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Verfasst von:Lenz, Christian [VerfasserIn]   i
 Rebel, Annette [VerfasserIn]   i
 Bucci, Enrico [VerfasserIn]   i
 Ackern, Klaus van [VerfasserIn]   i
 Kuschinsky, Wolfgang [VerfasserIn]   i
 Waschke, Klaus F. [VerfasserIn]   i
Titel:Lack of hypercapnic increase in cerebral blood flow at high blood viscosity in conscious blood-exchanged rats
Verf.angabe:Christian Lenz, Annette Rebel, Enrico Bucci, Klaus van Ackern, Wolfgang Kuschinsky, Klaus F. Waschke
E-Jahr:2001
Jahr:[2001]
Umfang:8 S.
Illustrationen:Diagramme
Fussnoten:Gesehen am 19.05.2021
Titel Quelle:Enthalten in: Anesthesiology
Ort Quelle:Hagerstown, Md. : Lippincott Williams & Wilkins, 1940
Jahr Quelle:2001
Band/Heft Quelle:95(2001), 2, Seite 408-415
ISSN Quelle:1528-1175
Abstract:The hypothesis of a compensatory dilation of cerebral vessels to maintain cerebral blood flow at a high blood viscosity was tested during hypercapnia in the study after replacement of blood by hemoglobin solutions of defined viscosities. If compensatory vasodilation exists at normocapnia at a high blood viscosity, vasodilatory mechanisms may be exhausted when hypercapnia is added, resulting in a lack of increase in cerebral blood flow at hypercapnia.In conscious rats, blood was replaced by ultrapurified cross-linked hemoglobin solutions that had defined and shear rate-independent low or high viscosities (low- and high-viscosity groups). Blood viscosity differed threefold between both groups (1.2 vs. 3.6 mP x s). Thereafter, rats inhaled either a normal or an increased concentration of carbon dioxide in air. Cerebral blood flow was determined by the iodo[14C]antipyrine method.During normocapnia, global and local cerebral blood flows did not differ between both groups. With increasing degrees of hypercapnia, global and local cerebral blood flows were gradually elevated in the low-viscosity group (2.8 ml x mmHg(-1) CO2 x 100 g(-1) x min(-1)), whereas they remained unchanged in the high-viscosity group.Changes in blood viscosity do not result in changes of cerebral blood flow as long as cerebral vessels can compensate for these changes by vasodilation or vasoconstriction. However, such vascular compensatory adjustments may be exhausted in their response to further pathophysiologic conditions in blood vessels that have already been dilated or constricted as a result of changes in blood viscosity.
DOI:doi:10.1097/00000542-200108000-00024
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1097/00000542-200108000-00024
 DOI: https://doi.org/10.1097/00000542-200108000-00024
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1758156554
Verknüpfungen:→ Zeitschrift

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