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Journal articles on the topic 'Cerebral circulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 June 2025

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1

Hickey, Joanne V. "Cerebral Circulation Demystified." AACN Advanced Critical Care 2, no. 4 (November 1, 1991): 657–64. http://dx.doi.org/10.4037/15597768-1991-4005.

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Basic anatomic and physiologic concepts related to cerebral circulation are summarized. The arterial blood supply is traced from its origins to the major divisions of anterior and posterior circulation. The circle of Willis, the major arterial vessels and territories, and the peculiarities of the cerebral venous circulation are discussed. Finally, concepts of cerebral circulations are applied to clinical practice to assist the nurse in accurately assessing, monitoring, and predicting human responses to alterations in cerebral blood supply

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2

Hamel, Edith. "Cerebral Circulation." Journal of Cardiovascular Pharmacology 65, no. 4 (April 2015): 317–24. http://dx.doi.org/10.1097/fjc.0000000000000177.

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3

Cipolla, Marilyn J. "The Cerebral Circulation." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 1, no. 1 (January 2009): 1–59. http://dx.doi.org/10.4199/c00005ed1v01y200912isp002.

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4

Townsend, P., and M. G. Knowles. "The cerebral circulation." Current Anaesthesia & Critical Care 10, no. 2 (April 1999): 77–82. http://dx.doi.org/10.1016/s0953-7112(99)90005-4.

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5

Moss, Edward. "The cerebral circulation." BJA CEPD Reviews 1, no. 3 (June 2001): 67–71. http://dx.doi.org/10.1093/bjacepd/1.3.67.

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6

Cipolla, Marilyn J. "The Adaptation of the Cerebral Circulation to Pregnancy: Mechanisms and Consequences." Journal of Cerebral Blood Flow & Metabolism 33, no. 4 (January 16, 2013): 465–78. http://dx.doi.org/10.1038/jcbfm.2012.210.

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The adaptation of the cerebral circulation to pregnancy is unique from other vascular beds. Most notably, the growth and vasodilatory response to high levels of circulating growth factors and cytokines that promote substantial hemodynamic changes in other vascular beds is limited in the cerebral circulation. This is accomplished through several mechanisms, including downregulation of key receptors and transcription factors, and production of circulating factors that counteract the vasodilatory effects of vascular endothelial growth factor (VEGF) and placental growth factor. Pregnancy both prevents and reverses hypertensive inward remodeling of cerebral arteries, possibly through downregulation of the angiotensin type 1 receptor. The blood–brain barrier (BBB) importantly adapts to pregnancy by preventing the passage of seizure provoking serum into the brain and limiting the permeability effects of VEGF that is more highly expressed in cerebral vasculature during pregnancy. While the adaptation of the cerebral circulation to pregnancy provides for relatively normal cerebral blood flow and BBB properties in the face of substantial cardiovascular changes and high levels of circulating factors, under pathologic conditions, these adaptations appear to promote greater brain injury, including edema formation during acute hypertension, and greater sensitivity to bacterial endotoxin.

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7

Nikitin, Vladislav Nikolaevich, and Ekaterina Valerevna Kozhemyakina. "MODELING REDISTRIBUTION CEREBRAL CIRCULATION." SOFT MEASUREMENTS AND COMPUTING 1, no. 4 (2021): 13–18. http://dx.doi.org/10.36871/2618-9976.2021.04.002.

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The brain is one of the most important organs responsible for the health and functioning of the entire body. The blood supply to the brain is carried out through 2 internal carotid and 2 vertebral arteries in norm. The brain, like other body systems, has protective (compensatory) mechanisms aimed at maintaining the necessary blood flow, one of which is the circle of Willis. The article proposes a mechanism for how blood flow is redistributed through the arteries feeding the brain, which is based on the assumption that the central nervous system controls in such a way that it minimizes flows through the connective arteries of the circle of Willis, the flows along which are normal (with symmetry of the left and right sides) practically equal to zero. Сase of the structure of the circle of Willis is considered in norm. The indicated redistribution mechanism is still only the first step towards an attempt to predict cases of changes in blood flow through the cerebral arteries, especially in stroke. In further works, it is planned to consider the inverse problem, i.e. determine the flows through the internal carotid and vertebral arteries, provided that the flows through the cerebral arteries extending from the circle of Willis have normal flow values.

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8

Tan, A., and D. Roberts. "Cerebral circulation 1: anatomy." BJA Education 21, no. 10 (October 2021): 390–95. http://dx.doi.org/10.1016/j.bjae.2021.05.004.

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9

Chang, Steven D., Stephen I. Ryu, and Gary K. Steinberg. "Posterior Cerebral Circulation Revascularization." Neurosurgery Clinics of North America 12, no. 3 (July 2001): 519–40. http://dx.doi.org/10.1016/s1042-3680(18)30041-x.

