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...
Gespeichert in:
| Hauptverfasser: | , , , , , , |
|---|---|
| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
25 May 2002
|
| In: |
Microvascular research
Year: 2001, Jahrgang: 62, Heft: 3, Pages: 284-292 |
| ISSN: | 1095-9319 |
| DOI: | 10.1006/mvre.2001.2342 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: http://dx.doi.org/10.1006/mvre.2001.2342 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/abs/pii/S0026286201923428 
|
| Verfasserangaben: | T.G. Lehmann, T.A. Koeppel, S. Münch, M. Heger, M. Kirschfink, E. Klar, S. Post |
| Zusammenfassung: | 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. |
|---|---|
| Beschreibung: | Gesehen am 17.02.2021 |
| Beschreibung: | Online Resource |
| ISSN: | 1095-9319 |
| DOI: | 10.1006/mvre.2001.2342 |