blood flow (CBF). Recent evidence, however, suggests that epoxygenases and sEH are present in perivascular vasodilator nerve fibers innervating the cerebral surface vasculature. In the present study, we tested the hypothesis that EETs are nerve-derived relaxing factors in the cerebral circulation. We first traced these fibers by retrograde labeling in the rat to trigeminal ganglia (TG) and sphenopalatine ganglia (SPG). We then examined the expression of CYP epoxygenases and sEH in these ganglia. RT-PCR and Western blot analysis identified CYP2J3 and CYP2J4 epoxygenase isoforms and sEH in both TG and SPG, and immunofluorescence double labeling identified CYP2J and sEH immunoreactivity in neuronal cell bodies of both ganglia. To evaluate the functional role of EETs in neurogenic vasodilation, we elicited cortical hyperemia by electrically stimulating efferent cerebral perivascular nerve fibers and by chemically stimulating oral trigeminal fibers with capsaicin. Cortical blood flow responses were monitored by laser-Doppler flowmetry. Local administration to the cortical surface of the putative EET antagonist 14,15-epoxyeicosa-5( Z)-enoic acid (30 μmol/l) attenuated CBF responses to electrical and chemical stimulation. These results suggest that EETs are produced by perivascular nerves and play a role in neurogenic vasodilation of the cerebral vasculature. The findings have important implications to such clinical conditions as migraine, vasospasm after subarachnoid hemorrhage, and stroke.
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Kumakura, Yoshitaka, Ingo Vernaleken, Gerhard Gründer, Peter Bartenstein, Albert Gjedde, and Paul Cumming. "PET Studies of Net Blood—Brain Clearance of FDOPA to Human Brain: Age-Dependent Decline of [18F]Fluorodopamine Storage Capacity." Journal of Cerebral Blood Flow & Metabolism 25, no. 7 (February 23, 2005): 807–19. http://dx.doi.org/10.1038/sj.jcbfm.9600079.
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Conventional methods for the graphical analysis of 6-[18F]fluorodopa (FDOPA)/positron emission tomography (PET) recordings ( Kappin) may be prone to negative bias because of oversubtraction of the precursor pool in the region of interest, and because of diffusion of decarboxylated FDOPA metabolites from the brain. These effects may reduce the sensitivity of FDOPA/PET for the detection of age-related changes in dopamine innervations. To test for these biasing effects, we have used a constrained compartmental analysis to calculate the brain concentrations of the plasma metabolite 3- O-methyl-FDOPA (OMFD) during 120 mins of FDOPA circulation in healthy young, healthy elderly, and Parkinson's disease subjects. Calculated brain OMFD concentrations were subtracted frame-by-frame from the dynamic PET recordings, and maps of the FDOPA net influx to brain were calculated assuming irreversible trapping ( Kapp). Comparison of Kappin and Kapp maps revealed a global negative bias in the conventional estimates of FDOPA clearance. The present OMFD subtraction method revealed curvature in plots of Kapp at early times, making possible the calculation of the corrected net influx ( K) and also the rate constant for diffusion of decarboxylated metabolites from the brain ( kloss). The effective distribution volume (EDV2; K/ kloss) for FDOPA, an index of dopamine storage capacity in brain, was reduced by 85% in putamen of patients with Parkinson's disease, and by 58% in the healthy elderly relative to the healthy young control subjects. Results of the present study support claims that storage capacity for dopamine in both caudate and putamen is more profoundly impaired in patients with Parkinson's disease than is the capacity for DOPA utilization, calculated by conventional FDOPA net influx plots. The present results furthermore constitute the first demonstration of an abnormality in the cerebral utilization of FDOPA in caudate and putamen as a function of normal aging, which we attribute to loss of vesicular storage capacity.