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10

Hermann, Dirk M., and Claudio L. Bassetti. "Cerebral circulation and sleep." Sleep Medicine Reviews 6, no. 6 (December 2002): 425–27. http://dx.doi.org/10.1053/smrv.2002.0259.

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11

Armstead, William M. "Age and cerebral circulation." Pathophysiology 12, no. 1 (July 2005): 5–15. http://dx.doi.org/10.1016/j.pathophys.2005.01.002.

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12

Ligon, R. Allen, Denver Sallee, Sassan Hashemi, Clifford M. Hawkins, and Christopher J. Petit. "Rerouting of Cerebral Circulation." JACC: Case Reports 2, no. 6 (June 2020): 855–59. http://dx.doi.org/10.1016/j.jaccas.2020.03.038.

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13

Nagata, Ken, Takashi Yamazaki, Daiki Takano, Tetsuya Maeda, Yumi Fujimaki, Taizen Nakase, and Yuichi Sato. "Cerebral circulation in aging." Ageing Research Reviews 30 (September 2016): 49–60. http://dx.doi.org/10.1016/j.arr.2016.06.001.

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14

Iedynak, G. A., M. B. Guska, Y. P. Kozak, V. I. Mazur, and M. V. Guska. "Cerebral circulation of highly qualified sumo and judo wrestlers." Pedagogical and social aspects of physical education and physical therapy, no. 1 (March 5, 2019): 81–93. http://dx.doi.org/10.32626/pasaopeapt.2019.81-93.

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15

Liu, James K., Michael S. Tenner, Oren N. Gottfried, Edwin A. Stevens, Joshua M. Rosenow, Neel Madan, Joel D. Macdonald, John R. W. Kestle, and William T. Couldwell. "Efficacy of multiple intraarterial papaverine infusions for improvement in cerebral circulation time in patients with recurrent cerebral vasospasm." Journal of Neurosurgery 100, no. 3 (March 2004): 414–21. http://dx.doi.org/10.3171/jns.2004.100.3.0414.

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Object. Cerebral vasospasm that is caused by aneurysmal subarachnoid hemorrhage and that is refractory to maximal medical management can be treated with selective intraarterial papaverine infusions. The effects of single papaverine treatments on cerebral circulation time are well known. The purpose of this study was to assess the efficacy of multiple, repeated papaverine infusions on the cerebral circulation time in patients with recurrent vasospasm. Methods. A retrospective study was conducted in 17 patients who received multiple intraarterial papaverine infusions in 91 carotid artery (CA) territories for the treatment of cerebral vasospasm. Cerebral circulation times were measured from the first angiographic image, in which peak contrast was seen above the supraclinoid internal CA, to the peak filling of cortical veins. Glasgow Outcome Scale (GOS) scores assessed 12 months after discharge were reviewed. Cerebral circulation times in 16 CA territories were measured in a control group of 11 patients. Seventeen patients received a total of 91 papaverine treatments. Prolonged cerebral circulation times improved after 90 (99%) of 91 papaverine treatments. The prepapaverine mean cerebral circulation time was 6.54 seconds (range 3.35–27 seconds) and the immediate postpapaverine mean cerebral circulation time was 4.19 seconds (range 2.1–12.6 seconds), an overall mean decrease of 2.35 seconds (36%, p < 0.001). Recurrent vasospasm reflected by prolonged cerebral circulation times continued to improve with subsequent papaverine infusions. Repeated infusions were just as successful quantitatively as the primary treatment (mean change 2.06 seconds). The mean cerebral circulation time in the control group was 5.21 seconds (range 4–6.8 seconds). In five patients a dramatic reversal of low-attenuation changes was detected on computerized tomography scans. The mean GOS score at 12 months after discharge was 3.4. Conclusions. The preliminary results indicate that multiple intraarterial papaverine treatments consistently improve cerebral circulation times, even with repeated infusions in cases of recurrent vasospasm.

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16

Aslan, Işıl, and Irmak Salt. "Collateral miracle: adequate cerebral circulation with only right ICA." Medical Science and Discovery 10, no. 3 (March 21, 2023): 204–7. http://dx.doi.org/10.36472/msd.v10i3.905.

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Objective: Collateral circulation is essential for cerebral perfusion and the maintenance of cerebral metabolism and function. The clinical factors affecting the collateral circulation in the brain is still unknown. In the presence of slowly developing stenosis, the decrease in cerebral blood flow can be compensated by adequate collateral circulation, and signs of cerebral hemodynamic deterioration may not be observed. Case: This case with a 6-year retrospective record and adequate cerebral circulation with only right Internal Carotid Artery (ICA) is presented.

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17

Park, Geo-seong, and Jung-soo Park. "Anatomical differences of the vertebrobasilar artery between normal subjects and patients with cerebral infarction." Medicine 103, no. 32 (August 9, 2024): e39105. http://dx.doi.org/10.1097/md.0000000000039105.

