Journal articles on the topic 'Cerebral arteries'
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1
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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Aydin, A., S. Yilmaz, Z. E. Ozkan, and R. Ilgun. "The morphology of the circulus arteriosus cerebri in the ground squirrel (Spermophilus citellus)." Veterinární Medicína 54, No. 11 (December 23, 2009): 537–42. http://dx.doi.org/10.17221/162/2009-vetmed.
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In this study, the circulus arteriosus cerebri of the ground squirrel (<i>Spermophilus citellus</i>) was investigated. Five ground squirrels were used as subjects. Coloured latex was injected from the left ventriculi of the hearts of all the squirrels. When the vertebral arteries of two of the animals were ligatured, it was found that there was no internal carotid artery. After careful dissection, the circulus arteriosus cerebri (the circle of Willis) was investigated. The right and left vertebral arteries gave rise to the caudal cerebellar artery before forming the basilar artery. The basilar artery formed the caudal communicans artery that was the caudal part of the circulus arteriosus cerebri on the pontocrural groove (sulcus pontocruralis). The caudal, medial, rostral cerebellar, the common root formed by the caudal cerebral and choroid arteries, the rostral choroid, the rostral and medial cerebral arteries arose from the vertebral, basilar and caudal communicans arteries and dispersed to the cerebrum and cerebellum from caudal to cranial. The termination and the branches of the rostral cerebral artery in ground squirrels varied. It was observed that the internal carotid artery does not supply the circulus arteriosus cerebri in ground squirrels.
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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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García Pisón, Joaquín, Matías Negrotto, Alejandra Garretano, Andrés Pouy, Carolina Fernández, and Eduardo Olivera. "RARE TRIPLE ANATOMICAL VARIATION OF THE CEREBRAL ARTERIAL CIRCLE; Rara triple variación del círculo arterial cerebral." Revista Argentina de Anatomía Clínica 9, no. 1 (April 10, 2017): 18–23. http://dx.doi.org/10.31051/1852.8023.v9.n1.15416.
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Se reporta la rara asociación de un aneurisma de arteria trigeminal persistente lateral derecha (Tipo II de Saltzman), aplasia del segmento pre-comunicante de ambas arterias cerebrales posteriores y la presencia de arterias cerebrales posteriores fetales en forma bilateral, en una mujer de 64 años que consultó de diplopía y parálisis del nervio abducens derecho, probablemente debida a compresión del nervio en el espacio latero-celar. Se realizó con éxito la embolización endovascular con coils, sin complicaciones inmediatas. Los hallazgos de CT, RM y angiografía son presentados. Aunque cada una de estas variaciones son infrecuentes en forma individual, la combinación de las mismas no ha sido reportada en la literatura hasta nuestro conocimiento, siendo de enorme importancia en el manejo diagnóstico y terapéutico de pacientes con stroke de mecanismo embolico, así como para la planificación de procedimientos endovasculares diagnósticos y terapéuticos. We report the rare association of an aneurysm of a lateral right persistent trigeminal artery (Saltzman type II), bilateral aplasia of the pre-communicating segment of both posterior cerebral arteries and bilateral fetal posterior cerebral arteries, in a 64 years old woman who suffered from progressive diplopia and right abducens nerve palsy, most likely due to nerve compression in the latero-cellar space. Successful endovascular coils embolization of the aneurysm was performed, with no immediate complications. CT, MR and angiographic findings are presented. Although infrequent as single variations, the association of these three arterial variations has not been reported in literature to our knowledge, having special importance in the diagnostic workup and therapeutic procedures in a patient with an embolic stroke, as well as in the planification of intracranial endovascular diagnostic and therapeutic procedures.
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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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Zarrinkoob, Laleh, Khalid Ambarki, Anders Wåhlin, Richard Birgander, Bo Carlberg, Anders Eklund, and Jan Malm. "Aging alters the dampening of pulsatile blood flow in cerebral arteries." Journal of Cerebral Blood Flow & Metabolism 36, no. 9 (July 20, 2016): 1519–27. http://dx.doi.org/10.1177/0271678x16629486.
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Excessive pulsatile flow caused by aortic stiffness is thought to be a contributing factor for several cerebrovascular diseases. The main purpose of this study was to describe the dampening of the pulsatile flow from the proximal to the distal cerebral arteries, the effect of aging and sex, and its correlation to aortic stiffness. Forty-five healthy elderly (mean age 71 years) and 49 healthy young (mean age 25 years) were included. Phase-contrast magnetic resonance imaging was used for measuring blood flow pulsatility index and dampening factor (proximal artery pulsatility index/distal artery pulsatility index) in 21 cerebral and extra-cerebral arteries. Aortic stiffness was measured as aortic pulse wave velocity. Cerebral arterial pulsatility index increased due to aging and this was more pronounced in distal segments of cerebral arteries. There was no difference in pulsatility index between women and men. Dampening of pulsatility index was observed in all cerebral arteries in both age groups but was significantly higher in young subjects than in elderly. Pulse wave velocity was not correlated with cerebral arterial pulsatility index. The increased pulsatile flow in elderly together with reduced dampening supports the pulse wave encephalopathy theory, since it implies that a higher pulsatile flow is reaching distal arterial segments in older subjects.
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Löhn, Matthias, Dietmar Kämpf, Chai Gui-Xuan, Hermann Haller, Friedrich C. Luft, and Maik Gollasch. "Regulation of arterial tone by smooth muscle myosin type II." American Journal of Physiology-Cell Physiology 283, no. 5 (November 1, 2002): C1383—C1389. http://dx.doi.org/10.1152/ajpcell.01369.2000.
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The initiation of contractile force in arterial smooth muscle (SM) is believed to be regulated by the intracellular Ca2+concentration and SM myosin type II phosphorylation. We tested the hypothesis that SM myosin type II operates as a molecular motor protein in electromechanical, but not in protein kinase C (PKC)-induced, contraction of small resistance-sized cerebral arteries. We utilized a SM type II myosin heavy chain (MHC) knockout mouse model and measured arterial wall Ca2+ concentration ([Ca2+]i) and the diameter of pressurized cerebral arteries (30–100 μm) by means of digital fluorescence video imaging. Intravasal pressure elevation caused a graded [Ca2+]i increase and constricted cerebral arteries of neonatal wild-type mice by 20–30%. In contrast, intravasal pressure elevation caused a graded increase of [Ca2+]i without constriction in (−/−) MHC-deficient arteries. KCl (60 mM) induced a further [Ca2+]i increase but failed to induce vasoconstriction of (−/−) MHC-deficient cerebral arteries. Activation of PKC by phorbol ester (phorbol 12-myristate 13-acetate, 100 nM) induced a strong, sustained constriction of (−/−) MHC-deficient cerebral arteries without changing [Ca2+]i. These results demonstrate a major role for SM type II myosin in the development of myogenic tone and Ca2+-dependent constriction of resistance-sized cerebral arteries. In contrast, the sustained contractile response did not depend on myosin and intracellular Ca2+ but instead depended on PKC. We suggest that SM myosin type II operates as a molecular motor protein in the development of myogenic tone but not in pharmacomechanical coupling by PKC in cerebral arteries. Thus PKC-dependent phosphorylation of cytoskeletal proteins may be responsible for sustained contraction in vascular SM.
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Geary, Greg G., John N. Buchholz, and William J. Pearce. "Maturation depresses mouse cerebrovascular tone through endothelium-dependent mechanisms." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 3 (March 1, 2003): R734—R741. http://dx.doi.org/10.1152/ajpregu.00510.2002.
