Impact of inhibition of complement by sCR1 on hepatic microcirculation after warm ischemia
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 isch...
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| Main Authors: | , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
25 May 2002
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| In: |
Microvascular research
Year: 2001, Volume: 62, Issue: 3, Pages: 284-292 |
| ISSN: | 1095-9319 |
| DOI: | 10.1006/mvre.2001.2342 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: http://dx.doi.org/10.1006/mvre.2001.2342 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/abs/pii/S0026286201923428 
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| Author Notes: | T.G. Lehmann, T.A. Koeppel, S. Münch, M. Heger, M. Kirschfink, E. Klar, S. Post |
MARC
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| 245 | 1 | 0 | |a Impact of inhibition of complement by sCR1 on hepatic microcirculation after warm ischemia |c T.G. Lehmann, T.A. Koeppel, S. Münch, M. Heger, M. Kirschfink, E. Klar, S. Post |
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| 520 | |a 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. | ||
| 534 | |c 2001 | ||
| 650 | 4 | |a Animals | |
| 650 | 4 | |a Cell Adhesion | |
| 650 | 4 | |a Complement C1 Inactivator Proteins | |
| 650 | 4 | |a Complement C1s | |
| 650 | 4 | |a Endothelium, Vascular | |
| 650 | 4 | |a Hemodynamics | |
| 650 | 4 | |a Injections, Intravenous | |
| 650 | 4 | |a Ischemia | |
| 650 | 4 | |a Laser-Doppler Flowmetry | |
| 650 | 4 | |a Leukocytes | |
| 650 | 4 | |a Liver Circulation | |
| 650 | 4 | |a Male | |
| 650 | 4 | |a Microcirculation | |
| 650 | 4 | |a Microscopy, Fluorescence | |
| 650 | 4 | |a Rats | |
| 650 | 4 | |a Rats, Wistar | |
| 650 | 4 | |a Receptors, Complement | |
| 650 | 4 | |a Reperfusion Injury | |
| 650 | 4 | |a Temperature | |
| 650 | 4 | |a Time Factors | |
| 650 | 4 | |a Venules | |
| 650 | 4 | |a Video Recording | |
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