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Previous studies have reported various anatomical differences in the cerebral artery between healthy subjects and patients with posterior circulation cerebral infarction. In particular, basilar artery angulation has been associated with posterior circulation cerebral infarction. We compared anatomical variations and the degree of anterior and lateral vertebrobasilar artery angulation and deviation to compare the incidence of cerebral infarction of healthy subjects and patients with posterior circulation cerebral infarction. We compared basilar artery anatomy using brain magnetic resonance angiography in 97 patients who underwent brain magnetic resonance angiography during health checkups at our hospital and in 92 patients diagnosed with posterior circulation cerebral infarction between 2012 and 2022. Anatomical variations, including fetal-type posterior cerebral artery, hypoplastic P1 segment, vertebrobasilar dolichoectasia, and dominant vertebral artery, as well as the degree of anterior and lateral deviation and angulation, were evaluated. Correlations between these variations and the occurrence of cerebral infarction were analyzed. The prevalence of hypoplastic P1 was significantly differences in patients with posterior circulation cerebral infarction (odds ratio: 5.655). Furthermore, patients with posterior circulation cerebral infarction exhibited more acute anterior and lateral angulation, as well as lateral deviation. Hypoplastic P1 and more acute anterior or lateral angulation of the vertebrobasilar artery are associated with increased frequency of cerebral infarction.

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18

Nakase, Hiroyuki. "Introduction: Venous brain circulation disorders." Neurosurgical Focus 27, no. 5 (November 2009): E1. http://dx.doi.org/10.3171/2009.9.focus.nov09.intro.

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Brain ischemia by arterial occlusion has been a focus of attention for decades, and cerebral venous disorders have been an underestimated condition of potentially good outcome if diagnosed and treated promptly. Recently, there has been considerable interest in cerebral injury following cerebral venous circulation disorders because diagnosis has improved as our understanding of the diseases and modern imaging technologies have advanced.

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19

Abilova, Guljakhan, Vitaly Kamkeh, and Zhanna Kalmatayeva. "Predictive Estimations for Patients Who Have Suffered From Acute Cerebrovascular Accident and Have Undergone Rehabilitation." Open Access Macedonian Journal of Medical Sciences 10, E (June 12, 2022): 1024–28. http://dx.doi.org/10.3889/oamjms.2022.9943.

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BACKGROUND: Acute cerebral circulation disorder is known to be one of the main causes of morbidity, mortality, long-term disability, and the overall so-called disability in society. Prevention of acute cerebral circulation disorder, mortality after acute cerebral circulation disorder, methods of rehabilitation after acute cerebral circulation disorder are studied all over the world, but there are so few studies in the literature on the relationship between rehabilitation and survival of patients after acute cerebral circulation disorder. AIM: The aim is to study the features of survival among patients who have suffered from acute cerebral circulation disorder (hereinafter referred to as ACCD) and have undergone rehabilitation. METHODS: Based on the register statistics on cases of acute cerebral circulation disorder among Almaty residents, the association of the fact of rehabilitation with a fatal outcome was studied and a survival analysis was performed using the Kaplan-Meyer method. RESULTS: In patients with acute cerebral circulation disorder who have not undergone rehabilitation, the chances of a fatal outcome increase by 3.830 times, in comparison with patients who have received an appropriate course of recovery. With the postponement of rehabilitation, the probability of death in patients with acute cerebral circulation disorder increased by 6−10%. The average survival rates in patients who did not receive a rehabilitation course are significantly lower compared to those who underwent rehabilitation: the average survival was 87 years (CI95% 87.0−87.0) and 82 years (CI95% 80.3 ÷ 83.7), respectively, (Log-rank test: test statistics χ2 = 7.916, for DF = 1, p = 0.005). CONCLUSIONS: The main conclusion that can be drawn is that the early rehabilitation care increases the probability of survival among patients who have undergone ACCD. At the same time, the predictive parameters of an unfavorable outcome are the sexual characteristic and the type of acute cerebral circulation disorder.

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20

Cipolla, Marilyn J. "The Cerebral Circulation, Second Edition." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 8, no. 1 (July 28, 2016): 1–80. http://dx.doi.org/10.4199/c00141ed2v01y201607isp066.

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21

Ogoh, Shigehiko. "Autonomic control of cerebral circulation." Medicine & Science in Sports & Exercise 39, Supplement (May 2007): 49. http://dx.doi.org/10.1249/01.mss.0000272469.79816.7d.

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22

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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23

Mancini, Marcello, Vincenzo Brescia Morra, Orlando Di Donato, Valentina Maglio, Roberta Lanzillo, Raffaele Liuzzi, Elena Salvatore, Arturo Brunetti, Vittorio Iaccarino, and Marco Salvatore. "Multiple Sclerosis: Cerebral Circulation Time." Radiology 262, no. 3 (March 2012): 947–55. http://dx.doi.org/10.1148/radiol.11111239.