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In light of previous observations that the range of arterial pressures over which cerebral blood flow is autoregulated differs dramatically in neonates and adults, the present experiments explored the hypothesis that pressure-induced intrinsic arterial tone is regulated differently in neonatal and adult cerebral arteries. In cannulated and pressurized endothelium-intact mouse cerebral arteries <150 μm in diameter, active intrinsic tone was evident at intraluminal pressures as low as 10 mmHg in neonatal arteries, but only at pressures of 60 mmHg or greater in adult arteries. Administration of 10 μM indomethacin produced no significant effect on tone at any pressure in either neonatal or adult arteries, but subsequent addition of 100 μM nitroarginine methyl ester (NAME) significantly vasoconstricted both neonatal and adult arteries at all pressures. Conversely, administration of 100 μM NAME alone significantly vasoconstricted adult arteries only, and subsequent addition of 10 μM indomethacin produced a significant additional vasoconstriction in adult arteries only, indicating an important interaction between the nitric oxide synthase and cyclooxygenase pathways, at least in adult arteries. In the presence of both indomethacin and NAME, intrinsic tone was significantly greater in neonatal than adult arteries, but when the endothelium was removed, tone was similar in neonatal and adult arteries at all pressures. Together, these results suggest that pressure-induced myogenic tone is regulated similarly in neonatal and adult mouse cerebral arteries but that the contribution of endothelial vasoactive factors to intrinsic tone is highly age dependent.
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Dizdarević, Kemal. "The Role of Nitric Oxide in Resolution of Vasospasam Corresponding with Cerebral Vasospasms after Subarachnoid Haemorrhage: Animal Model." Bosnian Journal of Basic Medical Sciences 8, no. 2 (May 20, 2008): 177–82. http://dx.doi.org/10.17305/bjbms.2008.2978.
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Intracranial aneurysmal rupture is the common cause of spontaneous subarachnoid haemorrhage (SAH). This haemorrhage is typically diffuse and located in extracerebral subarachnoid space in which main cerebral arterial branches are situated. The intimate and long-term contact of arterial wall and blood products in the closed space causes the cerebral vasospasm as a serious and frequent complication of SAH. It is connected with significant morbidity and mortality due to developing of focal cerebral ischaemia and subsequently cerebral infarction. The aim of our experimental research was to create the animal model of vasospasm using the femoral artery due to examination of reduced basic dilator activity cause in arterial wall after SAH. The important characteristic of major cerebral arteries is their localization in the closed subarachnoid space which enables their to have long-term contact with blood products after haemorrhage. Thirty six femoral arteries (FA) of eighteen female rats weighing about 300 g were used. In vivo, femoral arteries are microsurgically prepared in both inguinal regions in all rats. Eighteen arteries were encompassed by polytetrafluoroethylene (PTFE) material forming closed tube and autologous blood was injected in the tube around the arterial wall. Additional eighteen arteries, as a control group, were also put in PTFE tube but without exposing to the blood. All rats are left to live for eight days. Afterwards, rats were sacrificed and their arteries were in vitro examined including an isometric tension measurement and histological changes analysis. The tension was measured during application of vasoconstrictors and vasodilatators (nitric oxide, NO). FA exposed to periadventitial blood exhibit hyper reactivity to constrictors (KCl, phenylephrine, acetylcholine) compared to control group. It was also found that NO donor (sodium nitroprusside) diminished arterial spasm induced by blood and vasoconstrictors. In conclusion, FA can be used as a model for vasospasm correlating with cerebral vasospasm after SAH and therefore this model can be utilized in future experiments assessing cerebral vasospasm. The reduced basic dilator activity of spastic femoral artery is caused by an absence of gaseous messenger NO next to the arteries but not by diminished response vasculature to NO. Absence of NO after SAH probably causes the reduced basic dilator activity of cerebral arteries as well. The guanylate-cyclase level in the arterial wall is consequently reduced after SAH primary due to absence of NO but not due to direct reduction of enzyme activities caused by process of blood degradation inside of subarachnoid space.
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Han, Jin, Nari Kim, Hyun Joo, and Euiyong Kim. "Ketamine blocks Ca2+-activated K+ channels in rabbit cerebral arterial smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H1347—H1355. http://dx.doi.org/10.1152/ajpheart.00194.2003.
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Although ketamine and Ca2+-activated K+ (KCa) channels have been implicated in the contractile activity regulation of cerebral arteries, no studies have addressed the specific interactions between ketamine and the KCa channels in cerebral arteries. The purpose of this study was to examine the direct effects of ketamine on KCa channel activities using the patch-clamp technique in single-cell preparations of rabbit middle cerebral arterial smooth muscle. We tested the hypothesis that ketamine modulates the KCa channel activity of the cerebral arterial smooth muscle cells of the rabbit. Vascular myocytes were isolated from rabbit middle cerebral arteries using enzymatic dissociation. Single KCa channel activities of smooth muscle cells from rabbit cerebral arteries were recorded using the patch-clamp technique. In the inside-out patches, ketamine in the micromolar range inhibited channel activity with a half-maximal inhibition of the ketamine conentration value of 83.8 ± 12.9 μM. The Hill coefficient was 1.2 ± 0.3. The slope conductance of the current-voltage relationship was 320.1 ± 2.0 pS between 0 and +60 mV in the presence of ketamine and symmetrical 145 mM K+. Ketamine had little effect on either the voltage-dependency or open- and closed-time histograms of KCa channel. The present study clearly demonstrates that ketamine inhibits KCa channel activities in rabbit middle cerebral arterial smooth muscle cells. This inhibition of KCa channels may represent a mechanism for ketamine-induced cerebral vasoconstriction.
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Badhwar, AmanPreet, Danica B. Stanimirovic, Edith Hamel, and Arsalan S. Haqqani. "The Proteome of Mouse Cerebral Arteries." Journal of Cerebral Blood Flow & Metabolism 34, no. 6 (March 26, 2014): 1033–46. http://dx.doi.org/10.1038/jcbfm.2014.52.
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The cerebral vasculature ensures proper cerebral function by transporting oxygen, nutrients, and other substances to the brain. Distribution of oxygenated blood throughout the neuroaxis takes place at the level of the circle of Willis (CW). While morphologic and functional alterations in CW arteries and its main branches have been reported in cerebrovascular and neurodegenerative diseases, accompanying changes in protein expression profiles remain largely uncharacterized. In this study, we performed proteomics to compile a novel list of proteins present in mouse CW arteries and its ramifications. Circle of Willis arteries were surgically removed from 6-month-old wild-type mice, proteins extracted and analyzed by two proteomics approaches, gel-free nanoLC-mass spectrometry (MS)/MS and gel-based GelLC-MS/MS, using nanoAcquity UPLC coupled with ESI-LTQ Orbitrap XL. The two approaches helped maximize arterial proteome coverage. Six biologic and two technical replicates were performed. In all, 2,188 proteins with at least 2 unique high-scoring peptides were identified (6,630 proteins total). Proteins were classified according to vasoactivity, blood–brain barrier specificity, tight junction and adhesion molecules, membrane transporters/channels, and extracellular matrix/basal lamina proteins. Furthermore, we compared the identified CW arterial proteome with the published brain microvascular proteome. Our database provides a vital resource for the study of CW cerebral arterial protein expression profiles in health and disease.
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Tamaki, K., W. Mayhan, and D. Heistad. "Effects of vasodilator stimuli on resistance of large and small cerebral vessels." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 6 (December 1, 1986): H1176—H1182. http://dx.doi.org/10.1152/ajpheart.1986.251.6.h1176.
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We have examined effects of vasodilator stimuli on segmental resistance in the cerebral circulation. Our hypothesis was that resistance of large arteries, as well as small vessels, contributes to cerebral vascular responses to vasodilator stimuli. We measured cerebral blood flow with microspheres in anesthetized rabbits and measured pressure in pial arteries approximately 100 microns diameter using a servo-null method. These values were used to calculate resistance of large arteries (greater than 100 microns diameter) and small vessels (less than 100 microns diameter). Under control conditions, resistance of large arteries accounted for one-third to one-half of total cerebral vascular resistance. Intracarotid infusion of acetylcholine (1 microgram/min) reduced large arterial resistance by 69% and small vessel resistance by 58%. Adenosine also produced marked reductions in resistance of both large and small cerebral vessels. In contrast, seizures reduced large arterial resistance by 50% and small vessel resistance by 85%. Pial arterial pressure, which depends on the ratio of large and small vessel resistance, increased during infusion of acetylcholine and adenosine, but decreased during seizures. We conclude that both large and small cerebral vessels are responsive to acetylcholine and adenosine, and seizures produce preferential reduction in resistance of small vessels.
