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Academic literature on the topic 'Cerebral arteries'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 August 2024

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Journal articles on the topic "Cerebral arteries"

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Mizutani, Tohru, Hideaki Kojima, and Yoshimasa Miki. "Arterial dissections of penetrating cerebral arteries causing hypertension-induced cerebral hemorrhage." Journal of Neurosurgery 93, no. 5 (November 2000): 859–62. http://dx.doi.org/10.3171/jns.2000.93.5.0859.

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Object. For the past 130 years, it has been believed that hypertension-induced cerebral hemorrhages are the result of ruptures of microaneurysms or ruptures of arteries that have degenerative changes. The majority of previous investigations have focused on autopsied brain. In this study, the authors attempted to verify the cause of hypertension-induced cerebral hemorrhage by using surgical specimens of the penetrating arteries responsible for the hemorrhages.Methods. Between 1997 and 1999, the authors performed pathological studies in surgical specimens of lenticulostriate arteries that had been confirmed during microsurgery to be the cause of hypertension-induced hemorrhage of the putamen. Nineteen lenticulostriate arteries were collected from 12 patients. Fifteen of these arteries were verified as the pathological causes of hemorrhage. They included six arterial dissections, six arterial ruptures with substantial degenerative changes, and three arterial ruptures with few degenerative changes. The pathological findings in the lenticulostriate artery dissections were similar to those of typical arterial dissections in major cerebral arteries.Conclusions. To the best of the authors' knowledge, arterial dissections of lenticulostriate arteries have not been identified as a cause of hypertension-induced cerebral hemorrhages. When penetrating arteries are included as causative vessels, cerebral arterial dissections may be much more common than previously thought.

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Warnert, Esther AH, Kevin Murphy, Judith E. Hall, and Richard G. Wise. "Noninvasive Assessment of Arterial Compliance of Human Cerebral Arteries with Short Inversion Time Arterial Spin Labeling." Journal of Cerebral Blood Flow & Metabolism 35, no. 3 (March 2015): 461–68. http://dx.doi.org/10.1038/jcbfm.2014.219.

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A noninvasive method of assessing cerebral arterial compliance (AC) is introduced in which arterial spin labeling (ASL) is used to measure changes in arterial blood volume (aBV) occurring within the cardiac cycle. Short inversion time pulsed ASL (PASL) was performed in healthy volunteers with inversion times ranging from 250 to 850 ms. A model of the arterial input function was used to obtain the cerebral aBV. Results indicate that aBV depends on the cardiac phase of the arteries in the imaging volume. Cerebral AC, estimated from aBV and brachial blood pressure measured noninvasively in systole and diastole, was assessed in the flow territories of the basal cerebral arteries originating from the circle of Willis: right and left middle cerebral arteries (RMCA and LMCA), right and left posterior cerebral arteries (RPCA and LPCA), and the anterior cerebral artery (ACA). Group average AC values calculated for the RMCA, LMCA, ACA, RPCA, and LPCA were 0.56%±0.2%, 0.50%±0.3%, 0.4%±0.2%, 1.1%±0.5%, and 1.1%±0.3% per mm Hg, respectively. The current experiment has shown the feasibility of measuring AC of cerebral arteries with short inversion time PASL.

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Dieguez, G., J. L. Garcia, N. Fernandez, A. L. Garcia-Villalon, L. Monge, and B. Gomez. "Cerebrovascular and coronary effects of endothelin-1 in the goat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 4 (October 1, 1992): R834—R839. http://dx.doi.org/10.1152/ajpregu.1992.263.4.r834.

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In vivo and in vitro effects of endothelin-1 (ET-1) on cerebral and coronary vasculature of goats were examined and compared. In six anesthetized goats intravenous injections of ET-1 (0.1-0.8 nmol) increased arterial pressure, did not change the middle cerebral (MCA) and left anterior descending or left circumflex coronary (LCC) arterial blood flows (electromagnetically measured), and increased cerebral and coronary vascular resistances. In four other anesthetized goats intra-arterial injections of ET-1 (0.01-0.3 nmol) decreased the MCA flow less than the LCC flow (maximal reduction was 20 and 80%, respectively) and only the highest dose increased arterial pressure. In isolated segments from large arteries ET-1 (10(-11) to 10(-7) M) caused concentration-dependent isometric contractions, the concentration causing 50% of the maximal effect and the maximal contraction being lower in cerebral arteries than in coronary arteries. The in vitro reactivity of both arteries was unaffected by endothelium removal or by indomethacin (10(-5) M). Therefore ET-1 produces cerebral and coronary vasoconstriction in vivo and in vitro, probably by acting directly on vascular musculature. Although the sensitivity is higher in isolated cerebral arteries than in coronary arteries, the reactivity in vivo could be lower in the cerebral circulation than in the coronary circulation to this endothelium-derived peptide.

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Chyatte, Douglas, Jeffrey Reilly, and David M. Tilson. "Morphometric Analysis of Reticular and Elastin Fibers in the Cerebral Arteries of Patients with Intracranial Aneurysms." Neurosurgery 26, no. 6 (June 1, 1990): 939–43. http://dx.doi.org/10.1227/00006123-199006000-00003.

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Abstract Elastin and reticular fibers were identified using standard histological stains in middle cerebral arteries taken from patients who had died from aneurysmal subarachnoid hemorrhage and control patients who did not have cerebral aneurysms, Examination of cerebral arteries from normal individuals revealed a dense network of fine reticular fibers in the arterial media that were uniformly distributed. Computerized morphometric analysis indicated that reticular fibers in the arterial media of cerebral arteries were significantly decreased in patients with aneurysms. In addition, these fibers were irregularly distributed and shortened when compared to those seen in control arteries. In both patients with aneurysms and control patients, elastin fibers were limited almost exclusively to the internal elastin lamina. No differences were observed in the appearance or content of elastin fibers in control patients and patients with aneurysm. Although other explanations cannot be excluded, these observations are consistent with the hypothesis that “intrinsic“ abnormalities in the walls of cerebral arteries lead to conditions that favor the formation and rupture of cerebral aneurysms.