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24

STRANDGAARD, S., and O. B. PAULSON. "Antihypertensive drugs and cerebral circulation." European Journal of Clinical Investigation 26, no. 8 (August 1996): 625–30. http://dx.doi.org/10.1111/j.1365-2362.1996.tb02145.x.

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25

Fujishima, Masatoshi, Seizo Sadoshima, Takao Ishitsuka, Setsuro Ibayashi, and Kenichiro Fujii. "Antihypertensive agents and cerebral circulation." Nosotchu 11, no. 1 (1989): 1–10. http://dx.doi.org/10.3995/jstroke.11.1.

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26

Šulla, Igor, and Slavomír Horňák. "Canine cerebral circulation: a review." Acta Veterinaria Brno 93, no. 4 (2024): 405–15. https://doi.org/10.2754/avb202493040405.

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The cerebral vascular system (CVS) of mammals is a complicated three-dimensional structure that supplies brain parenchyma with oxygenated blood and nutrients, drains deoxygenated blood and catabolites out from it and participates in cerebrospinal fluid (CSF) resorption, maintenance of intracranial pressure (ICP) stability, and brain thermoregulation. A thorough understanding of the morphology and function of CVS is essential for human as well as veterinary neurologists and neurosurgeons as it helps to diagnose intracranial pathological processes, to choose an optimal therapeutic approach for the specific patient concerning configuration and possible anomalies of their CVS, and to execute intracranial surgical procedures. The number of brain operations in dogs has rapidly grown, which prompted the authors to review the literature on the complex issue of canine intracranial blood vessels. The research strategy involved a PubMed, MEDLINE (Ovid), EMBASE (Ovid), and Clarivate Analytics Web of Science search from January 1960 to January 2024 using the terms ‘canine brain blood vessels’ and ‘cerebral haemodynamics in dogs’ in the English language literature; references from selected papers were also scanned, and relevant articles were included.

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27

Burnstock, G. "Neurogenic Control of Cerebral Circulation." Cephalalgia 5, no. 2_suppl (May 1985): 25–33. http://dx.doi.org/10.1177/03331024850050s205.

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The cerebral vascular neuromuscular apparatus consists of a varicose perivascular nerve plexus at the adventitial-medial border and smooth muscle cells in the medial coat that are functionally connected. In addition to noradrenaline and acetylcholine, a number of putative non-adrenergic, non-cholingergic neurotransmitters have been identified in cerebral perivascular nerves, including serotonin, substance P, vasoactive intestinal polypeptide, gastrinreleasing peptide, cholecystokinin, somatostatin, neurotensin, calcitonin gene-related peptide and neuropeptide Y. The role of adenosine-5'-triphosphate as a cotransmitter with noradrenaline in some perivascular sympathetic nerves, and of endothelial cells in mediating the vasodilatation produced by some neurohumoral agents is discussed. Speculations are made about the relation between vascular neuroeffector mechanisms and migraine, including the possiblity of local vasospasm by serotoninergic nerves, reactive hyperaemia involving purine nucleotides and nucleosides, release of substance P from sensory nerve collaterals during antidromic ('axon reflex') impulses and secondary release of local agents such as prostanoids, histamine and bradykinin.

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28

Barker, J., and R. A. Duckworth. "Ketamine and the cerebral circulation." Anaesthesia 50, no. 8 (August 1995): 751–52. http://dx.doi.org/10.1111/j.1365-2044.1995.tb06132.x.

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29

RichardWinn, H., Ellen Gordon, Al Ngai, Seiji Morii, Setsuro Ibayashi, Toe Meno, and Kathryn Ko. "Adenosine and the cerebral circulation." Japanese Journal of Pharmacology 52 (1990): 47. http://dx.doi.org/10.1016/s0021-5198(19)32920-8.

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30

Coiteiro, Domingos N., Matthias Oertel, and Neil A. Martin. "Revascularization of Posterior Cerebral Circulation." Techniques in Neurosurgery 6, no. 2 (June 2000): 113–26. http://dx.doi.org/10.1097/00127927-200006020-00006.

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31

Kis, Béla, Csongor S. Ábrahám, Mária A. Deli, Hideyuki Kobayashi, Akihiko Wada, Masami Niwa, Hiroshi Yamashita, and Yoichi Ueta. "Adrenomedullin in the cerebral circulation." Peptides 22, no. 11 (November 2001): 1825–34. http://dx.doi.org/10.1016/s0196-9781(01)00533-2.

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32

Hakopian, V. P., L. Yedigarova, A. Manukian, A. Kocharian, L. Balian, and S. Barsegian. "Hypokinesia and cerebral blood circulation." Pharmacological Research 31 (January 1995): 237. http://dx.doi.org/10.1016/1043-6618(95)87206-x.