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Harraz, Osama F., Frank Visser, Suzanne E. Brett, Daniel Goldman, Anil Zechariah, Ahmed M. Hashad, Bijoy K. Menon, Tim Watson, Yves Starreveld, and Donald G. Welsh. "CaV1.2/CaV3.x channels mediate divergent vasomotor responses in human cerebral arteries." Journal of General Physiology 145, no. 5 (April 27, 2015): 405–18. http://dx.doi.org/10.1085/jgp.201511361.
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The regulation of arterial tone is critical in the spatial and temporal control of cerebral blood flow. Voltage-gated Ca2+ (CaV) channels are key regulators of excitation–contraction coupling in arterial smooth muscle, and thereby of arterial tone. Although L- and T-type CaV channels have been identified in rodent smooth muscle, little is known about the expression and function of specific CaV subtypes in human arteries. Here, we determined which CaV subtypes are present in human cerebral arteries and defined their roles in determining arterial tone. Quantitative polymerase chain reaction and Western blot analysis, respectively, identified mRNA and protein for L- and T-type channels in smooth muscle of cerebral arteries harvested from patients undergoing resection surgery. Analogous to rodents, CaV1.2 (L-type) and CaV3.2 (T-type) α1 subunits were expressed in human cerebral arterial smooth muscle; intriguingly, the CaV3.1 (T-type) subtype present in rodents was replaced with a different T-type isoform, CaV3.3, in humans. Using established pharmacological and electrophysiological tools, we separated and characterized the unique profiles of Ca2+ channel subtypes. Pressurized vessel myography identified a key role for CaV1.2 and CaV3.3 channels in mediating cerebral arterial constriction, with the former and latter predominating at higher and lower intraluminal pressures, respectively. In contrast, CaV3.2 antagonized arterial tone through downstream regulation of the large-conductance Ca2+-activated K+ channel. Computational analysis indicated that each Ca2+ channel subtype will uniquely contribute to the dynamic regulation of cerebral blood flow. In conclusion, this study documents the expression of three distinct Ca2+ channel subtypes in human cerebral arteries and further shows how they act together to orchestrate arterial tone.
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Wellman, G. C., L. Cartin, D. M. Eckman, A. S. Stevenson, C. M. Saundry, W. J. Lederer, and M. T. Nelson. "Membrane depolarization, elevated Ca2+ entry, and gene expression in cerebral arteries of hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 6 (December 1, 2001): H2559—H2567. http://dx.doi.org/10.1152/ajpheart.2001.281.6.h2559.
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Elevated intracellular Ca2+([Ca2+]i) has been implicated in contractile and phenotypic changes in arterial smooth muscle during hypertension. This study examined the role of membrane potential and [Ca2+]i in altered gene expression in cerebral arteries of a rat (Dahl) genetic model of salt-sensitive hypertension. Cerebral arteries from hypertensive animals (Dahl salt-sensitive) exhibited a tonic membrane depolarization of ∼15 mV compared with normotensive (Dahl salt-resistant) animals. Consistent with this membrane depolarization, voltage-dependent K+currents were decreased in cerebral artery myocytes isolated from hypertensive animals. Arterial wall Ca2+ was elevated in cerebral arteries from hypertensive animals, an effect reversed by diltiazem, a blocker of voltage-dependent Ca2+ channels. This depolarization-induced increase in [Ca2+]i was associated with increased activation of the transcription factor, cAMP response element binding protein, and increased expression of the immediate early gene c-fos, both of which are reversed by acute exposure to the voltage-dependent Ca2+ channel blocker nisoldipine. This study provides the first information linking altered Ca2+handling to changes in gene expression in cerebral arteries during hypertension.
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Goyal, Ravi, Ashwani Mittal, Nina Chu, Lijun Shi, Lubo Zhang, and Lawrence D. Longo. "Maturation and the role of PKC-mediated contractility in ovine cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 6 (December 2009): H2242—H2252. http://dx.doi.org/10.1152/ajpheart.00681.2009.
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Ca2+-independent pathways such as protein kinase C (PKC), extracellular-regulated kinases 1 and 2 (ERK1/2), and Rho kinase 1 and 2 (ROCK1/2) play important roles in modulating cerebral vascular tone. Because the roles of these kinases vary with maturational age, we tested the hypothesis that PKC differentially regulates the Ca2+-independent pathways and their effects on cerebral arterial contractility with development. We simultaneously examined the responses of arterial tension and intracellular Ca2+ concentration and used Western immunoblot analysis to measure ERK1/2, RhoA, 20 kDa regulatory myosin light chain (MLC20), PKC-potentiated inhibitory protein of 17 kDa (CPI-17), and caldesmon. Phorbol 12,13-dibutyrate (PDBu)-mediated PKC activation produced a robust contractile response, which was increased a further 20 to 30% by U-0126 (MEK inhibitor) in cerebral arteries of both age groups. Of interest, in the fetal cerebral arteries, PDBu leads to an increased phosphorylation of ERK2 compared with ERK1, whereas in adult arteries, we observed an increased phosphorylation of ERK1 compared with ERK2. Also, in the present study, RhoA/ROCK played a significant role in the PDBu-mediated contractility of fetal cerebral arteries, whereas in adult cerebral arteries, CPI-17 and caldesmon had a significantly greater role compared with the fetus. PDBu also led to an increased MLC20 phosphorylation, a response blunted by the inhibition of myosin light chain kinase only in the fetus. Overall, the present study demonstrates an important maturational shift from RhoA/ROCK-mediated to CPI-17/caldesmon-mediated PKC-induced contractile response in ovine cerebral arteries.
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Salmina, A., V. Levantsevich, D. Boris, and T. Semak. "COMPARATIVE ANATOMY OF THE STRUCTURE OF THE VILLISIAN CIRCLE IN PERSONS WITH CEREBRAL CIRCULATION DISORDERS AND WITHOUT SIGNS OF PATHOLOGY." EurasianUnionScientists 2, no. 2(83) (April 2, 2021): 23–25. http://dx.doi.org/10.31618/esu.2413-9335.2021.2.83.1255.
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The study is devoted to the study of the anatomy of the Willis circle of people with and without cerebral circulation pathology. We studied 243 angiograms (men and women of different age groups from 18 to 72 years old). Of these, 120 patients had no signs of cerebrovascular pathology, 123 patients had various kinds of cerebral circulation disorders. Only in 32% of cases, when studying 120 MR-angiograms of persons without cerebral circulation disorders, a classical type of structure of the arterial bed was revealed. In 68% of the subjects, structural anomalies were found, namely: 23% hypoplasia of the anterior communicating artery, 21% aplasia or hypoplasia of one of the posterior communicating arteries, 17% combination of aplasia of the anterior communicating arteries and aplasia of one of the posterior communicating arteries, 4% aplasia of the anterior and both posterior connecting arteries, 3% parietal contact of both anterior cerebral arteries. A study of the Willis circle of patients with cerebrovascular pathology revealed: 2% have a classic variant of the structure, 53% have aplasia of one of the posterior communicating arteries, aplasia of both posterior communicating arteries 26%, 19% a variant in which aplasia of the anterior and posterior communicating arteries is combined. Based on the foregoing, the classical type of structure of the arterial circle of the brain is the most optimal option for ensuring collateral blood flow.
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Vikner, Tomas, Lars Nyberg, Madelene Holmgren, Jan Malm, Anders Eklund, and Anders Wåhlin. "Characterizing pulsatility in distal cerebral arteries using 4D flow MRI." Journal of Cerebral Blood Flow & Metabolism 40, no. 12 (November 13, 2019): 2429–40. http://dx.doi.org/10.1177/0271678x19886667.
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Recent reports have suggested that age-related arterial stiffening and excessive cerebral arterial pulsatility cause blood–brain barrier breakdown, brain atrophy and cognitive decline. This has spurred interest in developing non-invasive methods to measure pulsatility in distal vessels, closer to the cerebral microcirculation. Here, we report a method based on four-dimensional (4D) flow MRI to estimate a global composite flow waveform of distal cerebral arteries. The method is based on finding and sampling arterial waveforms from thousands of cross sections in numerous small vessels of the brain, originating from cerebral cortical arteries. We demonstrate agreement with internal and external reference methods and show the ability to capture significant increases in distal cerebral arterial pulsatility as a function of age. The proposed approach can be used to advance our understanding regarding excessive arterial pulsatility as a potential trigger of cognitive decline and dementia.