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Warnert, Esther AH, Emma C. Hart, Judith E. Hall, Kevin Murphy, and Richard G. Wise. "The major cerebral arteries proximal to the Circle of Willis contribute to cerebrovascular resistance in humans." Journal of Cerebral Blood Flow & Metabolism 36, no. 8 (November 20, 2015): 1384–95. http://dx.doi.org/10.1177/0271678x15617952.

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Cerebral autoregulation ensures constant cerebral blood flow during periods of increased blood pressure by increasing cerebrovascular resistance. However, whether this increase in resistance occurs at the level of major cerebral arteries as well as at the level of smaller pial arterioles is still unknown in humans. Here, we measure cerebral arterial compliance, a measure that is inversely related to cerebrovascular resistance, with our novel non-invasive magnetic resonance imaging-based measurement, which employs short inversion time pulsed arterial spin labelling to map arterial blood volume at different phases of the cardiac cycle. We investigate the differential response of the cerebrovasculature during post exercise ischemia (a stimulus which leads to increased cerebrovascular resistance because of increases in blood pressure and sympathetic outflow). During post exercise ischemia in eight normotensive men (30.4 ± 6.4 years), cerebral arterial compliance decreased in the major cerebral arteries at the level of and below the Circle of Willis, while no changes were measured in arteries above the Circle of Willis. The reduction in arterial compliance manifested as a reduction in the arterial blood volume during systole. This study provides the first evidence that in humans the major cerebral arteries may play an important role in increasing cerebrovascular resistance.

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Sasaki, Tomio, Neal F. Kassell, Masanori Yamashita, Shigeru Fujiwara, and Mario Zuccarello. "Barrier disruption in the major cerebral arteries following experimental subarachnoid hemorrhage." Journal of Neurosurgery 63, no. 3 (September 1985): 433–40. http://dx.doi.org/10.3171/jns.1985.63.3.0433.

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✓ The effects of experimental subarachnoid hemorrhage (SAH) on the blood-arterial wall barrier in the major cerebral arteries were studied in 20 normotensive dogs. Horseradish peroxidase (HRP) was given intravenously before the animals were sacrificed to assess the integrity of the barrier. Transient elevation of intracranial pressure (ICP) produced by cisternal injection of saline solution resulted in HRP leakage at the branching points of the major cerebral arteries. Extensive disturbance of the blood-arterial wall barrier was consistently observed in the major cerebral arteries after SAH, with or without elevation of ICP. These results suggest that both subarachnoid clot and a sudden rise in the ICP are important factors causing the breakdown of the blood-arterial wall barrier, but that the effect of the clot is the most profound. Electron microscopy revealed that opening of the interendothelial junctions is one of the important mechanisms responsible for the HRP leakage in the major cerebral arteries following SAH. Disturbance of arterial permeability in the major cerebral arteries following SAH probably accounts for the abnormal post-contrast enhancement that occurs in patients who are prone to develop vasospasm following aneurysm rupture, and is probably involved in the pathogenesis of vasospasm.

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Ayajiki, Kazuhide, and Noboru Toda. "Regional Difference in the Response Mediated by β1-Adrenoceptor Subtype in Bovine Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 12, no. 3 (May 1992): 507–13. http://dx.doi.org/10.1038/jcbfm.1992.69.

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Helical strips of bovine rostral cerebral arteries (anterior cerebral, middle cerebral, and internal carotid artery) responded to norepinephrine with contractions, whereas the caudal cerebral arteries (posterior communicating, posterior cerebral, and basilar artery) relaxed in response to the amine. After blockade of α-adrenoceptors, norepinephrine-induced rostral artery contractions were reversed to relaxations, which were smaller than those in the caudal arteries. Isoproterenol, dobutamine, and terbutaline produced greater relaxations in caudal than in rostral arteries, but forskolin relaxed these arteries to a similar magnitude. The isoproterenol-induced relaxation was not affected by removal of the endothelium. Maximal relaxations induced by terbutaline in caudal arteries were much inferior to those by isoproterenol, norepinephrine, and dobutamine. Relaxations caused by isoproterenol, norepinephrine, and terbutaline in the caudal arteries were attenuated by metoprolol, but not influenced by butoxamine. Relaxations mediated possibly by β1-adrenoceptor subtype are greater in bovine caudal cerebral arteries than in the rostral arteries. The heterogeneity does not appear to be associated with the different ability of cyclic AMP to relax arterial smooth muscle but with the difference of β-adrenoceptor populations and/or processes from the receptors to adenylate cyclase.

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Sabec-Pereira, Dayane Kelly, Fabiano C. Lima, Fabiano R. Melo, Fabiana Cristina S. A. Melo, Kleber Fernando Pereira, and Valcinir Aloisio S. Vulcani. "Vascularization of the Alouatta belzebul brain base." Pesquisa Veterinária Brasileira 40, no. 4 (April 2020): 315–23. http://dx.doi.org/10.1590/1678-5150-pvb-6536.