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33

Magyar, Mária Tünde, and Dániel Bereczki. "Cholesterol and the cerebral circulation." Future Lipidology 2, no. 2 (April 2007): 211–28. http://dx.doi.org/10.2217/17460875.2.2.211.

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34

Fitch, William. "Physiology of the cerebral circulation." Best Practice & Research Clinical Anaesthesiology 13, no. 4 (December 1999): 487–98. http://dx.doi.org/10.1053/bean.1999.0043.

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35

OGOH, SHIGEHIKO. "Autonomic Control of Cerebral Circulation." Medicine & Science in Sports & Exercise 40, no. 12 (December 2008): 2046–54. http://dx.doi.org/10.1249/mss.0b013e318180bc6f.

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36

Mayhan, William G. "Cerebral circulation during diabetes mellitus." Pharmacology & Therapeutics 57, no. 2-3 (January 1993): 377–91. http://dx.doi.org/10.1016/0163-7258(93)90062-i.

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37

SOMA, Y., T. HIROTANI, R. YOZU, K. ONOGUCHI, T. MISUMI, K. KAWADA, T. INOUE, and H. MOHRI. "A Clinical Study of Cerebral Circulation During Extracorporeal Circulation." Survey of Anesthesiology 5, no. 2 (October 1989): 279. http://dx.doi.org/10.1097/00132586-198910000-00008.

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38

Soma, Yasuhiro, Takashi Hirotani, Ryohei Yozu, Katsuhisa Onoguchi, Takahiko Misumi, Kozo Kawada, Tadashi Inoue, and Hitoshi Mohri. "A clinical study of cerebral circulation during extracorporeal circulation." Journal of Thoracic and Cardiovascular Surgery 97, no. 2 (February 1989): 187–93. http://dx.doi.org/10.1016/s0022-5223(19)35323-1.

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39

Iwata, Tomonori, Takahisa Mori, Hiroyuki Tajiri, Yuichi Miyazaki, Masahito Nakazaki, and Koji Mizokami. "Initial Experience of a Novel Sheath Guide for Transbrachial Coil Embolization of Cerebral Aneurysms in the Anterior Cerebral Circulation." Operative Neurosurgery 72, no. 1 (August 15, 2012): ons15—ons20. http://dx.doi.org/10.1227/neu.0b013e31826e2cd9.

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Abstract Background: The transfemoral approach is a common technique for coil embolization of cerebral aneurysms in the anterior cerebral circulation. However, it is difficult to advance a guiding catheter into the carotid artery via the femoral route in patients with a tortuous aortic arch, an unfavorable supra-aortic takeoff, aortic diseases, or occlusion of the femoral artery. Objective: To report our initial experiences of coil embolization of cerebral aneurysms in the anterior cerebral circulation with a novel sheath guide for transbrachial carotid cannulation. Methods: A sheath guide designed specifically for transbrachial carotid cannulation was developed; transbrachial coil embolization for cerebral aneurysms began in May 2011. Included for analysis were patients who underwent transbrachial coil embolization for cerebral aneurysms in the anterior cerebral circulation from May 2011 to January 2012. Adjuvant techniques, angiographic results, procedural success, and periprocedural complications were investigated. Results: Ten patients underwent transbrachial coil embolization of cerebral aneurysms in the anterior cerebral circulation. All procedures were successful using the brachial route. No periprocedural complications occurred. Patients were permitted to get seated immediately after coil embolization even during hemostasis. Conclusion: The sheath guide specifically designed for transbrachial carotid cannulation was useful for coil embolization of cerebral aneurysms in the anterior cerebral circulation.

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40

Lansdell, Theresa A., Laura C. Chambers, and Anne M. Dorrance. "Endothelial Cells and the Cerebral Circulation." Comprehensive Physiology 12, no. 3 (June 29, 2022): 3449–508. https://doi.org/10.1002/j.2040-4603.2022.tb00220.x.

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AbstractEndothelial cells form the innermost layer of all blood vessels and are the only vascular component that remains throughout all vascular segments. The cerebral vasculature has several unique properties not found in the peripheral circulation; this requires that the cerebral endothelium be considered as a unique entity. Cerebral endothelial cells perform several functions vital for brain health. The cerebral vasculature is responsible for protecting the brain from external threats carried in the blood. The endothelial cells are central to this requirement as they form the basis of the blood‐brain barrier. The endothelium also regulates fibrinolysis, thrombosis, platelet activation, vascular permeability, metabolism, catabolism, inflammation, and white cell trafficking. Endothelial cells regulate the changes in vascular structure caused by angiogenesis and artery remodeling. Further, the endothelium contributes to vascular tone, allowing proper perfusion of the brain which has high energy demands and no energy stores. In this article, we discuss the basic anatomy and physiology of the cerebral endothelium. Where appropriate, we discuss the detrimental effects of high blood pressure on the cerebral endothelium and the contribution of cerebrovascular disease endothelial dysfunction and dementia. © 2022 American Physiological Society. Compr Physiol 12:3449‐3508, 2022.