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Lv, Xianli, Chen Li, and Weijian Jiang. "The intracranial vasculature of canines represents a model for neurovascular ischemia and training residents and fellows in endovascular neurosurgery." Neuroradiology Journal 33, no. 4 (May 5, 2020): 292–96. http://dx.doi.org/10.1177/1971400920920787.
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Background We describe use of a canine model to evaluate physiological effects and neuroprotective strategies in the setting of cerebral ischemia and endovascular neurosurgery training. Methods We performed transfemoral digital subtraction cerebral and cervical angiography on eight anesthetized dogs. Angiographic images of cerebral arteries were obtained following cannulation of the femoral artery. Cerebral ischemia models were made after angiography. Results The canine cerebral vasculature exhibited extensive tortuosity of the carotid and vertebral arteries. Conversely, the bilateral anterior spinal arteries were easily catheterized using microcatheters and microguidewires. The basilar artery and its branches were facilely cannulable. Circle of Willis continuity sans hypoplasia or aplasia of its constitutive segments was appreciated in all animals. The middle cerebral arteries could be easily accessed via the posterior communicating arteries. We generated an empirically evaluable therapeutically interventional experimental animal model of cerebral ischemia by occluding the middle cerebral artery using small coils for a duration between 15 and 60 min. Conclusion Unique amenability of the canine intracranial vasculature to selective and microcatheter cannulation renders experimentally induced cerebral, cerebellar, and brainstem via occlusion of the supratentorial and infratentorial arteries a simple matter. The neural vasculature irrigating the canine cerebrum, brainstem, and cerebellum may consequently prove useful in helping young and nascent endovascular neurosurgeons in developing and refining their skills of microcatheter navigation and manipulation and deployment of therapeutic devices to achieve effective occlusion of aneurysms, arteriovenous malformations, arteriovenous fistulas, and neoplasms of the intracranial cavity.
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Johansson, Barbro B., and Kent Fredriksson. "Cerebral Arteries in Hypertension." Journal of Cardiovascular Pharmacology 7 (1985): S90—S93. http://dx.doi.org/10.1097/00005344-198507002-00017.
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Rodríguez-Hernández, Ana, Susanna Miric, and Michael T. Lawton. "Twiglike Middle Cerebral Arteries." Neurosurgery 71, no. 2 (August 2012): E522. http://dx.doi.org/10.1227/neu.0b013e31825971a7.
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Lee, Robert M. K. W. "Morphology of cerebral arteries." Pharmacology & Therapeutics 66, no. 1 (January 1995): 149–73. http://dx.doi.org/10.1016/0163-7258(94)00071-a.
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Findlay, J. Max, R. Loch Macdonald, Bryce K. A. Weir, and Michael G. A. Grace. "Surgical manipulation of primate cerebral arteries in established vasospasm." Journal of Neurosurgery 75, no. 3 (September 1991): 425–32. http://dx.doi.org/10.3171/jns.1991.75.3.0425.
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✓ It is generally believed that surgery in the face of angiographic vasospasm is dangerous due to an increased incidence of postoperative cerebral ischemia. One theory is that arterial narrowing is exacerbated by surgical manipulation of vasospastic vessels during aneurysm dissection and clipping. This theory was tested in a primate model of cerebral vasospasm and the results reported. Six monkeys underwent baseline cerebral angiography, followed by induction of subarachnoid hemorrhage (SAH) on both sides of the circle of Willis. An equal amount of fresh autologous blood clot was placed around each internal carotid, anterior cerebral, and middle cerebral artery. Six days later, angiography was repeated and the right craniectomy was reopened for clot evacuation and surgical manipulation of the right cerebral arteries, including placement of a temporary aneurysm clip on the right middle cerebral artery. The left cerebral arteries were not exposed or manipulated, and served as controls. Twenty-four hours later angiography was repeated, then the animals were killed. Equal and significant vasospasm (> 40% reduction in vessel caliber compared to baseline, p < 0.05) was seen in the middle cerebral arteries on both sides of the circle of Willis in all animals 6 and 7 days after SAH. There was no significant change in the severity of vasospasm on Day 7 compared with Day 6 in the right cerebral arteries. Increased risk of postoperative cerebral ischemia for surgery in the peak vasospasm period may be due to mechanisms other than increased arterial narrowing precipitated by surgical manipulation.
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Hull, A. D., D. M. Long, L. D. Longo, and W. J. Pearce. "Pregnancy-induced changes in ovine cerebral arteries." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 1 (January 1, 1992): R137—R143. http://dx.doi.org/10.1152/ajpregu.1992.262.1.r137.
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We examined the effects of pregnancy on the ovine cerebral vasculature by comparing several characteristics of isolated endothelium-intact segments of three intracranial arteries including the middle cerebral (MCA), posterior communicating (PC), and basilar (BAS) arteries taken from pregnant sheep (138-143 days gestation, term approximately 145 days) and nonpregnant controls. For comparison, segments of the extracranial common carotid (COM) artery were also studied. With pregnancy, vessel water content increased (5.4-5.8%) in all arteries except the PC. Additionally, cellular protein content increased in all arteries (4.4-50.0%). Arterial stiffness, as determined by passive stress-strain determinations, was significantly decreased during pregnancy in the MCA but not in the larger arteries. Maximum contractile responses, when normalized to vessel wall cross-sectional area, were consistently greater in arteries from pregnant than in those from nonpregnant animals (10.1-49.7%). Relaxation to the endothelium-independent guanylate cyclase stimulator S-nitroso-N-acetyl penicillamine (SNAP) increased with pregnancy only in the distal MCA (approximately 17%). Endothelium-dependent relaxation to the calcium ionophore A23187 decreased only in the larger and more proximal COM (-39%). Thus pregnancy was associated with an increase in production of contractile force, a decrease in peripheral vascular stiffness, a decrease in the relaxant response to A23187 in the COM, and an increase in the relaxant response to SNAP in the MCA. Together, these findings indicate that pregnancy has widespread and important vessel specific cerebrovascular consequences that affect not only arterial composition, but also contractility and endothelial reactivity.
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ISHIBASHI, AKIRA, and YOSHITAKE YOKOKURA. "Massive Cerebral Infarctions in Main Cerebral Arteries." Kurume Medical Journal 50, no. 1/2 (2003): 35–39. http://dx.doi.org/10.2739/kurumemedj.50.35.
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Knot, H. J., and M. T. Nelson. "Regulation of membrane potential and diameter by voltage-dependent K+ channels in rabbit myogenic cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 1 (July 1, 1995): H348—H355. http://dx.doi.org/10.1152/ajpheart.1995.269.1.h348.
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The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) cerebral arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these arteries depolarized and the arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized cerebral arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) cerebral arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small cerebral arteries to changes in intravascular pressure.
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Sancho, Maria, Yuan Gao, Bjorn O. Hald, Hao Yin, Melfort Boulton, David A. Steven, Keith W. MacDougall, Andrew G. Parrent, J. Geoffrey Pickering, and Donald G. Welsh. "An assessment of KIR channel function in human cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 4 (April 1, 2019): H794—H800. http://dx.doi.org/10.1152/ajpheart.00022.2019.