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ABSTRACT: We studied the arterial circle in the brain of five specimens of the Alouatta belzebul primate. The material had the arterial system perfused (water at 40°C), injected with stained latex (Neoprene 650), fixed in aqueous formaldehyde solution (10%) and dissected for vessel verification. The arterial circle of this primate is composed of two vascular systems: the vertebra-basilar and the carotid ones, which anastomose to close the arterial circuit. In the caudal portion of the arterial circle, there are the vertebral arteries and their branches: the rostral spinal artery and the caudal inferior cerebellar artery. The anastomosis of the vertebral arteries gives rise to the basilar artery. It presented an anatomical variation at the beginning of its path, forming a double basilar artery, called arterial island. In its course, it emitted branches giving rise to the rostral inferior cerebellar artery, the pontine arteries, the rostral cerebellar arteries, the satellite rostral cerebellar arteries and its terminal branch, the caudal cerebral artery, which presented itself in two segments: the pre-communicating one and post-communicating, joining the internal carotid artery and originating the caudal communicating artery. This group of arteries and anastomoses enclose the caudal portion of the arterial circle. From the right and left internal carotid arteries begins the rostral portion of the arterial circle, which consists of the right and left rostral cerebral arteries and the right and left middle cerebral arteries. The rostral cerebral arteries anastomose into a single trunk, giving rise to the interhemispheric artery, and in A. belzebul and Sapajus libidinosus, the rostral communicating artery is absent. The interhemispheric artery goes to the midbrain region and the corpus callosum knee divides into pericalous artery and callosarginal artery, which will supply the pre and post-central regions of the cerebral hemispheres of this species, as well as other non-human and human primates. It is noted that in the first part of the left rostral cerebral artery, there is a direct inosculation between the recurrent branch of the rostral cerebral artery and left middle cerebral artery to supply the entorhinal region. This fact also occurs in Pongo spp. The middle cerebral artery travels along the lateral sulcus where it emits several superficial branches to irrigate the superior and inferior lateral cortical regions of the frontal, parietal and temporal lobes. It is not part of the arterial circle but is the terminal branch of the internal carotid artery. A. belzebul can be considered to depend on two sources of supply to the brain: the vertebra-basilar and carotid systems, contributing to the intervention of veterinarians during clinical and surgical procedures in other primates, as well as the preservation of wild animals.

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Mangiarua, Elsa I., and Robert M. K. W. Lee. "Increased sympathetic innervation in the cerebral and mesenteric arteries of hypertensive rats." Canadian Journal of Physiology and Pharmacology 68, no. 4 (April 1, 1990): 492–99. http://dx.doi.org/10.1139/y90-070.

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The density of catecholamine-containing nerve fibers was studied in the cerebral and mesenteric arteries from normotensive Wistar–Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) in the growing (SHR, WKY) and adult (SHR, SHRSP, WKY) animals. Cerebral arteries from SHR showed an increased adrenergic innervation from day 1. The nerve plexuses reached an adult pattern earlier in SHR than in WKY. The arteries from adult SHR and SHRSP (22 weeks old) showed a markedly higher nerve density than WKY. There was a positive linear correlation between blood pressure and nerve density for four cerebral arteries. The mesenteric arteries were not innervated at birth. However, hyperinnervation of these arteries in the SHR was already present at 10 days of age as compared with WKY. Sympathectomy with anti-nerve growth factor and guanethidine caused a complete disappearance of fluorescent fibers in the mesenteric arteries from SHR and WKY, and in the cerebral arteries of WKY. The same procedure caused only partial denervation of the cerebral arteries from hypertensive animals. We postulate that the increase in nerve density in the cerebral arteries from the hypertensive rats may contribute to the development of arterial hypertrophy in chronic hypertension through the trophic effect of the sympathetic innervation on vascular structure.Key words: sympathetic innervation, cerebral artery, mesenteric artery, spontaneously hypertensive rat, neonatal rat.

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Amin, Faisal Mohammad, Mohammad Sohail Asghar, Julie W. Ravneberg, Patrick JH de Koning, Henrik BW Larsson, Jes Olesen, and Messoud Ashina. "The effect of sumatriptan on cephalic arteries: A 3T MR-angiography study in healthy volunteers." Cephalalgia 33, no. 12 (April 15, 2013): 1009–16. http://dx.doi.org/10.1177/0333102413483374.

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Aim To explore a possible differential effect of sumatriptan on extracerebral versus cerebral arteries, we examined the superficial temporal (STA), middle meningeal (MMA), extracranial internal carotid (ICAextra), intracranial internal carotid (ICAintra), middle cerebral (MCA) and basilar arteries (BA). Methods The arterial circumferences were recorded blindly using high-resolution magnetic resonance angiography before and after subcutaneous sumatriptan injection (6 mg) in 18 healthy volunteers. Results We found significant constrictions of MMA (16.5%), STA (16.4%) and ICAextra (15.2%) ( p ≤ 0.001). Smaller, but statistically significant, constrictions were seen in MCA (5.5%) and BA (2.1%) ( p ≤ 0.012). ICAintra change 1.8% was not significant ( p = 0.179). The constriction of cerebral arteries was significantly smaller than the constriction of extracerebral arteries ( p < 0.000001). Conclusion Sumatriptan constricts extracerebral arteries more than cerebral arteries. We suggest that sumatriptan may exert its anti-migraine action outside of the blood–brain barrier.

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Dissertations / Theses on the topic "Cerebral arteries"

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Pierre, Lisa Natalie. "Endothelin receptors in human small coronary and cerebral arteries." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624843.

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Storer, Kingsley Paul School of Medicine UNSW. "Cerebral arteriovenous malformations: molecular biology and enhancement of radiosurgical treatment." Awarded by:University of New South Wales. School of Medicine, 2006. http://handle.unsw.edu.au/1959.4/31942.