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41

Camstra, Kevin M., Visish M. Srinivasan, Dalis Collins, Stephen Chen, Peter Kan, and Jeremiah Johnson. "Canine Model for Selective and Superselective Cerebral Intra-Arterial Therapy Testing." Neurointervention 15, no. 3 (November 1, 2020): 107–16. http://dx.doi.org/10.5469/neuroint.2020.00150.

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Purpose: With advancing endovascular technology and increasing interest in minimally invasive intra-arterial therapies such as stem cell and chemotherapy for cerebral disease, the establishment of a translational model with cerebral circulation accessible to microcatheters is needed. We report our experience catheterizing canine cerebral circulation with microcatheters, present high-resolution angiographic images of the canine vascular anatomy, describe arterial branch flow patterns and provide measurements of canine arterial conduits.Materials and Methods: Angiograms were performed on 10 intact purpose-bred hounds. Angiography, measurements of arterial conduits and catheterization information for intracranial arterial branches were obtained.Results: Selective and superselective cerebral angiography was successful in all subjects. Relevant arterial mean diameters include the femoral (4.64 mm), aorta (9.38 mm), external carotid (3.65 mm), internal carotid arteries (1.6 mm), vertebrobasilar system and Circle of Willis branches. Catheterization of the Circle of Willis was achieved via the posterior circulation in all subjects tested (n=3) and the use of flow directed microcatheters resulted in reduced arterial tree deformation and improved superselection of intracranial vessels. Catheterization of the intracranial circulation was attempted but not achieved via the internal carotid artery (n=7) due to its tortuosity and subsequent catheter related vasospasm.Conclusion: The canine cerebral vasculature is posterior circulation dominant. Anterior circulation angiography is achievable via the internal carotid artery, but direct cerebral arterial access is best achieved via the posterior circulation using flow-directed microcatheters. It is feasible to deliver intra-arterial therapies to selective vascular territories within the canine cerebral circulation, thus making it a viable animal model for testing novel intra-arterial cerebral treatments.

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42

Shestakov, V. V. "Changes in cerebral blood flow in formation and initial progressing of cerebrovascular Diseases." Neurology Bulletin XXX, no. 1-2 (March 15, 1998): 10–12. http://dx.doi.org/10.17816/nb80695.

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The author investigated 40 patients with initial manifestation of insufficient cerebral circulation and 46 patients with discirculatory encephalopathy. The author showed, that progressing and clinical manifestations of initial stages of cerebrovascular diseases are connected with imperfection of cerebral circulation regulation with phenomena of its depression. In stage of initial manifestation of insufficient cerebral circulation dimyelitic defect prevails in proximal departments of cerebral arteries, and in stage of discirculatory encephalopathy is spreading on parenchymatous vessels.

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43

Odinak, M. M., G. G. Khubulava, A. N. Kuznetcov, I. A. Vosnyuk, and N. A. Arsenova. "Modern angiotensmconverting enzyme inhibitors m correction of cerebral haemodynamics in hypertension." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 12, no. 4 (August 28, 2006): 347–50. http://dx.doi.org/10.18705/1607-419x-2006-12-4-347-350.

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The study addresses changes of cerebral circulation during perindopril therapy of hypertension. 33 hypertensive patients were included (males - 15 (45,5%); females - 18 (54,5%). 20 patients (60,6%) received perindopril e 4 mg per day, 13 patients of control group were treated by alternative antihypertensive drugs. Neurology status, cerebral circulation (Sonomed, Spectodem, Russia) were evaluated at baseline and after 6 months of treatment. Results obtained demonstrated that perindopril can improve cerebral circulation independently of blood pressure reduction and has angioprotective effect. In conclusion perindopril seems to be effective treatment of hypertension in patients with impaired cerebral blood flow. Transcranial Doppler can be used as effective tool for monitoring of cerebral circulation in such cases.

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Abramova, Ekaterina A., Oleg V. Voennov, Gennadii A. Boyarinov, and Аlexei O. Trofimov. "Cerebral Circulation and Metabolism of Patients with Cerebral Injury." General Reanimatology 14, no. 1 (March 11, 2018): 4–11. http://dx.doi.org/10.15360/1813-9779-2018-1-4-11.

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Umemnra, Kazuo. "Cerebral circulation impairment following the middle cerebral artery occlusion." Japanese Journal of Pharmacology 71 (1996): 9. http://dx.doi.org/10.1016/s0021-5198(19)36297-3.

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Grant, Daniel A., Carlo Franzini, Jennene Wild, and Adrian M. Walker. "Cerebral Circulation in Sleep: Vasodilatory Response to Cerebral Hypotension." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (June 1998): 639–45. http://dx.doi.org/10.1097/00004647-199806000-00006.