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In the rodent cerebral circulation, inward rectifying K+ (KIR) channels set resting tone and the distance over which electrical phenomena spread along the arterial wall. The present study sought to translate these observations into human cerebral arteries obtained from resected brain tissue. Computational modeling and a conduction assay first defined the impact of KIR channels on electrical communication; patch-clamp electrophysiology, quantitative PCR, and immunohistochemistry then characterized KIR2.x channel expression/activity. In keeping with rodent observations, computer modeling highlighted that KIR blockade should constrict cerebral arteries and attenuate electrical communication if functionally expressed. Surprisingly, Ba2+ (a KIR channel inhibitor) had no effect on human cerebral arterial tone or intercellular conduction. In alignment with these observations, immunohistochemistry and patch-clamp electrophysiology revealed minimal KIR channel expression/activity in both smooth muscle and endothelial cells. This absence may be reflective of chronic stress as dysphormic neurons, leukocyte infiltrate, and glial fibrillary acidic protein expression was notable in the epileptic cortex. In closing, KIR2.x channel expression is limited in human cerebral arteries from patients with epilepsy and thus has little impact on resting tone or the spread of vasomotor responses. NEW & NOTEWORTHY KIR2.x channels are expressed in rodent cerebral arterial smooth muscle and endothelial cells. As they are critical to setting membrane potential and the distance signals conduct, we sought to translate this work into humans. Surprisingly, KIR2.x channel activity/expression was limited in human cerebral arteries, a paucity tied to chronic brain stress in the epileptic cortex. Without substantive expression, KIR2.x channels were unable to govern arterial tone or conduction.
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Silva, Roberto Sávio Bessa da, Gleidson Benevides de Oliveira, Carlos Magno Oliveira Junior, Ferdinando Vinicius Fernandes Bezerra, Felipe Venceslau Câmara, Radan Elvis Matias de Oliveira, and Moacir Franco de Oliveira. "Arterial vascularization of the brain of the agouti (Dasyprocta aguti Linnaeus, 1766)." Semina: Ciências Agrárias 37, no. 2 (April 16, 2016): 773–84. http://dx.doi.org/10.5433/1679-0359.2016v37n2p773.
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The agouti, a rodent that is geographically distributed throughout South America, is greatly valued for its meat. This paper describes the arterial vascularization of the base of the agouti’s brain, characterizing behavior, and arterial origin and distribution. Ten animals from the Center for the Multiplication of Wild Animals (CEMAS/UFERSA) were used and the study was approved by SISBIO (report number 32413- 1) and the Ethics Committee on Animal Use (CEUA/UFERSA) (protocol 02/2010). After euthanasia, the animals were incised in the thoracic cavity by an injection of red-stained Neoprene latex 650 and the skulls were subsequently opened. The brains were extracted from the skulls for ventral surface analysis and then fixed in an aqueous 10% formaldehyde solution. The agouti’s arterial vascularization of the brain has two main components, namely the carotid and vertebrobasilar systems. The agouti’s carotid system accounts for vascularization of almost the entire forebrain, while the vertebrobasilar system accounts for vascularization of almost the entire posterior brain (medulla oblongata, pyramid, trapezoid body, cerebellum, bridge, and part of the third caudal section of the forebrain) through the caudal cerebral arteries originating from the terminal branches of the basilar artery. The main arteries on the brain surface include the basilar artery, which is unique, and the arterial pairs, specifically the vertebral arteries, cerebellar caudal arteries, trigeminal artery, rostral cerebellar artery, basilar terminal branch artery, cerebral caudal artery, communicating caudal branch of the cerebral carotid artery, cerebral carotid artery, communicating branch rostral cerebral carotid artery, choroidal rostral artery, medial branch of the communicating branch rostral artery, internal ophthalmic artery, middle cerebral artery, and rostral cerebral artery.
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Costa, Herson Da Silva, Hélio Norberto De Araújo Júnior, Ferdinando Vinícius Fernandes Bezerra, Carlos Eduardo Vale Rebouças, Danilo José Ayres De Menezes, Carlos Eduardo Bezerra De Moura, and Moacir Franco De Oliveira. "Macroscopic Anatomy and Brain Vascularization in the Greater Rhea (Rhea americana americana)." Acta Scientiae Veterinariae 46, no. 1 (March 16, 2018): 8. http://dx.doi.org/10.22456/1679-9216.86671.
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Background: The Rhea americana americana is a wild bird belonging to the group of Ratites, and is important from the scientific point of view given their adaptability to captivity. Considering that information about its morphology is important for the viability of domesticating the species, the aim of this study was to macroscopically identify the brain regions, as well as the cerebral arteries and the cerebral arterial circuit in order to establish the cerebral vascular pattern and systematization.Materials, Methods & Results: Twenty one brains from young and adult Greater Rheas of both sexes were used from animals that had died due to natural causes and were then kept in a freezer. The specimens were thawed and incised in the cervical region to allow exposure of the left common carotid artery, which was cannulated. The vascular system was rinsed with 0.9% saline solution, then perfused with latex Neoprene 650 stained with red pigment. The animals were subsequently fixed in 3.7% aqueous formaldehyde solution for 72 h, and then they were dissected by removing the bones from the skull cap. The brains were analyzed, and the structures were identified, photographed, schematized and denominated. Morphometric measurements were performed on the basilar and cerebellar ventral caudal arteries, recording the values of length and width in millimeters with the aid of a digital caliper. The brain was divided into: telencephalon, diencephalon, brainstem and cerebellum; while externally, the observed structures are: olfactory bulbs, optical lobes, optic nerves, optic chiasm, pituitary and pineal glands. Vascularization was performed by the following arteries: ventral spinal artery, basilar artery, ventricular cerebellar arteries, medium ventricular cerebellar arteries, caudal branches of the carotid arteries of the brain, ventral mesencephalic artery, cerebral caudal arteries, rostral branches of the carotid arteries of the brain, middle cerebral arteries, cerebroethmoidal arteries, rostral intercerebral anastomosis, rostral cerebral arteries, ethmoidal arteries, internal ophthalmic arteries, inter-hemispheric artery, pituitary arteries, dorsal mesencephalic tectal arteries, dorsal cerebellar arteries, occipital, pineal and dorsal hemispherical branches. The cerebral arterial circuit was both caudally and rostrally closed in 100.0% of the samples, being composed of the arteries: basilar artery, caudal branches of the carotid brain, rostral branches of the brain carotid, cerebroethmoidal arteries and rostral intercerebral anastomosis.Discussion: Encephalon classification regarding the presence or absence of gyri is a characteristic associated to evolutionary aspects among vertebrates, being respectively considered as lisencephalon or girencecephalus when it presents or does not present convolutions. In Greater Rheas, the telencephalon was quite developed, with a relatively rounded shape and the absence of sulci and convolutions in the cortex, which allowed it to be classified as a lisencephalon. Such findings resemble those described for the ostrich and in a comparative study involving kiwis, emus, owls and pigeons, although different sizes and forms of telencephalon development were observed in the latter. Regarding the cerebral arterial circuit, this structure in Rheas was complete and both caudally and rostrally closed in 100.0% of the specimens. Our findings differ from those observed for ostriches, in which a rostrally open behavior has been described, while it is caudally closed in 20.0% of cases and opened in 80.0%. Regarding the vascular type of the brain, in the Rhea it was observed that there was only contribution of the carotid system, similar to that found for birds such as ostriches and turkeys which confer a type I encephalic vascularization.
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Macdonald, R. L., B. K. A. Weir, M. G. A. Grace, M. H. Chen, T. P. Martin, and J. D. Young. "Mechanism of Cerebral Vasospasm Following Subarachnoid Hemorrhage in Monkeys." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 4 (November 1992): 419–27. http://dx.doi.org/10.1017/s0317167100041597.
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ABSTRACT:This paper reviews our recent studies on the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH) in monkeys. Middle cerebral artery (MCA) vasospasm was maximal at 7 days, resolving by 14 days, and absent at 28 days after SAH. Arterial fibrosis was not detected during vasospasm, although there was intimal hyperplasia with fibrosis 28 days after SAH. On scanning electron microscopy, smooth muscle cells from vasospastic arteries had corrugated cell membranes and appeared similar to cells contracted pharmacologically, suggesting that vasospastic smooth muscle is contracted. Morphometric analysis of arteries obtained 7 days after SAH showed no significant increases in arterial wall area of vasospastic arteries compared with normal MCAs. The results suggest vasospasm in monkeys is not due to hypertrophy, hyperplasia, or fibrosis in the arterial wall. Vasospasm may be mainly vascular smooth muscle contraction, which damages the arterial wall, leading to secondary structural changes in the arterial wall which occur after angiographic vasospasm.