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Object Rupture of intracranial arteriovenous malformations is a leading cause of stroke in children and young adults. Treatment options include surgery and highly focused radiation (stereotactic radiosurgery). For large and deep seated lesions, the risks of surgery may be prohibitively high, while radiosurgery has a disappointingly low efficacy and long latency. Radiosurgery carries the most promise for significant advances, however the process by which radiosurgery achieves obliteration is incompletely understood. Inflammation and thrombosis are likely to be important in the radiation response and may be amenable to pharmacological manipulation to improve radiosurgical efficacy. Materials and methods Immunohistochemistry and electron microscopy were used to study normal cerebral vessels, cavernous malformations and AVMs, some of which had previously been irradiated. An attempt was made to culture AVM endothelial cells to study the immediate response of AVM endothelium to radiosurgery. The effects of radiosurgery in a rat model of AVM were studied using immunohistochemistry and the results used to determine the choice of a pharmacological strategy to enhance the thrombotic effects of radiosurgery. Results Vascular malformations have a different endothelial inflammatory phenotype than normal cerebral vessels. Radiosurgery may cause long term changes in inflammatory molecule expression and leads to endothelial loss with exposure of pro-thrombotic molecules. Ultrastructural effects of irradiation include widespread cell loss, smooth muscle cell (SMC) proliferation and thrombosis. Endothelial culture from AVMs proved difficult due to SMC predominance in initial cultures. Radiosurgery upregulated several endothelial inflammatory molecules in the animal model and may induce pro-thrombotic cell membrane alterations. The administration of lipopolysaccharide and soluble tissue factor to rats following radiosurgery led to selective thrombosis of irradiated vessels. Conclusions Inflammation and thrombosis are important in the radiosurgical response of AVMs. Lumen obliteration appears to be mediated by proliferation of cells within the vessel wall and thrombosis. Upregulation of inflammatory molecules and perhaps disruption of the normal phospholipid asymmetry of the endothelial and SMC membranes are some of the earliest responses to radiosurgery. The alterations induced by radiation may be harnessed to selectively initiate thrombus formation. Stimulation of thrombosis may improve the efficacy of radiosurgery, increasing treatable lesion size and reducing latency.

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Corrêa, José Fernando Guedes. ""Dificuldades no tratamento microcirúrgico dos aneurismas gigantes e complexos da circulação anterior do polígono de Willis: proposta de escala técnica prognóstica"." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/5/5132/tde-27092005-145748/.

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Para desenvolver e avaliar a aplicabilidade de uma escala técnica prognostica das dificuldades no tratamento microcirúrgico dos aneurismas gigantes e complexos da circulação anterior do polígono de Willis, 50 lesões foram operadas. Um valor numérico foi dado a cada uma das 8 variáveis da escala. Somando-se os valores para cada variável, uma nota (de 1 a 14) foi obtida, para cada uma das 50 cirurgias. Dois grupos, portanto, foram definidos: cirurgia difícil (nota de 1 a 8) e cirurgia extremamente difícil (nota de 9 a 14). Foi feita análise estatística comparando-se os 2 grupos em relação a diversas variáveis demográficas e clínicas. Concluiu-se que a escala proposta é útil no planejamento pré-operatório, intra-operatório e prognóstico neste tipo de aneurisma
In order to develop and verify the applicability of a technical and prognostic scale of the difficulties in the microsurgical treatment of giant and complex aneurysms of the anterior circulation of the Cicle of Willis, 50 lesions were operated. A numeric amount was given for each of 8 variants of the scale. By adding each amount for each variant a score(from 1 to 14) was achieved, for each of the 50 surgeries. Two groups, therefore, were established: difficult surgery (scores from 1 to 8) and extremely difficult surgery (scores from 9 to 14). Statistical assessment comparing both groups in relation to several demographic and clinical variants was done. It was concluded that the proposed scale is useful in preoperative, intraoperative and prognostic planning in microsurgery for this kind of aneurysms

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Almeida, Lygia Maria de. "Sistematização das artérias da base do encéfalo, distribuição e territórios das artérias cerebrais rostral, média e caudal e da artéria mesencefálica na superfície do encéfalo em jacaré do papo-amarelo (Cayman latirostris)." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2010. http://hdl.handle.net/10183/22679.

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Foram utilizados 30 encéfalos de jacaré do papo-amarelo (Cayman latirostris), injetados com látex, corado em vermelho, com objetivo de sistematizar e descrever a distribuição e territórios das artérias carótidas internas e suas principais ramificações na superfície do encéfalo. As artérias carótidas internas apresentaram uma anastomose intercarótica e a artéria oftálmica interna. Na altura da hipófise estas se dividiram num ramo rostral e num curto ramo caudal, que continuou naturalmente como artéria cerebral caudal. O ramo rostral formou a rede da artéria cerebral média, a artéria cerebral rostral e a artéria comunicante rostral. A artéria cerebral caudal antes de penetrar na fissura transversa do cérebro emitiu o Iº ramo central, e em seu interior originou a artéria diencefálica, o IIº ramo central, ramos hemisféricos occipitais e a artéria pineal. Ao abandonar a fissura, a artéria cerebral caudal, curvou-se caudodorsalmente, emergindo no pólo occipital do hemisfério cerebral, projetou-se rostralmente, sagital a fissura longitudinal do cérebro como artéria interhemisférica. Esta lançou ramos hemisféricos convexos e hemisféricos mediais para as respectivas faces dos hemisférios cerebrais, e anastomosou-se com sua homóloga contralateral formando a artéria etmoidal comum, que se dividiu nas artérias etmoidais: direita e esquerda, as quais progrediram para as cavidades nasais, vascularizando-as. O curto ramo caudal emitiu sua porção de médio calibre, que lançou as artérias mesencefálica e cerebelar ventral rostral. Esta porção do ramo caudal anastomosou-se com seu homólogo contralateral formando a artéria basilar. A artéria basilar acompanhou a fissura mediana ventral da medula oblonga, e lançou as artérias cerebelares ventrais caudais e espinhais dorsais, e abandonou a cavidade craniana como artéria espinhal ventral. A artéria mesencefálica formou as artérias tectais, cerebelar dorsal rostral e cerebelar dorsal caudal. A artéria espinhal dorsal originou a artéria trigeminal. O círculo arterial cerebral apresentou-se fechado tanto rostral como caudalmente e o suprimento sanguíneo cerebral foi feito exclusivamente pelo sistema carótico.
It was utilized 30 brains of broad- snouted Cayman (Cayman latirostris), injected with red stained latex, aiming to systematize and describe the distribution and territories of the internal carotid arteries and their main branches on the surface of the brain. The internal carotid arteries showed an anastomosis intercarótica and internal ophthalmic artery. At the level of the hypophysis divided into a rostral branch and a short caudal branch, which continued naturally as caudal cerebral artery. The rostral branch formed a middle cerebral artery network, the rostral cerebral artery and the rostral communicating artery. The caudal cerebral artery before entering the cerebral transverse fissure gave of the Iº central branch and inside emitted the diencephalic artery, the IIº central branch, occipital hemispheric branches and the pineal artery. After leaving the cerebral transverse fissure, the caudal cerebral artery curved caudodorsalwards, emerging at the occipital pole of the cerebral hemisphere and projected rostrally sagittal to the cerebral longitudinal fissure, as interhemispheric artery. This gave off convex hemispheric branches and medial hemispheric branches of the same, and anastomosed with its contralateral homologous to form the common ethmoidal artery, which divided into the ethmoidal arteries: right and left, which progressed to the nasal cavities, vascularizing them. The short caudal branch gave off his portion of medium caliber, which originated the mesencephalic and ventral rostral cerebellar arteries. This portion of the caudal branch anastomosed with its contralateral homologous to form the basilar artery. The basilar artery accompanied the ventral median fissure of medulla oblongata, and emitted the ventral caudal cerebellar artery and dorsal spinal artery, and abandoned the cranial cavity as ventral spinal artery. The mesencephalic artery formed: the tectal, dorsal rostral cerebellar and dorsal caudal cerebellar arteries. The dorsal spinal artery originated a trigeminal artery. The cerebral arterial circle was rostral and caudally closed with cerebral blood supply provided, exclusively, by the carotid system.