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Little is known of the factors that regulate CBF in sleep. We therefore studied 10 lambs to assess the vasodilatory processes that underlie cerebral autoregulation during sleep. Lambs, instrumented to measure CBF (flow probe on the superior sagittal sinus), sleep state, and cerebral perfusion pressure (CPP), were rapidly made hypotensive by inflating a cuff around the brachiocephalic artery to reduce CPP to 30 mm Hg in each state. During control periods, cerebral vascular resistance (CVR in mm Hg/mL/min) was lower in active sleep (2.8±0.3, mean±SD, P ≤ 0.001) than in wakefulness (3.9±0.6) and quiet sleep (4.3±0.6). The CVR decreased promptly in each state as CPP was lowered. The time (seconds) required for maximal cerebral vasodilation to occur was longer in active sleep (35±11) than in quiet sleep (20±6, P ≤ 0.001) and wakefulness (27±11, P ≤ 0.05). The CVR decreased less in active sleep (0.6±0.3, P ≤ 0.001) than in quiet sleep (1.5±0.3), although the changes in CPP induced with brachiocephalic occlusion were equal in each state. In conclusion, our studies provide the first evidence that the vasoactive mechanisms that underlie autoregulation of the cerebral circulation function during sleep. Moreover, our data reveal that the speed and the magnitude of the vasodilatory reserves available for autoregulation are significantly less in active sleep than in quiet sleep.

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Kawashima, Masatou, Albert L. Rhoton, Necmettin Tanriover, Arthur J. Ulm, Alexandre Yasuda, and Kiyotaka Fujii. "Microsurgical anatomy of cerebral revascularization. Part II: Posterior circulation." Journal of Neurosurgery 102, no. 1 (January 2005): 132–47. http://dx.doi.org/10.3171/jns.2005.102.1.0132.

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Object. Revascularization is an important component of treatment for complex aneurysms, skull base tumors, and vertebrobasilar ischemia in the posterior circulation. In this study, the authors examined the microsurgical anatomy related to cerebral revascularization in the posterior circulation and demonstrate various procedures for bypass surgery. Methods. The microsurgical anatomy of cerebral and cerebellar vessels as they relate to revascularization procedure and techniques, including extracranial-to-intracranial bypass grafting, arterial interposition grafting, and side-to-side anastomosis, were examined by performing stepwise dissections in 22 adult cadaveric specimens. The arteries and veins in the specimens were perfused with colored silicone. Dominant cerebral and cerebellar revascularization procedures in the posterior circulations include superficial temporal artery (STA)—posterior cerebral artery (PCA), STA—superior cerebellar artery (SCA), occipital artery (OA)—anterior inferior cerebellar artery, OA—posterior inferior cerebellar artery (PICA), and PICA—PICA anastomoses. These procedures are effective in relatively small but critical areas including the brainstem and cerebellum. For revascularization of larger areas a saphenous vein graft is used to create a bypass between the PCA and the external carotid artery. Surgical procedures are generally difficult to perform in deep and narrow operative spaces near critical vital structures. Conclusions. Although a clear guideline for cerebral revascularization procedures has not yet been established, it is important to understand various microsurgical techniques and their related anatomical structures. This will help surgeons consider surgical indications for treatment of patients with vertebrobasilar ischemia caused by aneurysms, tumors, or atherosclerotic diseases in the posterior circulation.

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Monti, Lucia, Lucia Morbidelli, Lorenzo Bazzani, and Alessandro Rossi. "Influence of Circulating Endothelin-1 and Asymmetric Dimethylarginine on Whole Brain Circulation Time in Multiple Sclerosis." Biomarker Insights 12 (January 1, 2017): 117727191771251. http://dx.doi.org/10.1177/1177271917712514.

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Blood-brain barrier (BBB) breakdown, inflammatory and immune cell activation, and chronic cerebral hypoperfusion are features of multiple sclerosis (MS). The aim is to determine the influence of endothelin-1 (ET1) and asymmetric dimethylarginine (ADMA) on cerebral circulation time (CCT) in patients with MS. In all, 64 patients with MS (39 relapsing-remitting [RR]-MS; 25 secondary progressive [SP]-MS subtype) and 37 controls (C) were studied. Cerebral circulation time was obtained by angiography. Plasmatic ET1 and ADMA were measured by enzyme-linked immunosorbent assay. Lesion load (LL) and brain volume (BV) were obtained by magnetic resonance imaging. Cerebral circulation time was correlated to ET1, ADMA, LL, BV, disease duration (DD), and Expanded Disability Status Scale (EDSS). In MS, both ET1 and ADMA were significantly higher than C ( P < .0001); CCT was approximately 2 times lower than C ( P < .0001) and significantly slower in SP than in RR-MS ( P = .0215). Cerebral circulation time significantly correlated with ET1 in SP-MS ( r = 0.38), whereas in RR-MS CCT significantly correlated with DD ( r = 0.75). The LL, BV, and EDSS did not correlate with CCT. Endothelin-1 significantly influences CCT delay in SP-MS. Diversely, CCT in RR-MS is independent of ET1 and correlates significantly with DD. We conclude that in RR-MS, DD responds to neurovascular damage accumulation. It is supposed that high ET1 and ADMA levels stem from a protective response to early insults, aimed at opposing nitric oxide overproduction, whereas persistent pathological ET1 and ADMA levels translate into detrimental long-term effects, due to increased brain micro-vessel resistance.

