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Journal articles on the topic 'Cerebral circulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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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

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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16

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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17

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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18

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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19

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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20

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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21

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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22

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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23

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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24

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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25

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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26

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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27

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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28

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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29

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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30

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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31

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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32

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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33

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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34

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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35

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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36

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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37

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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38

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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39

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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40

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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41

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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42

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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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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44

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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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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Panerai, Ronney B. "Complexity of the human cerebral circulation." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 367, no. 1892 (February 27, 2009): 1319–36. http://dx.doi.org/10.1098/rsta.2008.0264.

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The cerebral circulation shows both structural and functional complexity. For time scales of a few minutes or more, cerebral blood flow (CBF) and other cerebrovascular parameters can be shown to follow a random fractal point process. Some studies, but not all, have also concluded that CBF is non-stationary. System identification techniques have been able to explain a substantial fraction of the CBF variability by applying linear and nonlinear multivariate models with classical determinants of flow (arterial blood pressure, arterial CO 2 and cerebrovascular resistance, CVR) as inputs. These findings raise the hypothesis that fractal behaviour is not inherent to CBF but might be simply transmitted from its determinants. If this is the case, future investigations could focus on the complexity of the residuals or the unexplained variance of CBF. In the low-frequency range (below 0.15 Hz), changes in CVR due to pressure and metabolic autoregulation represent an important contribution to CBF variability. A small body of work suggests that parameters describing cerebral autoregulation can also display complexity, presenting significant variability that might also be non-stationary. Fractal analysis, entropy and other nonlinear techniques have a role to play to shed light on the complexity of cerebral autoregulation.

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48

Tuor, U. I., P. A. T. Kelly, L. Edvinsson, and J. McCulloch. "Neuropeptide Y and the Cerebral Circulation." Journal of Cerebral Blood Flow & Metabolism 10, no. 5 (September 1990): 591–601. http://dx.doi.org/10.1038/jcbfm.1990.110.

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The significance of neuropeptide Y (NPY) in the cerebral circulation has been examined in the rat using immunocytochemistry, isolated cerebral artery preparations, and quantitative autoradiographic techniques for determining local CBF and glucose utilisation. In the rat the middle cerebral artery and the lenticulostriate artery from which blood is supplied to the caudate nucleus were found to be invested with numerous perivascular NPY immunoreactive nerve fibres. NPY (3–300 n M) contracted rat middle cerebral artery segments in a concentration-dependent manner. Intracerebral microinjections of NPY (200 pmol) or vehicle (1 μl) were performed in rats after full recovery from anaesthesia via previously implanted guide cannulae. Following injection of NPY into the striatum, local blood flow was markedly decreased by 36% throughout the ipsilateral caudate nucleus (e.g., from 104 ± 25 to 67 ± 15 ml 100 g−1 min −1; mean ± SD), whereas glucose use in this region was not altered significantly (e.g., 73 ± 8 and 74 ± 10 μmol 100 g−1 min−1 with vehicle and NPY, respectively). Intrastriatal NPY did not alter CBF or glucose use in the majority of other brain areas, including all of the 40 contralateral regions examined and almost all regions within the ipsilateral hemisphere. In a small number of highly discrete brain areas remote from the injection site (e.g., amygdala), there were significant reductions in blood flow with minimal changes in glucose use. Since NPY is present around rat cerebral blood vessels, is capable of evoking their contraction, and has the ability to produce reductions in blood flow independently of oxidative metabolism, this neuropeptide may be of major importance in cerebrovascular regulation.

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Morrison, N., and D. L. Neuhardt. "Foam sclerotherapy: cardiac and cerebral monitoring." Phlebology: The Journal of Venous Disease 24, no. 6 (December 2009): 252–59. http://dx.doi.org/10.1258/phleb.2009.009051.

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Objectives To investigate and review collected and reported transcutaneous ultrasound, transthoracic echocardiography (TTE) and transcranial Doppler (TCD) data obtained during ultrasound-guided foam sclerotherapy (USGFS) of incompetent saphenous, tributary and perforating veins of the lower extremities. Methods TTE and/or middle cerebral artery TCD were performed during USGFS. Ultrasound (US) findings and adverse events were recorded. Existing literature was reviewed. Results Ultrasound detected emboli circulating in superficial, perforating, communicating and deep veins and into the central circulation. TTE detected bright echoes in the right heart after every injection and in the left heart in up to 65% of selected patients. TCD high-intensity transient signals (HITS) were detected in 14–42% of the patients. Incidence of HITS was higher than patient reports of adverse events. Incidence of HITS was independent of foam volumes injected. Conclusion Echogenic signals were detected in non-treated veins, in heart chambers and in the cerebral circulation by transcutaneous US, TTE and TCD. Pathological consequences of such findings remain to be investigated.

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Olesen, Jes. "Beta-Adrenergic Effects on Cerebral Circulation." Cephalalgia 6, no. 5_suppl (May 1986): 41–46. http://dx.doi.org/10.1177/03331024860060s505.

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Noradrenaline, adrenaline, and isoprenaline were infused intracarotidly and the regional cerebral blood flow measured with the intracarotid injection-stationary detector method in patients undergoing carotid angiography. No effect was seen, and beta blockade with intracarotid propranolol also had no effect. The adrenergic effects on cerebral blood vessels are probably neurogenic, and circulating adrenergic agonists and antagonists are unlikely to play a role. Pertubations of adrenergic substances in blood are therefore unlikely to be important in migraine pathophysiology.

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