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4 edition of Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume found in the catalog.

Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume

proceedings of the statellite symposium, Brain Section, Fourth World Congress for Microcirculation, Osaka, Japan, 1-2 August 1987

by World Congress for Microcirculation (4th 1987 Tokyo, Japan and Osaka, Japan).

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  • 38 Currently reading

Published by Excerpta Medica in Amsterdam, New York .
Written in English

    Subjects:
  • Cerebral ischemia -- Congresses.,
  • Brain -- Congestion -- Congresses.,
  • Blood volume -- Congresses.,
  • Blood Volume -- congresses.,
  • Blood Volume Determination -- methods -- congresses.,
  • Cerebral Ischemia -- physiopathology -- congresses.,
  • Cerebrovascular Circulation -- congresses.

  • Edition Notes

    Includes bibliographies and index.

    Statementeditors, M. Tomita ... [et al.].
    SeriesInternational congress series ;, 764, International congress series ;, no. 764.
    ContributionsTomita, M.
    Classifications
    LC ClassificationsRC388.5 .W66 1987
    The Physical Object
    Paginationxxi, 280 p. :
    Number of Pages280
    ID Numbers
    Open LibraryOL2528248M
    ISBN 100444809732
    LC Control Number88003576

    Cerebral vasospasm implies narrowing of blood vessels resulting in decreased cerebral blood flow to distal tissues resulting in ischemia. It has been variously defined 1 in the literature by different authors. 1. Clinical vasospasm defined as neurological deterioration deemed secondary to vasospasm after other causes are eliminated. It is seen in 20–40% of patients. Reduction of functional capillary density in human brain after stroke. J Cereb Blood Flow Metab. ; – Crossref Medline Google Scholar; Tomita M. Significance of cerebral blood volume. In: Tomita M, Sawata T, Naritomi H, Heiss WD, eds. Cerebral Hyperemia and Ischemia: From the Standpoint of Cerebral Blood Volume.

    THE brain, as a vital organ, disproportionately receives about 12% of cardiac output (CO) even though it weighs only 2% of the body weight. 1 Cerebral blood flow (CBF) is regulated by a set of powerful mechanisms that include cerebral autoregulation, 2 neurovascular coupling, 3 and cerebrovascular carbon dioxide and oxygen reactivity. 4 It is common to presume that a stable blood .   37 Tomita M. Significance of cerebral blood volume. Cerebral Hyperemia and Ischemia: From the Standpoint of Cerebral Blood Volume, Tomita M., Sawada T., Naritomi H., Heiss W. D. Excerpta MedicaAmsterdam Google Scholar; 38 Ursino M. A mathematical study of human intracranial hydrodynamics. 1. The cerebrospinal fluid pulse pressure. Ann.

    There is a delicate balance among vasoconstriction and vasodilation factors. During ischemia/stroke, cerebral blood flow autoregulation may be compromised triggering hyperemia (early phase) or hypoperfusion (late phase or post-ischemia) deranging cerebral blood flow that can lead to subsequent neuronal cell death due to blood flow abnormalities. Remote Hyperemia After Focal Cerebral Ischemia: Disinhibition Mechanism of Remote Hyperemia.- Cerebral Hyperemia and Breakthrough During Hypertension.- Maintenance of Constant Cerebral Blood Volume by Veni-Arterial Reflex.- Bordering Zone Hyperemia and Glucose Metabolism in Experimental Cerebral Ischemia.- 5 Myocardial Ischemia


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Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume by World Congress for Microcirculation (4th 1987 Tokyo, Japan and Osaka, Japan). Download PDF EPUB FB2

Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume. Amsterdam ; New York: Excerpta Medica, (OCoLC) Online version: World Congress for Microcirculation (4th: Tokyo, Japan and Osaka, Japan). Brain Section.

Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume. In: Cerebral hyperemia and ischemia: From the standpoint of cerebral blood volume (Tomita, M, Sawada, T, Naritomi, H, Heiss, WD, eds), Amsterdam: Excerpta Medica, pp 81 – 90 Google Scholar Kety, SS, Schmidt, CF () The effects of altered arterial tensions of carbon dioxide and oxygen on cerebral blood flow and cerebral oxygen consumption Cited by: Cerebral Hyperemia and Ischemia: From the Standpoint of Cerebral Blood Volume.

Amsterdam, The Netherlands: Elsevier Science Publishers BV; Significance of cerebral blood volume. 3– Ferrari M, Wilson D A, Hanley D F, Traystmen R J. Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in by: It is multifactorial in causation and varies with magnitude of injury severity and the increase in edema and cerebral blood volume.

Cerebral hyperemia and ischemia: From the standpoint of cerebral blood volume. Amsterdam, Netherlands: Excerpta Medica; pp. Cited by:   Tomita M. Significance of cerebral blood volume. In: Tomita M, Sawada T, Naritomi H, Heiss W-D, eds.

Cerebral Hyperemia and Ischemia: From the Standpoint of Cerebral Blood Volume. Amsterdam: Elsevier Science Publishers BV; Cited by: 9. Using our photoelectric method, the local cerebral blood volume, mean transit time of blood, and cerebral blood flow in the parieto-temporal region were measured during and for 3 h after ventricular tachycardia.