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Han, M. H., K. H. Chang, D. H. Han, K. M. Yeon, and M. C. Han. "Preembolization Functional Evaluation in Supratentorial Cerebral Arteriovenous Malformations with Superselective Intraarterial Injection of Thiopental Sodium Solution." Acta Radiologica 35, no. 3 (May 1994): 212–16. http://dx.doi.org/10.1177/028418519403500303.
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Superselective intraarterial injections of thiopental sodium solution for evaluation of local brain function were performed before embolization in 38 consecutive patients with supratentorial arteriovenous malformations to evaluate the role of the test using thiopental sodium solution. Thiopental sodium (30–50 mg) was injected in 68 arteries (44 middle cerebral arteries, 13 anterior cerebral arteries, 7 posterior cerebral arteries, 3 external carotid arteries, and 1 thalamo-perforating artery) through superselective microcatheters just before the injection of cyanoacrylate mixture for the embolization. The test was negative in 57 arteries and there were neurologic dysfunctions in 3 of them after embolization. The neurologic deficits in these cases were caused by reflux of embolic material, spasm of the main arterial trunk, or neglected mild sensory change, respectively, and there was no real false-negative test. The embolization could not be performed due to positive test in 9 arteries. Two arteries with positive tests but acceptable symptoms were embolized and the same neurologic deficits developed immediately after embolization. There was no local arterial complication by an injection of the thiopental sodium solution. All neurologic deficits caused by positive tests developed immediately and were completely relieved within 5 min without specific management. Superselective intraarterial injection of thiopental sodium solution is a safe and reliable test for the evaluation of local brain function before embolization of supratentorial arteriovenous malformations.
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Katusic, Z. S. "Endothelial L-arginine pathway and regional cerebral arterial reactivity to vasopressin." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 5 (May 1, 1992): H1557—H1562. http://dx.doi.org/10.1152/ajpheart.1992.262.5.h1557.
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Experiments were designed to characterize the mechanism of vasopressin action in small arteries of brain stem and cerebrum and to determine the role of L-arginine pathway in reactivity of these vessels to vasopressin. Secondary branches of canine basilar arteries (425 +/- 63 microns ID, n = 6) and middle cerebral arteries (466 +/- 30 microns ID, n = 6) were dissected and mounted on glass microcannulas in organ chambers. Changes in intraluminal diameter of the pressurized arteries were measured using a video dimension analyzer. Vasopressin caused endothelium-dependent relaxation in the brain stem arteries [-log half-maximal effective concentration (EC50) = 9.2 +/- 0.4, n = 5] but not in the branches of middle cerebral arteries. In contrast, bradykinin caused identical endothelium-dependent relaxations in arteries of both regions (-log EC50 = 8.0 +/- 0.2, n = 5, and 7.7 +/- 0.1, n = 4 for brain stem and cerebrum, respectively). Relaxations to vasopressin (but not to bradykinin) were reduced in the presence of V1-vasopressinergic antagonist [1-(beta-mercapto-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5-Tyr(Me)AVP;10(-7) M], pertussin toxin (100 ng/ml), and NG-monomethyl-L-arginine (L-NMMA; 10(-4) M). The inhibitory effect of L-NMMA was prevented by L-arginine (3 x 10(-4) M) but not D-arginine (3 x 10(-4) M). These studies suggest that vasopressin causes endothelium-dependent relaxation in canine brain stem arteries. The effect of the neuropeptide appears to be mediated by activation of endothelial V1-vasopressinergic receptors coupled to nitric oxide synthase. This signal transduction pathway is not functional in endothelial cells of branches of middle cerebral arteries.
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Nakakita, Kazuo. "Peptidergic Innervation in the Cerebral Blood Vessels of the Guinea Pig: An Immunohistochemical Study." Journal of Cerebral Blood Flow & Metabolism 10, no. 6 (November 1990): 819–26. http://dx.doi.org/10.1038/jcbfm.1990.138.
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The distribution of peptidergic nerve fibers containing substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY) in the cerebral arteries and veins of the guinea pig was studied using immunohistochemical techniques. The ultrastructure of these immunoreactive nerve terminals was also compared. The cerebral arteries were innervated by abundant peptidergic nerve fibers with characteristic running patterns, i.e., SP fibers in a meshwork, VIP and NPY fibers in a spiral fashion. Only CGRP fibers showed both meshwork and spiral patterns. In the cerebral veins, the abundant SP fibers innervated the cortical veins, deep cerebral veins, and dural sinuses. However, CGRP, VIP, and NPY fibers in extremely low density were noted merely in the cortical veins. Electron microscopic observations demonstrated that SP-immunoreactive nerve terminals existed apart from the arterial smooth muscle cells, while VIP- and NPY-immunoreactive nerve terminals adjoined them. As for CGRP nerve terminals, some existed close to the arterial smooth muscle cells, and others were found some distance from them. These morphological characteristics observed by light and electron microscopy suggest that SP fibers are not related directly to the vasomotor function, but VIP and NPY fibers are, and that CGRP fibers have a more complicated function. The distribution patterns of the peptidergic nerve fibers are consistent with the suggestion that vasomotor peptidergic fibers may function actively on cerebral arteries and passively on cerebral veins and that SP fibers regarded as sensory fibers may provide information regarding cerebral vascular conditions, innervating every part of both cerebral arteries and veins.
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Mayhan, W. G., S. M. Amundsen, F. M. Faraci, and D. D. Heistad. "Responses of cerebral arteries after ischemia and reperfusion in cats." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 4 (October 1, 1988): H879—H884. http://dx.doi.org/10.1152/ajpheart.1988.255.4.h879.
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Our goal was to determine whether responses of cerebral arteries are altered after cerebral ischemia and reperfusion. We measured diameter of cerebral arteries (150-180 micron) in cats in response to topical application of acetylcholine (ACh) and serotonin, which release endothelium-derived relaxing factor (EDRF), and adenosine and angiotensin, which do not release EDRF. Diameter of arteries was measured before and after 10 or 30 min of cerebral ischemia, when base-line diameter had returned to control levels. Under control conditions, serotonin and angiotensin constricted cerebral arteries by 16 +/- 2 and 23 +/- 3% (means +/- SE), respectively, and ACh and adenosine dilated cerebral arteries by 22 +/- 2 and 23 +/- 3%, respectively. During reperfusion after 10 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. Vasodilator responses of arteries to ACh after 10 min of ischemia were heterogeneous. In 6 of 15 cats, vasodilatation in response to ACh was preserved. In contrast, in 9 of 15 cats, vasodilatation in response to ACh was impaired (7 +/- 3%). In both groups, vasodilatation in response to adenosine was not impaired after 10 min of ischemia. During reperfusion after 30 min of cerebral ischemia, constrictor responses of cerebral arteries were preserved. In contrast, dilatation of cerebral arteries in response to ACh and adenosine was impaired. We speculate that impaired cerebral vasodilatation after ischemia, with maintenance of vasoconstriction, may contribute to impaired reperfusion after cerebral ischemia.
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Findlay, J. M., B. K. A. Weir, K. Kanamaru, and F. Espinosa. "Arterial Wall Changes in Cerebral Vasospasm." Neurosurgery 25, no. 5 (November 1, 1989): 736–46. http://dx.doi.org/10.1227/00006123-198911000-00008.
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Abstract A right-sided subarachnoid hemorrhage (SAH) was created in 12 monkeys. Only the right (clot-side) cerebral arteries developed angiographic vasospasm (VSP), which was maximal 7 days after SAH. Eight animals were killed at this time and the remainder at 14 days. At the time of killing the middle cerebral arteries (MCAs) were harvested, and four normal, left (non-clot-side) MCAs were vasoconstricted in vitro with prostaglandin F2… All MCAs were studied with scanning and transmission electron microscopy. Right MCAs in maximal VSP 7 days from SAH were undistinguishable on scanning electron microscopy from normal arteries vasoconstricted in vitro: both groups demonstrated a mean 57% reduction in vessel caliber and a 5-fold increase in vessel wall thickness compared to normal, nonvasoconstricted left MCAs. On transmission electron microscopy, however, arteries in SAH-induced VSP showed degenerative changes in the tunica intima and media. These changes were still evident at 14 days. despite considerable resolution of VSP. These findings, as well as those from other pathological studies of animal and human cerebral arteries in VSP, suggest that the arterial narrowing and vessel wall thickening seen within several weeks of SAH is due primarily to medial contraction, but unlike simple vasoconstruction, is associated with degenerative ultrastructural changes in the endothelium and vascular smooth muscle cells which may denote a temporarily irreversible state.