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Chen, Zhihong, Weiwei Hu, Mynor J. Mendez, Zachary C. Gossman, Anthony Chomyk, Brendan T. Boylan, Grahame J. Kidd, Timothy W. Phares, Cornelia C. Bergmann, and Bruce D. Trapp. "Neuroprotection by Preconditioning in Mice is Dependent on MyD88-Mediated CXCL10 Expression in Endothelial Cells." ASN Neuro 15 (January 2023): 175909142211463. http://dx.doi.org/10.1177/17590914221146365.
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The central nervous system (CNS) can be preconditioned to resist damage by peripheral pretreatment with low-dose gram-negative bacterial endotoxin lipopolysaccharide (LPS). Underlying mechanisms associated with transient protection of the cerebral cortex against traumatic brain injury include increased neuronal production of antiapoptotic and neurotrophic molecules, microglial-mediated displacement of inhibitory presynaptic terminals innervating the soma of cortical projection neurons, and synchronized firing of cortical projection neurons. However, the cell types and signaling responsible for these neuronal and microglial changes are unknown. A fundamental question is whether LPS penetrates the CNS or acts on the luminal surface of brain endothelial cells, thereby triggering an indirect parenchymal neuroprotective response. The present study shows that a low-dose intraperitoneal LPS treatment increases brain endothelial cell activation markers CD54, but does not open the blood–brain barrier or alter brain endothelial cell tight junctions as assessed by electron microscopy. NanoString nCounter transcript analyses of CD31-positive brain endothelial cells further revealed significant upregulation of Cxcl10, C3, Ccl2, Il1β, Cxcl2, and Cxcl1, consistent with identification of myeloid differentiation primary response 88 (MyD88) as a regulator of these transcripts by pathway analysis. Conditional genetic endothelial cell gene ablation approaches demonstrated that both MyD88-dependent Toll-like receptor 4 (TLR4) signaling and Cxcl10 expression are essential for LPS-induced neuroprotection and microglial activation. These results suggest that C-X-C motif chemokine ligand 10 (CXCL10) production by endothelial cells in response to circulating TLR ligands may directly or indirectly signal to CXCR3 on neurons and/or microglia. Targeted activation of brain endothelial receptors may thus provide an attractive approach for inducing transient neuroprotection.
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Saad Shaukat, Muhammad Hamza, Mamoon Ahmed, Terezia Petraskova, Alex Georgiev, and Orvar Jonsson. "Abstract 16831: Provoked PFO Shunt And Posterior Circulation Stroke: An Underrecognized Association." Circulation 144, Suppl_2 (November 16, 2021). http://dx.doi.org/10.1161/circ.144.suppl_2.16831.
Full textAbstract:
Case Presentation: A 50 year old man presented with nausea and weakness. MRI brain showed a small acute infarct in the right pons. CT angiography of the head and neck was unremarkable. No thrombus, vegetation, or inter-atrial communication was seen on transthoracic echocardiogram: LVEF was 55-60% with normal left atrial size. No history of atrial fibrillation, hypertension, diabetes or drug abuse was reported; lower extremity duplex was negative for deep venous thrombosis. TSH was normal. Transesophageal echocardiography showed an aneurysmal atrial septum: agitated saline injection did not demonstrate an inter-atrial communication (figure 1). Repeat saline injection during the same procedure with Valsalva maneuver demonstrated a moderate-sized, provoked right-to-left, patent foramen ovale (PFO) shunt (figure 2). Discussion: Physiologically decreased sympathetic innervation spares posterior cerebral circulation from Valsalva-induced vasoconstriction. The disproportionate increase in posterior cerebral blood flow when venous return/cardiac output increases in the immediate post-strain period explains the association of provoked PFO shunt and paradoxical embolism to posterior circulation. Although the association has been described in literature, it remains underappreciated. Recognition of the association expedited secondary prevention of stroke in this non-elderly patient by circumventing the need to exclude atrial fibrillation on ambulatory rhythm monitoring (3-6 months) before referral for PFO closure.