Journals / SSK İzmir Eğitim Hastanesi Tıp Dergisi / 2004 / Cilt: 10 - Sayı: 1

The effect of intravenous UDCA in experimental endotoxemia

Deneysel endotoksemide intravenöz ursodeoksikolik asitin (UDCA) etkisi

Pages
27–31
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

According to the results of various studies bile salts could have a role as a natural defence mechanism against the effects of the endotoxemia.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Endotoxin, which is in the form liposaccharide and is at the outermost of the bacteria cell, has still been conntinuing to be one of the reasons of high mortality rate by causing synthesis and secretion of eytokins which have roles on teh development of multiple organ failure and shock.
📊
Key Findings & Data:It has been reported that bile acid concentration is reduced in endotoxemia, and at portal venous side by administiring bile acid, ehdotoxemia is getting decreased.
💡
Conclusion & Impact:According to the results of various studies bile salts could have a role as a natural defence mechanism against the effects of the endotoxemia.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Endotoksemi · Ursodeoksikolik asit · Hayvan deneyleri

Abstract

Endotoxin, which is in the form liposaccharide and is at the outermost of the bacteria cell, has still been conntinuing to be one of the reasons of high mortality rate by causing synthesis and secretion of eytokins which have roles on teh development of multiple organ failure and shock. It has been reported that bile acid concentration is reduced in endotoxemia, and at portal venous side by administiring bile acid, ehdotoxemia is getting decreased. According to the results of various studies bile salts could have a role as a natural defence mechanism against the effects of the endotoxemia. This study has been planned to find out the effects of IV given UDCA on an experimental endotoxemia model at rabbits.The study consisted a control (n= 10) and a study group (n= 10). Under ketamine HCI and Xylasine anesthesia, it was given IV 0.1 mg/kg endotoxin of E. Coli after the administration IV UDCA with dose of mg/kg to the study group. Only was endotoxin given with same dose to the control group. The groups were compared with regards to mortality and survival after 24 hours. The histopathologic samples of livers, kidneys and lungs that had been taken from animals deceased or sacrified at the end the experiment period were examined. Nine out 10 in the control (90%) and 4 out of 10 (40%) in the study group died (p <0.02). Histopathologic changes were less in the study group than the control group. We concluded that IV administered UDCA might have some utility in an experimental endotoxemia model of rabbits. However, we believe more advanced stuies are needed in this field.

Özet

Bakteri hücresinin en dış kısmında bulunan liposakkarit yapısındaki endotoksin, multipl organ yetmezliği ve şok gelişiminde rol oynayan sitokinlerin yapım ve salınımına neden olarak, hala yüksek mortalite sebeplerinden birisi olamaya devam etmektedir. Endotoksemide serum safra asiti konsantrasyonlarının azaldığı ve safra tuzlarının verilmesinin portal venöz alandaki endotoksemiyi azalttığı rapor edilmiştir. Çeşitli çalışmalarda elde edilen veriler endotokseminin ektilerine karşı safra tuzlarının doğal bir savunma mekanizması olarak rol oynadıklarına işaret etmektedir. Bu çalışma tavşanlarda deneysel olarak oluşturlan endotoksemi üzerine intrayenöz yolla verilen UDCA'in etkilerini ortaya çıkartmak amacıyla yapıldı. Çalışmamız tavşanlar üzerinde kontrol (n=10) ve çalışma (n=10) grupları olmak üzere iki kolda yürütüldü. Çalışma grubuna Ketamin HCI+Ksilazin anestezisi altında 5 mg/kg dozunda İV UDCA verilmesini takiben, 0.1 mg/kg E. Coli endotoksini verildi. Kontrol grubuna aynı dozda yanlızca endotoksin verildi. Gruplar 24 saat sonra mortalite ve sağkalım açısından kıyaslandılar. Ölen veya deney sonunda sakrifiye edilen hayvanlardan alınan karaciğer, böbrek ye akciğer dokularının histopatolojik incelemesi yapıldı. Kontrol grubunda 10 tavşanın 9'u (%90), çalışma grubunda ise 4'ü (%40) öldü (p <0.02). Çalışma grubundaki histopatolojik değişiklikler kontrol grubuna oranla daha az idi. İV yolla verilen UDCA'in tavşanlardaki endotoksemi modeline yararlı olabileceeği sonucuna varıldı. Bu konuda daha ileri çalışmalara gereksinim vardır.

🔖

Cite This Article

GENÇ, H., YOLCUOĞLU, B., HACIYANLI, M., TAVUSBAY, C., ÖZGÜN, H., ÖZKAL, S., CANDA, Ş. (2004). The effect of intravenous UDCA in experimental endotoxemia. SSK İzmir Eğitim Hastanesi Tıp Dergisi, Cilt: 10 - Sayı: 1, 27–31. https://ajindex.com/articles/313034

References (15)

  1. Shenep JL, Magan KA: Kinetics of endotoxin release during antibiotic therapy for experimental gram-negative bacterial sepsis. J Infect Dis 1984; 150: 380-388
  2. Cannon JG, Tompkins RG, Gelfand JA, et al: Circulating interleukin 1 and tumor necrosis factor in septic shock and experimental endotoxin fever. J Infect Dis 1990; 161: 79-84
  3. Thompson JN, Cohen J, Moore RH, etal: Endotoxemia in obstructive jaundice. Am J Surg 1988; 155: 314-321
  4. Gouma DJ, Coelho JC, Fisher JD, et all. Endotoxemia after relief of biliary obstruction by internal and external drainage in rats. Am J Surg 1986; 151: 476-9
  5. Hori Y, Ohyanagi H.: Protective effect of the intravenous administration of ursodeoxycholic acid against endotoxemia in rats with obstructive jaundice. Surg Today 1997; 27:140-144
  6. Schwarzenberg SJ, Bundy M: Ursodeoxycholic acid modifies gut-derived endotoxemia in neonatal rats. Pediatr Res 1994; 35: 214-217
  7. Baldwin G, Alpert G, Caputo GL, et al: Effect of polymyxin B on experimental shock from meningococcal and Escherichia Coli v endotoxins. J Infect Dis 1991; 165: 542-549
  8. Yoshioka T, Goto M, Gottschalk ME et all. Plasma endotoxin concentration after an intraperitoneal injection of endotoxin in fed and fasted suckling rats. Shock 1994; 1: 362-365
  9. Raetz, CRH: Biochemistry of endotoxins. Ann Rev.Bio-chem 1990; 59:129
  10. Cue Jl, Dipiro JT, Bruner JL, et. all. Reconstituted high density lipoprotein inhibits physiologic and tumor necrosis factor a responses lipopolysaccharide in rabbits. Arch Surg 1994; 129:193-197
  11. Liao W, Floren CH. Hiperlipidemic response to endotoxin. Scand J Infect Dis 1993; 25: 675-682
  12. Munford RS, Hall CL, Dietschy JM: Binding of salmonella thphimurium lipopolysaccharides to rat high density lipoproteins. Infect Immunol. 1981; 34: 835-843
  13. Harris HW, Grunfeld C, Feingold KR, et al.: Chylomicrons alter the fate of endotoxin, decreasing tumor necrosis factor release and preventing death. J Clin Invest 1993; 91: 1028-1034
  14. Parker MM, Parrillo JE. Septic shock hemodynamics and pathogenesis. JAMA 1983; 250: 3324-3331
  15. Pain JA, Bailey ME.Prevention of endotoxemia in obstructive jaundice HPB Surg 1988; 1: 21-27.