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Hoiland, Ryan Leo. "Carbon dioxide mediated vasomotion of extra-cranial cerebral arteries : a role for prostaglandins?" Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54108.

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Cerebrovascular regulation during perturbations in arterial CO₂ is thought to occur solely at the level of the pial vessels. However, recent evidence implicates large extra-cranial cerebral blood vessels in this regulatory process. Although the mechanisms governing CO₂ mediated vasomotion remain unclear, animal and human studies support a large role of prostaglandins. Thus, we examined two hypotheses: 1) vasomotion of the internal carotid artery (ICA) would occur in response to both hyper and hypocapnia; and 2) pharmacological inhibition of prostaglandin synthesis with Indomethacin (INDO; a non-selective cyclooxygenase inhibitor) would reduce the vasomotor response of the ICA to changes in end-tidal PCO₂ (PETCO₂). Using a randomized single-blind placebo controlled study, subjects (n=10) were tested on two occasions. Before and 90-minutes following either oral INDO (1.2mg/kg) or placebo capsule, concurrent measures of beat-by-beat blood flow, velocity and diameter of the ICA were made at rest and during steady state stages (4 min) of iso-oxic hypercapnia (+3, +6, +9mmHg above baseline) and hypocapnia (-3, -6, -9mmHg below baseline). End-tidal forcing was employed for the control of blood gases. To examine if INDO affected ICA vasomotion in a cyclooxygenase inhibition independent manner, a subset of subjects (n=5) were tested before and 45-minutes following oral Ketorolac (0.25mg/kg). During pre-drug testing in the INDO trial, the ICA dilated during hypercapnia at +6mmHg (4.72±0.45 vs. 4.95±0.51mm; P<0.001) and +9mmHg (4.72±0.45 vs. 5.12±0.47mm; P<0.001), and constricted during hypocapnia at -6mmHg (4.95±0.33 vs. 4.88±0.27mm; P<0.05) and -9mmHg (4.95±0.33 vs. 4.82±0.27mm; P<0.001). Following INDO, dilation of the ICA was still observed at +6mmHg (4.50±0.54 vs. 4.57±0.52mm; P<0.05) and +9mmHg (4.50±0.54 vs. 4.61±0.50mm; P<0.01); however, INDO reduced the vasomotor responsiveness by 67±28% (0.045±0.015 vs. 0.015±0.012mm ⋅ mmHgPETCO₂-¹). In the Ketorolac condition, there was no effect of the drug on the vasomotor response to hyper or hypocapnia. We conclude that: 1) changes in PETCO₂ mediate vasomotion of the ICA, 2) inhibition of non-selective prostaglandin synthesis via INDO markedly reduces the vasomotor response to changes in PETCO₂; and 3) INDO may be acting via a mechanism(s) independent of cyclooxygenase inhibition to reduce CO₂ mediated vasomotion.
Graduate Studies, College of (Okanagan)
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Dhital, Kumud Kumar. "Perivascular innervation of cerebral arteries and vasa nervorum : changes in development and disease." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322304.

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Mathewson, Alastair Munro. "The modulation of no-mediated in porcine cerebral arteries by inducible nitric oxide synthase." Thesis, University of Strathclyde, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269936.

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Mughal, Amreen. "Regulation of Vascular Tone in Cerebral and Coronary Arteries by Apelin/APJ Receptor Mechanisms." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/27847.

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The peptide, apelin, is expressed in fat cells, endothelial cells, and CNS neurons. Increasing evidence (e.g. inotropic and vasomotor effects) supports a role for apelin in the regulation of the cardiovascular system. This research aimed to understand vascular effects of apelin and bridge gaps in the knowledge about apelin-induced effects on different vascular beds i.e. cerebral and coronary arteries. My first objective was to assess apelin-induced vascular effects in cerebral arteries. Based on current data, one could conclude that apelin by itself has no effects on vasomotor tone of cerebral arteries, but it does impair nitric oxide dependent relaxations of cerebral arteries, possibly by inhibiting functions of large conductance calcium activated potassium (BKCa) channels. Apelin increases coronary blood flow; however, the involved mechanism(s) has not yet been elucidated. Hence, my next aim was to determine the mechanism(s) involved in apelin-induced vascular effects. The results suggest that apelin causes endothelium APJ receptor dependent relaxation of coronary arteries, which is possibly mediated by nitric oxide dependent direct activation of BKCa channels. Interestingly, my results also suggest that pathways involved in apelin-induced coronary arteries relaxation are markedly different from another endothelium dependent vasodilator, acetylcholine. This research is the first to report that nitric oxide, generated in response to different stimuli, can likely activate more than one signaling pathways in coronary arteries. In my final aim, I determined effects of apelin on smooth muscle BKCa channel functions in coronary arteries. My data suggest that functionally active apelin-APJ signaling has no inhibitory effects on BKCa channel functions and does not inhibit nitric oxide-induced relaxations of coronary arteries. Possible reasons for difference in apelin response between cerebral and coronary arteries could be associated with differences in activation of G-proteins and PI3K signaling pathways between these two vascular beds. Altogether, this research provides an improved understanding about apelin-induced vascular effects in cerebral and coronary arteries, and highlights some key mechanistic differences in apelin-induced vascular effects between these two blood vessels. Moreover, this knowledge may have important therapeutic implications in future design and development of apelin analogs for treatment of cardiovascular diseases.
NIH National Heart, Lung and Blood Institute (HL124338)