Transient ventricular tachycardia of as short as 1 min caused cerebral ischemia with a blood flow reduction of approximately 30%. Although cerebral ischemia may be observed after TBI and cause an increase in extracellular cerebral lactate, recent data found aerobic utilizat 13 and uptake 14 of endogenous lactate by the injured human brain, pointing towards alternative mechanisms of lactate release other than hypoxia/ischemia.

These findings suggest a potential role. Cerebral Vessel Anatomy. The anatomy of the cerebral circulation was recently eloquently described in detail (); therefore, discussion here will be limited to the intracranial arteries frequently studied in basilar artery, which arises from the vertebral arteries, runs along the midline of the brain stem and connects with the circle of Willis, an.

intracranial blood volume and disruption of the blood-brain barrier with vasogenic brain edema formation. This may ultimately result in elevated ICP. Alternatively, cerebral ischemia may result if CBF is too low (i.e., less than 20 ml per grams of brain tissue per minute), and the neurovasculature is unable to.

Cerebral metabolism (as reflected by cerebral oxygen and glucose consumption) and cerebral energy state (as reflected by tissue concentrations of phosphocreatine and ATP or indirectly by the lactate/pyruvate ratio) are frequently reduced after TBI and present with considerable temporal and spatial heterogeneity.

15, 12, 18, 23 The degree of. Background—Cerebral blood flow is tightly coupled to neuronal metabolic activity, a phenomenon referred to as functional mechanisms underlying functional hyperemia in the brain have been extensively studied, but the link between neuronal activation and nutritive blood flow has yet to be defined.

MISHRA: CEREBRAL BLOOD FLOW 87 SL No. – 9 Indian J. Anaesth. ; 46 (2): Adequate cerebral blood flow to each part of the brain is essential for its normal functioning as cerebral tissues are very intolerant of hypoxia.

The cessation of cerebral blood flow/ circulation for a few minutes can produce permanent damage to the brain. Cerebral Hyperemia and Ischemia. From the standpoint of cerebral blood volume, Elsevier, Amsterdam, pp 65–72 Google Scholar 3. Yoshimine T, Yanagihara T () Regional cerebral ischemia by occlusion of the posterior communicating artery and the middle cerebral artery in gerbils.

Brain Section. Title(s): Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume: proceedings of the satellite symposium, Brain Section, Fourth World Congress for Microcirculation, Osaka, Japan, August / editors, M.

Tomita. Eke, Reflectometric imaging of local tissue hematocrit in the cat brain cortex, in: “Cerebral Hyperemia and Ischemia: From the Standpoint of Cerebral Blood Volume,” M.

Tomita, T Sawada, H. Naritomi and W.D. Heiss, ed., Elsevier Science Publishers BV, Amsterdam, New York, Oxford (). Google Scholar. Middle Cerebral Artery Middle Cerebral Artery Occlusion Cerebral Blood Volume Cerebral Circulation Reactive Hyperemia These keywords were added by machine and not by the authors.

This process is experimental and the keywords may be. Cerebral Blood Flow and Metabolism After Resuscitation. A pattern of early transient postischemic hyperemia and subsequent delayed postischemic hypoperfusion has been observed almost universally in global cerebral ischemia models, including asphyxia-induced cardiac arrest.

The level of hyperemia and subsequent hypoperfusion varies in relation. Bruce Pike, R.D. Hoge, in Brain Mapping, Cerebral Blood Volume. CBV changes associated with neuronal activity modulations are believed to be both active, via the smooth muscle in the arteriolar wall and vascular pericytes, causing a change in the arteriolar vascular resistance, and passive, via dilation (constriction) of the venules and veins due to the increase.

Tomita M () Significance of cerebral blood volume. In: Tomita M, Sawada T, Naritomi H, Heiss WD (eds) Cerebral hyperemia and ischemia: from the standpoint of cerebral blood volume.

Excerta Medica, Amsterdam, pp 3–31 Google Scholar. t~rain Resear~ ~i, ~, j ii ~ I c~9(!) iSJ Elscvicl BRES Atrophy of the i lateral substantia nigra followir middle a ery occlusion in the rat Akira Tamura, Takaaki Kirino, Keiji Sano, Kiyoshi Takagi and Hidemune Oka Department of Neurosurgery, Teikyo University School of Medicine, Tokyo (Japan) (Accepted 14 November ) Key words: Rat; Middle cerebral artery; Ischemia.

To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/ g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, simultaneous measurements of ICP and CBF (xenon method) were obtained in 59 patients with moderate and severe head injury.Bouma GJ, & Muizelaar JP: Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury.

J Neurotrauma 9 (Suppl 1): S – S, Bouma GJ, Muizelaar JP: Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma 9 (Suppl 1): S–S, sulting in resolution of post-ischemic brain edema (Hossmann, ). A sensitive indicator of this process is post­ ischemic blood flow (Fig.

3). During recirculation, vessels are maximally dilated because lactacidosis and extracellular hypocalcemia cause a relaxation of vascular smooth muscles. If post-ischemic brain.