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McCarron, J. G., J. M. Quayle, W. Halpern, and M. T. Nelson. "Cromakalim and pinacidil dilate small mesenteric arteries but not small cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 2 (August 1, 1991): H287—H291. http://dx.doi.org/10.1152/ajpheart.1991.261.2.h287.
Full textAbstract:
Small elevations in external K+ hyperpolarize and dilate small cerebral arteries. The hyperpolarization and dilation to K+ are blocked by barium (less than 0.1 mM). Since membrane hyperpolarization appears to be an important mechanism for dilation of these small cerebral arteries, we investigated the effects of the hyperpolarizing vasodilators, cromakalim and pinacidil, on isolated pressurized rat cerebral arteries (diameter of 158 +/- 5 microns at 50% of the systolic blood pressure). Cromakalim and pinacidil, which are potent relaxants of a variety of muscle types, were without effect on posterior cerebral arteries at concentrations that completely dilate similarly sized rat mesenteric arteries (diameter 134 +/- 6 microns at 50% of the systolic blood pressure). The mesenteric artery dilation to cromakalim and pinacidil was reversed by glibenclamide. However, unlike the cerebral arteries, mesenteric arteries did not exhibit a barium-sensitive dilation to external K+. Thus it appears that there may be differences in the types of K+ channels that are activated by dilating mechanisms in small cerebral and mesenteric arteries.
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Adebiyi, Adebowale, Guiling Zhao, Sergey Y. Cheranov, Abu Ahmed, and Jonathan H. Jaggar. "Caveolin-1 abolishment attenuates the myogenic response in murine cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 3 (March 2007): H1584—H1592. http://dx.doi.org/10.1152/ajpheart.00584.2006.
Full textAbstract:
Intravascular pressure-induced vasoconstriction (the “myogenic response”) is intrinsic to smooth muscle cells, but mechanisms that underlie this response are unresolved. Here we investigated the physiological function of arterial smooth muscle cell caveolae in mediating the myogenic response. Since caveolin-1 (cav-1) ablation abolishes caveolae formation in arterial smooth muscle cells, myogenic mechanisms were compared in cerebral arteries from control (cav-1+/+) and cav-1-deficient (cav-1−/−) mice. At low intravascular pressure (10 mmHg), wall membrane potential, intracellular calcium concentration ([Ca2+]i), and myogenic tone were similar in cav-1+/+ and cav-1−/− arteries. In contrast, pressure elevations to between 30 and 70 mmHg induced a smaller depolarization, [Ca2+]i elevation, and myogenic response in cav-1−/− arteries. Depolarization induced by 60 mM K+ also produced an attenuated [Ca2+]i elevation and constriction in cav-1−/− arteries, whereas extracellular Ca2+ removal and diltiazem, an L-type Ca2+ channel blocker, similarly dilated cav-1+/+ and cav-1−/− arteries. Nω-nitro-l-arginine, an nitric oxide synthase inhibitor, did not restore myogenic tone in cav-1−/− arteries. Iberiotoxin, a selective Ca2+-activated K+ (KCa) channel blocker, induced a similar depolarization and constriction in pressurized cav-1+/+ and cav-1−/− arteries. Since pressurized cav-1−/− arteries are more hyperpolarized and this effect would reduce KCa current, these data suggest that cav-1 ablation leads to functional KCa channel activation, an effect that should contribute to the attenuated myogenic constriction. In summary, data indicate that cav-1 ablation reduces pressure-induced depolarization and depolarization-induced Ca2+ influx, and these effects combine to produce a diminished arterial wall [Ca2+]i elevation and constriction.
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Baltsavias, Gerasimos, Anton Valavanis, Venko Filipce, and Nadia Khan. "Selective and Superselective Angiography of Pediatric Moyamoya Disease Angioarchitecture: The Anterior Circulation." Interventional Neuroradiology 20, no. 4 (January 1, 2014): 391–402. http://dx.doi.org/10.15274/inr-2014-10050.
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The angioarchitecture of the so-called moyamoya vessels in children has not been explicitly analyzed. We aimed to investigate the precise anatomy of the vascular anastomotic networks in patients with childhood moyamoya disease. Six children diagnosed with moyamoya disease for the first time underwent an angiographic investigation with selective and superselective injections. We recorded the arterial branches feeding the moyamoya anastomotic networks, their connections and the recipient vessels. Depending on the level of the steno-occlusive lesion, the feeding vessels included the medial striate arteries, the perforators of the choroidal segment of the carotid, the uncal artery, the medial and lateral branches of the intraventricular segment of the anterior choroidal artery, perforators of the communicating segment, the superior hypophyseal arteries, the prechiasmal branches of the ophthalmic artery, the ethmoidal arteries and the dural branches of the cavernous carotid. Through connections, which are described, the recipient vessels were the lateral striate arteries and the middle cerebral, the medial striate arteries and the anterior cerebral, medullary arteries around the ventricular system, anterior temporal branches of the middle cerebral, orbitofrontal and frontopolar branches of the anterior cerebral, as well as other cortical branches of the anterior and middle cerebral territories. The use of high quality selective and superselective angiography enabled us to clearly demonstrate for the first time aspects of the microangiographic anatomy of the moyamoya anastomotic network previously only vaguely or incompletely described.
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Adebiyi, Adebowale, Elizabeth M. McNally, and Jonathan H. Jaggar. "Vasodilation induced by oxygen/glucose deprivation is attenuated in cerebral arteries of SUR2 null mice." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1360—H1368. http://dx.doi.org/10.1152/ajpheart.00406.2011.
Full textAbstract:
Physiological functions of arterial smooth muscle cell ATP-sensitive K+ (KATP) channels, which are composed of inwardly rectifying K+ channel 6.1 and sulfonylurea receptor (SUR)-2 subunits, during metabolic inhibition are unresolved. In the present study, we used a genetic model to investigate the physiological functions of SUR2-containing KATP channels in mediating vasodilation to hypoxia, oxygen and glucose deprivation (OGD) or metabolic inhibition, and functional recovery following these insults. Data indicate that SUR2B is the only SUR isoform expressed in murine cerebral artery smooth muscle cells. Pressurized SUR2 wild-type (SUR2wt) and SUR2 null (SUR2nl) mouse cerebral arteries developed similar levels of myogenic tone and dilated similarly to hypoxia (<10 mmHg Po2). In contrast, vasodilation induced by pinacidil, a KATP channel opener, was ∼71% smaller in SUR2nl arteries. Human cerebral arteries also expressed SUR2B, developed myogenic tone, and dilated in response to hypoxia and pinacidil. OGD, oligomycin B (a mitochondrial ATP synthase blocker), and CCCP (a mitochondrial uncoupler) all induced vasodilations that were ∼39–61% smaller in SUR2nl than in SUR2wt arteries. The restoration of oxygen and glucose following OGD or removal of oligomycin B and CCCP resulted in partial recovery of tone in both SUR2wt and SUR2nl cerebral arteries. However, SURnl arteries regained ∼60–82% more tone than did SUR2wt arteries. These data indicate that SUR2-containing KATP channels are functional molecular targets for OGD, but not hypoxic, vasodilation in cerebral arteries. In addition, OGD activation of SUR2-containing KATP channels may contribute to postischemic loss of myogenic tone.
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Kellawan, J. Mikhail, Garrett L. Peltonen, John W. Harrell, Alejandro Roldan-Alzate, Oliver Wieben, and William G. Schrage. "Differential contribution of cyclooxygenase to basal cerebral blood flow and hypoxic cerebral vasodilation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 2 (February 1, 2020): R468—R479. http://dx.doi.org/10.1152/ajpregu.00132.2019.