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Miller, Alastair Leslie. "Investigation of the mechanisms underlying the myogenic response in resistance blood vessels from the rat cerebral vasculature." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322245.

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Sutherland, Brad Alexander, and n/a. "Heme oxygenase and the use of tin protoporphyrin in hypoxia-ischaemia-induced brain damage : mechanisms of action." University of Otago. Department of Pharmacology & Toxicology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090119.150318.

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Stroke is the third largest cause of death, and the leading cause of disability worldwide. Treatments are sought to reduce mortality, and increase survival time following an ischaemic stroke. Hypoxia-ischaemia (HI) is the combination of cerebral ischaemia and global hypoxia that can lead to neuronal damage, particularly perinatally. The complex neurodegenerative cascade following ischaemic stroke and HI activates many stress pathways, including heme oxygenase (HO). HO metabolises free heme to release iron, carbon monoxide, and biliverdin, which is subsequently metabolised to bilirubin. This thesis aims to elucidate the role HO plays following HI, and assess any neuroprotective mechanisms using HO modulators. The 26 day old rat model of HI was used to induce the neurodegenerative cascade. All animals were sacrificed 3 days post-insult. Immunohistochemistry and Western blotting demonstrated that HO-1 was increased in the ipsilateral hemisphere of both HI (by 1.7 � 0.1 fold: p = 0.016, n = 4) and middle cerebral artery occlusion (MCAO) brains (by 1.6 � 0.1 fold: p = 0.037, n = 4), compared to controls. HO-2 was constitutively expressed throughout the control brain, but HI upregulated HO-2 expression (by 1.7 � 0.2 fold: p = 0.027, n = 4) ipsilaterally, whereas MCAO did not alter HO-2 expression. Administration of the HO inhibitor tin protoporphyrin (SnPP; 30[mu]mol/kg intraperitoneally) daily, beginning 1 day prior to HI until sacrifice, reduced infarct volume to 50% � 10 of saline-treated animals (p = 0.039, n = 6-8). The HO inducer ferriprotoporphyrin (FePP; 30[mu]mol/kg) had no effect on infarct volume. HO activity and protein expression were not significantly altered following treatment with SnPP. Therefore, the neuroprotective actions of SnPP may be through alternative mechanisms. SnPP treatment increased HI + saline-induced total nitric oxide synthase (NOS) activity by 1.5 � 0.06 fold (p < 0.001, n = 6-8). Conversely, SnPP inhibited both inducible NOS (50% � 7 of HI + saline; p = 0.045, n = 7-8) and cyclooxygenase (COX) activity (32% � 6 of HI + saline; p = 0.049, n = 4-8). SnPP treatment also increased mitochondrial complex I activity by 1.6 � 0.25 fold (p = 0.04, n = 4-8) and complex V activity by 1.7 � 0.26 fold (p = 0.046, n = 4-8) in the ipsilateral hemisphere. It appears that SnPP is acting on inflammatory and mitochondrial enzymes to produce neuroprotection. In vitro analysis of cultured RAW264.7 macrophages exposed to lipopolysaccharide (LPS; 10[mu]g/mL) treated with SnPP (dose range: 10⁻�⁰M - 10⁻⁵M) did not alter nitrite levels or cell viability. However, high dose SnPP (10⁻⁵M) in the absence of LPS increased nitrite levels from control cells by 2.7 � 0.7 fold (p = 0.043, n = 6), complementing the in vivo total NOS data. Other mechanisms such as NMDA receptor activation were not affected by 100[mu]M SnPP or 100[mu]M SnCl₂ in patch clamped cortical pyramidal neurons. Overall, the role that HO plays following HI remains unclear, but this thesis provides definitive evidence that SnPP (an established HO inhibitor) provides neuroprotection. This neuroprotection may be due to its effects on inducible pathways such as NOS and COX. Therefore, further experimentation is required to fully elucidate the role that HO plays following cerebral ischaemia, and additional in vivo evidence will be necessary to establish HO inhibitors as a putative candidate for cerebral ischaemia neuroprotection.

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Books on the topic "Cerebral arteries"

1

Robert, Courbier, ed. Basis for a classification of cerebral arterial diseases: Proceedings of a symposium held in Marseilles, 28-29 September 1984. Amsterdam: Excerpta Medica, 1985.

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W, Baumgartner R., ed. Handbook on cerebral artery dissection. Basel: Karger, 2005.

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Berguer, Ramon. Surgery of the arteries to the head. New York: Springer-Verlag, 1992.

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Takahashi, Shōki. Neurovascular imaging: MRI & microangiography. Dordrecht: Springer, 2010.

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K, Perktold, ed. Computer Simulation lokaler arterieller Strömungsformen unter besonderer Beachtung der cerebralen Gefässe. Graz: Forschungsgesellschaft Joanneum, 1987.

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Hajime, Handa, Kikuchi Haruhiko, Yonekawa Yasuhiro 1939-, and International Symposium on Microvascular Anastomoses for Cerebral Ischemia (6th : 1982 : Kyoto, Japan), eds. Microsurgical anastomoses for cerebral ischemia. New York: Igaku-Shoin, 1985.

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Noé, Battistini, ed. Acute brain ischemia: Medical and surgical therapy. New York: Raven Press, 1986.

