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Verfasst von:Lehmann, Thorsten G. [VerfasserIn]   i
 Koeppel, Thomas [VerfasserIn]   i
 Münch, Steffen [VerfasserIn]   i
 Heger, Michael [VerfasserIn]   i
 Kirschfink, Michael [VerfasserIn]   i
 Klar, Ernst [VerfasserIn]   i
 Post, Stefan [VerfasserIn]   i
Titel:Impact of inhibition of complement by sCR1 on hepatic microcirculation after warm ischemia
Verf.angabe:T.G. Lehmann, T.A. Koeppel, S. Münch, M. Heger, M. Kirschfink, E. Klar, S. Post
E-Jahr:2001
Jahr:25 May 2002
Jahr des Originals:2001
Umfang:9 S.
Fussnoten:Gesehen am 17.02.2021
Titel Quelle:Enthalten in: Microvascular research
Ort Quelle:Orlando, Fla. : Academic Press, 1968
Jahr Quelle:2001
Band/Heft Quelle:62(2001), 3, Seite 284-292
ISSN Quelle:1095-9319
Abstract:Recent observations provide evidence that complement is implicated as an important factor in the pathophysiology of ischemia/reperfusion injury (IRI). Here, we assessed the effects of complement inhibition on hepatic microcirculation by in vivo microscopy (IVM) using a rat model of warm hepatic ischemia clamping the left pedicle for 70 min. Ten animals received the physiological complement regulator soluble complement receptor type 1 (sCR1) intravenously 1 min prior to reperfusion. Controls were given an equal amount of Ringer's solution (n = 10). Microvascular perfusion and leukocyte adhesion were studied 30 to 100 min after reperfusion by IVM. Microvascular perfusion in hepatic sinusoids was significantly improved in the sCR1 group (80.6 +/- 0.6% of all observed sinusoids were perfused [sCR1] vs 67.3 +/- 1.2% [controls]). The number of adherent leukocytes was reduced in sinusoids (49.9 +/- 3.4 [sCR1] vs 312.3 +/- 14.2 in controls [adherent leukocytes per square millimeter of liver surface]; P < 0.001) as well as in postsinusoidal venules after sCR1 treatment (230.9 +/- 21.7 [sCR1] vs 1906.5 +/- 93.5 [controls] [adherent leukocytes per square millimeter of endothelial surface]; P < 0.001). Reflecting reduced hepatocyte injury, liver transaminases were decreased significantly upon sCR1 treatment compared to controls. Our results provide further evidence that complement plays a decisive role in warm hepatic IRI. Therefore, we conclude that complement inhibition by sCR1 is effective as a therapeutical approach to reduce microcirculatory disorders after reperfusion following warm organ ischemia.
DOI:doi:10.1006/mvre.2001.2342
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: http://dx.doi.org/10.1006/mvre.2001.2342
 Volltext: https://www.sciencedirect.com/science/article/abs/pii/S0026286201923428
 DOI: https://doi.org/10.1006/mvre.2001.2342
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Cell Adhesion
 Complement C1 Inactivator Proteins
 Complement C1s
 Endothelium, Vascular
 Hemodynamics
 Injections, Intravenous
 Ischemia
 Laser-Doppler Flowmetry
 Leukocytes
 Liver Circulation
 Male
 Microcirculation
 Microscopy, Fluorescence
 Rats
 Rats, Wistar
 Receptors, Complement
 Reperfusion Injury
 Temperature
 Time Factors
 Venules
 Video Recording
K10plus-PPN:1748479733
Verknüpfungen:→ Zeitschrift

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