DENEYSEL PERİTONEAL SEPSİS MODELİNDE SPLENEKTOMİ SONRASI KARACİĞER KUPFFER HÜCRE PROLİFESYONUNUN ETKİLERİ

Splenektomili ve splenektomisiz ratlarda , Karaciğer makrofajları olan Kupffer hücrelerinin E. Coli’ye yanıtları araştırılmıştır. Splenektomi yapılan ratlarda belirgin olarak fazla miktarda Kupffer hücre proliferasyonu görülmektedir. Bizde eksperimentel model üzerinde daha önceleri üzerinde çalışılmış olan Kupffer hücrelerinin peritonitteki koruyucu etkilerini araştırdık. Bu çalışmada 32 rat dört gruba ayrıldı.Birinci grup sham ,ikinci grup splenektomi,üçüncü grup splenektomi ve intraperitoneal E.Coli solüsyonu grubuydu. Son gruba ise splenektomi yapılmayıp,intraperitoneal bakteri verildi. Çalışma sonunda splenektomili ratlarda 2.Grup Kupffer hücre proliferasyonu olduğu ve splenektomiye ilaveten E.Coli ile peritonit yapılan grupla 3.Grup splenektomisiz grupta 4 Grup belirgin farklılık bulamadık

THE EFFECT OF POSTSPLENECTOMIC KUPFFER CELL PROLIFERATION IN THE EXPERIMENTAL MODEL OF PERITONEAL SEPSIS

The response of liver macrophages Kupffer cells to the pathogenic material E.Coli was investigate by comparing splenectomized versus non splenectomized rats. In response to splenectomy much more Kupffer cell proliferation was detected than splenic rats. Since previous studies have demonstrated that Kupffer cells proliferation in the liver were a protective effect of the peritonitis induced by E. Coli, we investigated it in experimental model.In this study 32 rats divided into four groups. The group one is sham,second group is splenectomy, third is splenectomy and intraperitoneal E.Coli inoculated group and last one is nonsplenectomized intraperitoneal E.Coli inoculated group. The results of this study suggest that Kupffer cell was significantly increased in rats with splenectomy Group 2 . There is no different correlation between splenectomy plus E.Coli group Group 3 and E.Coli inoculated group Group 4

___

  • Boulton RA, Allison MR, Goldina M, Selden C, Hodgkin HJ. Augmentation of the early phase of liver regeneration after 70 % partial hepatectomy in rats following selective kupffer cell depletion. J. Hepatol 1998; 29: 271-280
  • Mc Cuskey RS, Mc Cuskey PA The structure and function of kupffer cells. J.Electron-Microsc. Tech 1990; 14: 237-246
  • Okabayashi K, Ohtani M, Morio M, Kajihara H. Structural changes of Kupffer cells in rat liver following experimental termal injury. Burns 1990; 16: 83-88.
  • Eallery MP, Kamen T, Flye M. Kupffer cell blockade increases mortality during intraabdiminal sepsis despite improving systemic immunity. Arch Surg 1990; 125: 36-40
  • Baykal A, Ağlar F. Bakteriyel Translokasyon.In:Sayek İ, Coker A, Sökmen S, editörler. Cerrahi İnfeksiyon.1.Baskı Güneş Kitabevi; 2001: s.74-82
  • Decker K. The response of liver macrophages to inflamatory stimulation. Keio J. Med 1998; 47: 1-9
  • Busam KJ, Bauer TM, Bauer J et al. Interleukin 6 relase by rat liver macrophages. J. Hepatol 1990; 11: 367-373
  • Chaudry H, Zellweger R, Ayala A. The role of bacteriel translocation on kupffer cellimmune function following hemorhage. Prog. Clin. Biol. Res. 1995; 392: 209-218
  • Tiqhe D, Moss R, Boghossion S et al. Multiorgan demage resulting from experimental faecal peritonitis. Clin Sci 1989; 76: 269- 276.
  • Rotstein OD, Kao J, Houston K. Reciprocal synergy between Escherichia coli and Bacteroides Fragillis in an intra-abdominal infection model. J. Med. Microbiol, 1989; 29: 269-276.
  • Verwej-Van Vught A, Namauar F, Sparrius M et al. Pathogenic synergy between E. Coli and Bacteroides Fragillis: studies in an experimental mouse model. J. Med. Microbiol. 1985; 19: 325-331.