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U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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U, Sliwka, and United States. National Aeronautics and Space Administration., eds. Effects of sustained low-level elevations of carbon dioxide on cerebral blood flow and autoregulation of the intracerebral arteries in humans. [Washington, DC: National Aeronautics and Space Administration, 1996.

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N, Tulenko Thomas, and Cox Robert H, eds. Recent advances in arterial diseases: Atherosclerosis, hypertension, and vasospasm : proceedings of the A.N. Richards Symposium, held in Philadelphia, Pennsylvania, May 10-11, 1984. New York: Liss, 1986.

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Book chapters on the topic "Cerebral arteries"

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Schäberle, Wilhelm. "Extracranial Cerebral Arteries." In Ultrasonography in Vascular Diagnosis, 291–375. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02509-9_5.

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Schäberle, Wilhelm. "Extracranial Cerebral Arteries." In Ultrasonography in Vascular Diagnosis, 291–387. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-64997-9_5.

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Hacke, Werner, Herman J. Gelmers, Michael Hennerici, and Günter Krämer. "Applied Anatomy of the Cerebral Arteries." In Cerebral Ischemia, 1–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75548-4_1.

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Antochi, Florina, and Athena Mergeani. "Cervico-cerebral Arteries Dissection." In Arterial Revascularization of the Head and Neck, 301–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-34193-4_14.

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Bradac, Gianni Boris. "Spontaneous Dissection of Carotid and Vertebral Arteries." In Cerebral Angiography, 289–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54404-0_16.

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Bradac, Gianni Boris. "Spontaneous Dissection of Carotid and Vertebral Arteries." In Cerebral Angiography, 255–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-15678-6_16.

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Widder, Bernhard, and Gerhard F. Hamann. "Cerebral Vasospasms." In Duplex sonography of the brain-supplying arteries, 263–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-65566-5_22.

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Bradac, Gianni Boris. "Aortic Arch and Origin of the Cranial Cerebral Arteries." In Cerebral Angiography, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54404-0_1.

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Bradac, Gianni Boris. "Aortic Arch and Origin of the Cranial Cerebral Arteries." In Cerebral Angiography, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-15678-6_1.

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Bradac, Gianni Boris. "Spontaneous Dissection of Carotid and Vertebral Arteries." In Applied Cerebral Angiography, 371–92. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57228-4_16.

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Conference papers on the topic "Cerebral arteries"

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Fonck, E., G. G. Feigl, J. Fasel, D. Sage, M. Unser, D. A. Rüfenacht, and N. Stergiopulos. "Effect of Ageing on Elastin Functionality in Human Cerebral Arteries." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192727.

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The ageing process affects elastin, a key component of the arterial wall integrity and functionality. Elastin may play an important role in cerebral vessels because elastin degradation is linked to cerebrovascular disease [1]. The goal of this study is to assess the biomechanical properties of human cerebral arteries, their composition and geometry, with particular focus on the functional alterations of elastin in cerebral arteries due to ageing.

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Fabbri, Dario, Quan Long, Saroj Das, and Michele Pinelli. "Study of Embolic Particle Migration in Cerebral Arteries by Computational Modelling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80314.

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As known, embolism is one of the major causes of stroke, which represents the rapid loss of brain functions. Two major sources of emboli which may cause ischemic attack were emboli formed in heart and from a ruptured arterial plaque in carotid arties. Due to the different characteristics of emboli formed from different mechanisms, the migration route of specific emboli in cerebral arteries may be different, so does the territory of the ischemic attack caused by them. Therefore, a good understanding of emboli migration in the complex cerebral arterial network may provide a good guidance for the diagnosis and treatment of stroke. Studies on the emboli motion in cerebral arteries so far were based on phantom models [1]. Although CFD simulation has been used on prediction of cerebral blood perfusion for many years, CFD particle tracking technique is rarely applied on study emboli migration in cerebral arteries. The present study aims to demonstrate the feasibility of using CFD particle tracking on emboli migration study with emphasis on the discussions of the particle tracking result by different coupling algorithms between blood flow and embolic particles.

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Jin, Kazuyoshi, Ko Kitamura, Shunji Mugikura, Naoko Mori, Makoto Ohta, and Hitomi Anzai. "Evaluation of Normalization Methods in a Cerebral Artery Atlas for Automatic Labeling." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-71097.

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Abstract An existence probability atlas has been used for automatic labeling of cerebral arteries. However, the number of arteries varies frequently because of image quality and individual variation of the artery structure. To moderate the influence of number imbalance on labeling accuracy, we propose a new normalized atlas for automatic labeling of cerebral artery centerlines. The number of arteries, which was obtained from magnetic resonance angiography, varies from 11 to 46 among the artery sites. Based on the centerline and diameter, the arterial volume was reconstructed into a voxel space for each subject. After superimposing arteries from 46 subjects, three normalization methods were compared: dividing by the number of subjects (N), by N and the arterial length (L), and by N and the arterial volume (V). To compare the labeling accuracy and precision, the summation of probability and labeling method was also used. The accuracy of all normalization methods was > 85% in all arteries. The precision improved in some parts, with the atlas normalized by N-L and by N-V. The use of N-L and N-V changed the relative value of the existence probability among the parts. Consequently, some normalization methods changed the tendency toward misclassification, which changed the precision.

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Northcutt, Avione, and Hai-Chao Han. "Finite Element Analysis of Buckling of Arteries With Aneurysms." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206275.

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Tortuosity of arteries occurs when a normally straight artery starts to take on a twisted path. This is often referred to as tortuosity and kinking of arteries. This phenomenon occurs in arteries throughout the body including the aorta and cerebral [1, 2]. Arterial tortuosity is a potentially dangerous condition that can lead to cerebrovascular symptoms, ischemia, and stroke [3].

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Harazawa, M., and T. Yamaguchi. "Computational Fluid Dynamics Simulation of the Blood Flow in the Circle of Willis." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32516.