Full textAbstract:
Cyclooxygenase (COX) is proposed to regulate cerebral blood flow (CBF); however, accurate regional contributions of COX are relatively unknown at baseline and particularly during hypoxia. We hypothesized that COX contributes to both basal and hypoxic cerebral vasodilation, but COX-mediated vasodilation is greater in the posterior versus anterior cerebral circulation. CBF was measured in 9 healthy adults (28 ± 4 yr) during normoxia and isocapnic hypoxia (fraction of inspired oxygen = 0.11), with COX inhibition (oral indomethacin, 100mg) or placebo. Four-dimensional flow magnetic resonance imaging measured cross-sectional area (CSA) and blood velocity to quantify CBF in 11 cerebral arteries. Cerebrovascular conductance (CVC) was calculated (CVC = CBF × 100/mean arterial blood pressure) and hypoxic reactivity was expressed as absolute and relative change in CVC [ΔCVC/Δ pulse oximetry oxygen saturation ([Formula: see text])]. At normoxic baseline, indomethacin reduced CVC by 44 ± 5% ( P < 0.001) and artery CSA ( P < 0.001), which was similar across arteries. Hypoxia ([Formula: see text] 80%–83%) increased CVC ( P < 0.01), reflected as a similar relative increase in reactivity (% ΔCVC/−Δ[Formula: see text]) across arteries ( P < 0.05), in part because of increases in CSA ( P < 0.05). Indomethacin did not alter ΔCVC or ΔCVC/Δ[Formula: see text] to hypoxia. These findings indicate that 1) COX contributes, in a largely uniform fashion, to cerebrovascular tone during normoxia and 2) COX is not obligatory for hypoxic vasodilation in any regions supplied by large extracranial or intracranial arteries.
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Kostreva, D. R., J. McNeely, and E. J. Zuperku. "Effect of arterial PCO2 on 2-[1-14C]deoxy-D-glucose uptake by feline cerebral arteries." Journal of Applied Physiology 61, no. 4 (October 1, 1986): 1288–92. http://dx.doi.org/10.1152/jappl.1986.61.4.1288.
Full textAbstract:
The effect of high and low arterial CO2 on the glucose utilization of nine major cerebral arteries was studied in cats anesthetized with pentothal using the quantitative 2-[1–14C]deoxy-D-glucose autoradiographic technique. All nine cerebral arteries from animals subjected to an arterial partial pressure of CO2 (PCO2) of 20 Torr utilized significantly more (P less than 0.025) glucose than the group subjected to an arterial PCO2 of 60 Torr. Mean relative glucose utilization of the 20-Torr PCO2 group was 105 +/- 9.5 mumol X 100g-1 X min-1 (+/- SE, n = 18) as compared with 49 +/- 6 mumol X 100g-1 X min-1 (+/- SE, n = 26) for the 60-Torr PCO2 group. This study demonstrates that blood vessels can be studied in vivo using the 2-[1-14C]deoxy-D-glucose autoradiographic technique. It also demonstrates that a physiological stimulus like CO2 can produce measurable changes in glucose utilization of cerebral arteries in vivo.
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Onoue, H., N. Kaito, M. Tomii, S. Tokudome, M. Nakajima, and T. Abe. "Human basilar and middle cerebral arteries exhibit endothelium-dependent responses to peptides." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 1994): H880—H886. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h880.
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We examined the activities of bradykinin, substance P, and vasopressin in isolated human cerebral arteries to better understand humoral control of cerebrovascular tone. Basilar and middle cerebral arteries were isolated from human cadavers during autopsy, and isometric tension was measured in helical strips of the arteries. Both bradykinin and substance P relaxed strips of both arteries precontracted with prostaglandin F2 alpha to similar extents. The relaxations induced by both peptides were abolished by removal of the vascular endothelium and were markedly reduced by pretreatment with NG-nitro-L-arginine, an inhibitor of endothelium-derived relaxing factor. Treatment with indomethacin, a cyclooxygenase inhibitor, did not attenuate the relaxations. These results indicate that the responses of human cerebral arteries to bradykinin and substance P are mediated by endothelium-derived relaxing factor. In contrast, vasopressin primarily produced endothelium-independent contractions in human cerebral arteries. Contractions of basilar arteries induced by vasopressin were much less than those of middle cerebral arteries. Two of eighteen basilar arteries, but none of the middle cerebral arteries, responded to vasopressin with endothelium-dependent relaxation. This suggests that the function of vasopressin receptors differs in basilar and middle cerebral arteries.
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Wickramasekera, Nadi T., Debebe Gebremedhin, Koryn A. Carver, Padmanabhan Vakeel, Ramani Ramchandran, Aaron Schuett, and David R. Harder. "Role of dual-specificity protein phosphatase-5 in modulating the myogenic response in rat cerebral arteries." Journal of Applied Physiology 114, no. 2 (January 15, 2013): 252–61. http://dx.doi.org/10.1152/japplphysiol.01026.2011.
Full textAbstract:
The present study examined the role of the dual-specificity protein phosphatase-5 (DUSP-5) in the pressure-induced myogenic responses of organ-cultured cerebral arterial segments. In these studies, we initially compared freshly isolated and organ-cultured cerebral arterial segments with respect to responses to step increases in intravascular pressure, vasodilator and vasoconstrictor stimuli, activities of the large-conductance arterial Ca2+-activated K+ (KCa) single-channel current, and stable protein expression of DUSP-5 enzyme. The results demonstrate maintained pressure-dependent myogenic vasoconstriction, DUSP-5 protein expression, endothelium-dependent and -independent dilations, agonist-induced constriction, and unitary KCa channel conductance in organ-cultured cerebral arterial segments similar to that in freshly isolated cerebral arteries. Furthermore, using a permeabilization transfection technique in organ-cultured cerebral arterial segments, gene-specific small interfering RNA (siRNA) induced knockdown of DUSP-5 mRNA and protein, which were associated with enhanced pressure-dependent cerebral arterial myogenic constriction and increased phosphorylation of PKC-βII. In addition, siRNA knockdown of DUSP-5 reduced levels of phosphorylated ROCK and ERK1 with no change in the level of phosphorylated ERK2. Pharmacological inhibition of ERK1/2 phosphorylation significantly attenuated pressure-induced myogenic constriction in cerebral arteries. The findings within the present studies illustrate that DUSP-5, native in cerebral arterial muscle cells, appears to regulate signaling of pressure-dependent myogenic cerebral arterial constriction, which is crucial for the maintenance of constant cerebral blood flow to the brain.
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Toda, Noboru. "Hemolysate Inhibits Cerebral Artery Relaxation." Journal of Cerebral Blood Flow & Metabolism 8, no. 1 (February 1988): 46–53. http://dx.doi.org/10.1038/jcbfm.1988.7.
Full textAbstract:
In helical strips of dog middle cerebral arteries partially contracted with prostaglandin (PG) F2α, relaxations induced by angiotensin-II, possibly mediated by PGI2, and those induced by PGH2 were reversed to a contraction or markedly reduced by treatment with hemolysate, which, however, attenuated the PGI2-induced relaxation only slightly. The relaxant response of human middle cerebral arterial strips to PGH2 was also suppressed by hemolysate. Dog and monkey middle cerebral arteries responded to transmural electrical stimulation and nicotine with transient relaxations, which were quite susceptible to tetrodotoxin and hexamethonium, respectively; the relaxations were abolished almost completely by hemolysate and methylene blue. On the other hand, the relaxant response of dog cerebral arteries to a low concentration of K+ was not influenced by hemolysate or by methylene blue, but was reversed to a contraction by treatment with ouabain. Relaxations induced by substance-P and nitroglycerin were markedly inhibited by hemolysate; removal of endothelium abolished the relaxation by substance-P, but did not influence the nitroglycerin-induced relaxation. Hemolysate may interfere with the biosynthesis of PGI2 in the vascular wall, thereby reversing the relaxation induced by angiotensin-II and PGH2 to a contraction. Relaxations induced by electrical and chemical stimulation of vasodilator nerves innervating cerebral arteries appear to be elicited by a mechanism dependent on cellular cyclic guanosine monophosphate (GMP), like that underlying the substance-P-induced and nitroglycerin-induced relaxation. These actions of hemolysate may be involved in the genesis of cerebral vasospasm after subarachnoid hemorrhage.