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Pearce, William. "Hypoxic regulation of the fetal cerebral circulation." Journal of Applied Physiology 100, no. 2 (February 2006): 731–38. http://dx.doi.org/10.1152/japplphysiol.00990.2005.

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Fetal cerebrovascular responses to acute hypoxia are fundamentally different from those observed in the adult cerebral circulation. The magnitude of hypoxic vasodilatation in the fetal brain increases with postnatal age although fetal cerebrovascular responses to acute hypoxia can be complicated by age-dependent depressions of blood pressure and ventilation. Acute hypoxia promotes adenosine release, which depresses fetal cerebral oxygen consumption through action of adenosine on neuronal A1 receptors and vasodilatation through activation of A2 receptors on cerebral arteries. The vascular effect of adenosine can account for approximately half the vasodilatation observed in response to hypoxia. Hypoxia-induced release of nitric oxide and opioids can account for much of the adenosine-independent cerebral vasodilatation observed in response to hypoxia in the fetus. Direct effects of hypoxia on cerebral arteries account for the remaining fraction, although the vascular endothelium contributes relatively little to hypoxic vasodilatation in the immature cerebral circulation. In contrast to acute hypoxia, fetal cerebral blood flow tends to normalize during acclimatization to chronic hypoxia even though cardiac output is depressed. However, uncompensated chronic hypoxia in the fetus can produce significant changes in brain structure and function, alteration of respiratory drive and fluid balance, and increased incidence of intracranial hemorrhage and periventricular leukomalacia. At the level of the fetal cerebral arteries, chronic hypoxia increases protein content and depresses norepinephrine release, contractility, and receptor densities associated with contraction but also attenuates endothelial vasodilator capacity and decreases the ability of ATP-sensitive and calcium-sensitive potassium channels to promote vasorelaxation. Overall, fetal cerebrovascular adaptations to chronic hypoxia appear prioritized to conserve energy while preserving basic contractility. Many gaps remain in our understanding of how the effects of acute and chronic hypoxia are mediated in fetal cerebral arteries, but studies of adult cerebral arteries have produced many powerful pharmacological and molecular tools that are simply awaiting application in studies of fetal cerebral artery responses to hypoxia.

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Fan, Weijian, Weihao Shi, Jianjie Rong, Wencheng Guo, Shuangshuang Lu, Jinyun Tan, and Bo Yu. "Different Grades of Collateral Circulation for Evaluating Cerebral Hemodynamic Status in Carotid Artery Stenosis." Journal of Healthcare Engineering 2022 (February 2, 2022): 1–9. http://dx.doi.org/10.1155/2022/8484977.

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Normally, ipsilateral hemodynamic compromise of patients with carotid stenosis (CS) is subjectively identified by collateral circulation through cerebral angiography in the clinical process. It is unclear whether collaterals would linearly determine cerebral perfusion in CS patients. This study aimed to investigate the independent role of collateral circulation on cerebral perfusion in CS patients and the underlying interrelations among them. From 2017 to 2020, 124 CS patients who underwent carotid endarterectomy (CEA) with both preoperative CTP and digital substruction angiography (DSA) images were enrolled. Division of subgroups was based on degree of CS (50–70%, 70–90%, and near-occlusion (NO)) and grades of collateral circulation by DSA. Differences in CTP parameters between CS patients with different collateral circulation were analyzed. Among 124 CS patients, grades 2 and 3 were highly associated with carotid NO (n = 22, 32.35% and n = 22, 32.35%) compared with others ( P < 0.0001 ). The collateral circulation was found to have poor relation with cerebral perfusion parameters in all enrolled patients but significantly improved ipsilateral cerebral perfusion in patients with carotid NO ( P < 0.05 ). Linear hemodynamic compromise was barely related to degree of CS in lobes supplied by middle cerebral artery (MCA) except the frontal lobe ( P < 0.05 ). The grades of collateral circulation are positively associated with degree of CS while having nonsignificant effect on cerebral perfusion. Overall, severity of CS is poorly related to hemodynamic status while the perfectibility of compensation defined by grades of collateral circulation effectively alleviates ipsilateral cerebral perfusion deficit in carotid NO.

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