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This Article Full Text Full Text (PDF) All Versions of this Article: 286/5/G791    most recent 00407.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (11) Citing Articles via Google Scholar Google Scholar Articles by von Dobschuetz, E. Articles by Messmer, K. Search for Related Content PubMed PubMed Citation Articles by von Dobschuetz, E. Articles by Messmer, K.

INFLAMMATION/IMMUNITY/MEDIATORS

Soluble complement receptor 1 preserves endothelial barrier function and microcirculation in postischemic pancreatitis in the rat

¹Department of General and Visceral Surgery, Albert Ludwigs University, 79106 Freiburg; ²Institute for Surgical Research, Ludwig Maximilians University, 81366 Munich; ³Department of Urology, University of Mainz, 55101 Mainz; ⁴Department of Otorhinolaryngology, Ludwig Maximilians University, 81377 Munich, Germany; and ⁵Maria Theresia Klinik, 80336 Munich, Germany

Submitted 17 September 2003 ; accepted in final form 18 December 2003

Components of the activated complement cascade are considered to play a pivotal role in ischemia-reperfusion-induced organ injury. With the use of intravital epifluorescence microscopy, we investigated the effect of complement inhibition by the recombinant soluble complement receptor 1 (sCR1; TP10) on the effect of macromolecular microvascular permeability, functional capillary perfusion, and leukocyte endothelium interaction in postischemic pancreatitis. Anaesthetized Sprague-Dawley rats were subjected to 60 min of normothermic pancreatic ischemia induced by microclipping of the blood-supplying arteries of the organ. Rats who received sCR1 (15 mg/kg body wt iv; n = 7) during reperfusion showed a significant reduction of permeability (1.77 ± 1.34 x 10^-8 cm/s; n = 7) of tetramethylrhodamine isothiocyanate-labeled albumin injected 90 min after the onset of reperfusion compared with vehicletreated animals (6.95 ± 1.56 x 10^-8 cm/s; n = 7). At 120 min after the onset of reperfusion, the length of red blood cell-perfused capillaries (functional capillary density) was significantly improved (from 279 ± 15.7 to 330 ± 3.7 cm^-1; n = 7) and the number of leukocytes adherent to postcapillary venules was significantly reduced (from 314 ± 87 to 163 ± 71 mm^-2; n = 7) by sCR1 compared with vehicle treatment. Complement inhibition by sCR1 effectively ameliorates pancreatic ischemia-reperfusion-induced microcirculatory disturbances and might be considered for treatment of postischemic pancreatitis.

permeability; ischemia; reperfusion; acute pancreatitis; transplantation

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				W. Hartwig, M. Klafs, M. Kirschfink, T. Hackert, L. Schneider, M.-M. Gebhard, M. W. Buchler, and J. Werner Interaction of complement and leukocytes in severe acute pancreatitis: potential for therapeutic intervention. Am J Physiol Gastrointest Liver Physiol, November 1, 2006; 291(5): G844 - G850. [Abstract] [Full Text] [PDF]