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Complement inhibition by soluble complement receptor type 1 improves microcirculation after rat liver transplantation.
Transplantation. 1998 Sep 27; 66(6):717-22.T

Abstract

BACKGROUND

Recent observations provide evidence that complement is involved in the pathophysiology of ischemia/reperfusion injury. In this study, we assessed the impact of complement inhibition on hepatic microcirculation and graft function using a rat model of liver transplantation.

METHODS

Arterialized orthotopic liver transplantation was performed in Lewis rats after cold preservation (University of Wisconsin solution, 4 degrees C, 24 h). Eight animals received the physiological complement regulator soluble complement receptor type 1 (sCR1) intravenously 1 min before reperfusion. Controls received Ringer's solution (n=8). Microvascular perfusion, leukocyte adhesion, and Kupffer cell phagocytic activity were studied 30-100 min after reperfusion by in vivo microscopy.

RESULTS

Microvascular perfusion in hepatic sinusoids was improved in the sCR1 group (87+/-0.7% vs. 50+/-1%; P < 0.001). The number of adherent leukocytes was reduced in sinusoids (68.3+/-4.7 vs. 334.1+/-15.8 [adherent leukocytes per mm < or = liver surface]; P < 0.001) and in postsinusoidal venules after sCR1 treatment (306.6+/-21.8 vs. 931.6+/-55.9 [adherent leukocytes per mm < or = endothelial surface]; P < 0.001). Kupffer cell phagocytic activity was decreased in the sCR1 group compared to controls. Postischemic bile production reflecting hepatocellular function was increased by almost 200% (P = 0.004) after complement inhibition. Plasmatic liver enzyme activity was decreased significantly upon sCR1 treatment, indicating reduced parenchymal cell injury.

CONCLUSIONS

Our results provide further evidence that the complement system plays a decisive role in hepatic ischemia/reperfusion injury. We conclude that complement inhibition by sCR1 represents an effective treatment to prevent reperfusion injury in liver transplantation.

Authors+Show Affiliations

Department of General Surgery, University of Heidelberg, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9771834

Citation

Lehmann, T G., et al. "Complement Inhibition By Soluble Complement Receptor Type 1 Improves Microcirculation After Rat Liver Transplantation." Transplantation, vol. 66, no. 6, 1998, pp. 717-22.
Lehmann TG, Koeppel TA, Kirschfink M, et al. Complement inhibition by soluble complement receptor type 1 improves microcirculation after rat liver transplantation. Transplantation. 1998;66(6):717-22.
Lehmann, T. G., Koeppel, T. A., Kirschfink, M., Gebhard, M. M., Herfarth, C., Otto, G., & Post, S. (1998). Complement inhibition by soluble complement receptor type 1 improves microcirculation after rat liver transplantation. Transplantation, 66(6), 717-22.
Lehmann TG, et al. Complement Inhibition By Soluble Complement Receptor Type 1 Improves Microcirculation After Rat Liver Transplantation. Transplantation. 1998 Sep 27;66(6):717-22. PubMed PMID: 9771834.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Complement inhibition by soluble complement receptor type 1 improves microcirculation after rat liver transplantation. AU - Lehmann,T G, AU - Koeppel,T A, AU - Kirschfink,M, AU - Gebhard,M M, AU - Herfarth,C, AU - Otto,G, AU - Post,S, PY - 1998/10/15/pubmed PY - 1998/10/15/medline PY - 1998/10/15/entrez SP - 717 EP - 22 JF - Transplantation JO - Transplantation VL - 66 IS - 6 N2 - BACKGROUND: Recent observations provide evidence that complement is involved in the pathophysiology of ischemia/reperfusion injury. In this study, we assessed the impact of complement inhibition on hepatic microcirculation and graft function using a rat model of liver transplantation. METHODS: Arterialized orthotopic liver transplantation was performed in Lewis rats after cold preservation (University of Wisconsin solution, 4 degrees C, 24 h). Eight animals received the physiological complement regulator soluble complement receptor type 1 (sCR1) intravenously 1 min before reperfusion. Controls received Ringer's solution (n=8). Microvascular perfusion, leukocyte adhesion, and Kupffer cell phagocytic activity were studied 30-100 min after reperfusion by in vivo microscopy. RESULTS: Microvascular perfusion in hepatic sinusoids was improved in the sCR1 group (87+/-0.7% vs. 50+/-1%; P < 0.001). The number of adherent leukocytes was reduced in sinusoids (68.3+/-4.7 vs. 334.1+/-15.8 [adherent leukocytes per mm < or = liver surface]; P < 0.001) and in postsinusoidal venules after sCR1 treatment (306.6+/-21.8 vs. 931.6+/-55.9 [adherent leukocytes per mm < or = endothelial surface]; P < 0.001). Kupffer cell phagocytic activity was decreased in the sCR1 group compared to controls. Postischemic bile production reflecting hepatocellular function was increased by almost 200% (P = 0.004) after complement inhibition. Plasmatic liver enzyme activity was decreased significantly upon sCR1 treatment, indicating reduced parenchymal cell injury. CONCLUSIONS: Our results provide further evidence that the complement system plays a decisive role in hepatic ischemia/reperfusion injury. We conclude that complement inhibition by sCR1 represents an effective treatment to prevent reperfusion injury in liver transplantation. SN - 0041-1337 UR - https://www.unboundmedicine.com/medline/citation/9771834/Complement_inhibition_by_soluble_complement_receptor_type_1_improves_microcirculation_after_rat_liver_transplantation_ L2 - https://doi.org/10.1097/00007890-199809270-00005 DB - PRIME DP - Unbound Medicine ER -