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The blood supply for the brain is born by four arteries, that is, two internal carotid arteries and two vertebral arteries. They are mutually connected at the cerebral base, and form a closed arterial circle, called the circle of Willis, so that the safety of the brain blood supply is increased. However their anastomoses show a very wide variety of atypism. If some of anastomses are very thin, or even do not exist, the safety of the blood supply is not secured. This is particularly important when some diseases such as cerebral thrombosis occurs and the blood flow supply stops unilaterally. Redistribution of the blood supply in such cases is thought to be strongly affected by geometrical configuration of the anastomoses. It is also known that cerebral aneurysms, which may induce serious cerebrovascular diseases, preferentially occur at the circle of Willis. Complex blood flow pattern has been suspected of having an influence on this preference. This is again dependent on complex geometry of the circle.

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Zhu, Guangyu, Qi Yuan, and Joon Hock Yeo. "Experimental Study of Hemodynamics in the Circle of Willis." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14162.

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The Circle of Willis (CoW) is a ring like structure located at the base of brain, which is composed of a single anterior communicating artery (ACoA), paired anterior cerebral arteries (ACAs), paired internal carotid arteries (ICAs), paired posterior communicating arteries (PCoAs), paired posterior cerebral arteries (PCAs), paired vertebral arteries (VAs) and a single basilar artery (BA). It is the main cerebral blood perfusion pathway and provides an important collateral channel in patients with severe carotid or vertebral artery disease. Over 50% of stroke cases are related to the stenosis of arteries in the CoW, so the detailed information of the cerebral hemodynamics under different pathology situations is important for a variety of clinical applications. Numerous experimental studies have been performed on this field from different perspectives, include the mechanism of stenosis in the CoW [1], risk assessment of cerebral aneurysm [2] and the impact of pathological variations on the flow distribution [3]. However, none of these researches focus on the influence of ICA stenosis rates on cerebral perfusion and the specific collateral mechanism of the Circle of Willis under such situations. In this paper, an experimental study on cerebral blood perfusion and the collateral mechanism under a series of ICA stenosis rates was carried out.

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Yuan, Qi, Zhen Chen, and Guangyu Zhu. "Blood Flow Dynamic and Fluid-Structure Interaction in Patient-Specific Circle of Willis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206230.

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Over 50% stroke is related to the cerebral artery stenosis. The most common position is in the Circle of Willis (CoW), which is composed of a single anterior communicating artery (ACoA), paired anterior cerebral arteries (ACA), paired middle cerebral arteries (MCA), internal carotid arteries (ICA), posterior communicating arteries (PCoA) and posterior cerebral arteries (PCA). Detailed knowledge of the cerebral hemodynamics is important for a variety of clinical applications [1]. There has been a significant body of research performed on blood flow in the CoW [1,2] treating the cerebral vasculature as a 2D structure. To obtain more accurate hemodynamic results, 3D models should be considered. Studies have been performed on 3D models of the CoW generated from magnetic resonance imaging (MRI) data [3,4]. However, those 3D models neglected the effects of fluid-structure interaction (FSI) between the vessel wall and blood. In this paper, a patient-specific model of CoW from CT scan data was reconstructed and FLUENT 6.1 was used to simulate the blood flow in the CoW. On a special part of CoW, a 3D FSI model for the arteries was introduced to investigate both flow and structure behaviors, as well as their interaction by ADINA 8.3.

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Reymond, Philippe, Fabrice Merenda, Fabienne Perren, Daniel Rüfenacht, and Nikos Stergiopulos. "Validation of 1D Model of the Systemic Arterial Tree Including the Cerebral Circulation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192529.

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The aim of this study is to develop a distributed model of the entire systemic arterial tree, coupled to a heart model and including a detailed description of the cerebral arteries. Distributed models of the arterial tree have been studied extensively in the past (Avolio [1], Stergiopulos et al [2], Westerhof et al [3]), however, no model has been developed so far that offers a physiologically relevant coupling to the heart and includes the entire cerebral arterial tree.

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Reymond, Philippe, Fabrice Merenda, Fabienne Perren, Daniel Rüfenacht, and Nikos Stergiopulos. "One Dimensional Model of the Systemic Arterial Tree Including Cerebral Circulation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176452.

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The aim of this study is to develop a distributed model of the entire systemic arterial tree, coupled to a heart model and including a detailed description of the cerebral arteries. Distributed models of the arterial tree have been studied extensively in the past (Avolio [1]; Cassot et al [2]; Meister [3]; Schaaf and Abbrecht [4]; Stergiopulos et al [5]; Westerhof et al [6]; Zagzoule and Marc-Vergnes [7]), however, no model has been developed so far that offers a physiologically relevant coupling to the heart and includes the entire cerebral artery network.

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Fonck, E., G. Feigl, L. Augsburger, D. A. Rüfenacht, and N. Stergiopulos. "Structural Properties of Human Cerebral Arteries as Assessed by a Constituent-Based Biomechanical Model." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176122.

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Human cerebral arteries may develop aneurysms, as a result of geometrical and structural modifications in the arterial wall resulting from a variety of genetic, epigenetic and biomechanical factors. Aneurysms exhibit a markedly different wall composition and structure, characterized by relatively low elastin content as shown in Figure 1.

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Reports on the topic "Cerebral arteries"

1

Alshammari, Mohammed Kanan. Efficacy of Complementary and Alternative Medicine in Peripheral Arterial Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0001.

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Review question / Objective: To explore various CAM therapies available and to generate evidence that these therapies are effective for managing the disease. Condition being studied: Peripheral arterial disease (PAD) is described as the atherosclerotic process of arteries other than cerebral and coronary arteries i.e. the abdominal aorta, iliac, and arteries of the lower limb which leads to the narrowing and blocking of arteries. Information sources: An online systematic literature search will be done from the time of database inception from 5 electronic databases namely PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Ovid SP, ISI Web of Science, Elsevier Science Direct, and Wiley Online Library.

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