You are here

Home » Content

Sepsis Oluşturulan Ratlarda Kan Glukoz Düzeyinin Mortaliteye Etkisi

The effect of blood glucose level in experimental of sepsis rats on mortality

Journal Name:

  • Fırat Tıp Dergisi

Publication Year:

  • 2007

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
Objectives: The recent multitask studies made in the intensive care unites, it is detected that blood glucose level is one of the most determining factors for mortality. In this study the blood glucose level in experimental of sepsis in rats is altered and the effect of blood glucose level alterations on mortality is studied. Material and Methods: 60 wistard rats are included into the study. An artificial sepsis model is designed in all subjects by matching an intraperitoneal injection of 5 mg/kg E.Coli LPS in order to determine the bacterial translocation. The subjects are divided into two groups which include the group coith blood glucose level between 85-110 and the diabetic group with blood glucose level between 180-215. Tissue samples (mesenteric lymph node, liver, spleen) are taken from the subjects which died after shocoing symptoms of shock. Bacterial translocation is studied by using PCR and blood culture methods. Results: All the subjects in the diabetic group died in the first five day and all the subjects in the control group died in the first twelve days after LPS application. The mortality rate in the diabetic group is detected as statistically significant higher than the mortality rate in the control group (p<0.05) Conculation: In this study mortality of experimental sepsis in rats with only alterations in blood glucose level is studied. We come to the conclusion that mortality rate is decreasing experimental sepsis in rats by keeping the blood glucose level between 80-110 mg/dl. ©2007, Firat University, Medical Faculty
Bookmark/Search this post with
Abstract (Original Language): 
Giriş: Son yıllarda yoğun bakım ünitelerinde yapılan çok merkezli çalışmalarda mortalitenin önemli belirleyicilerinden birisinin de kan glukoz düzeyi olduğu saptanmıştır. Bu çalışmada sepsis oluşturulan ratlarda sadece kan glukoz düzeyi değişken tutulup bunun mortaliteye etkileri araştırıldı. Gereç ve Yöntem: 60 adet wistard türü rat çalışmaya alındı.Tüm hayvanlarda bakteriyel translokasyonu tespit edebilmek amacıyla; E. Coli lipopolisakkarit'i (LPS) 5 mg/kg intraperitoneal olarak uygulanarak sepsis modeli oluşturuldu. Denekler kontrol grubunda kan glukoz düzeyi 85-110 mg/dl olanlar ve diabetik grupta ise 180-215 mg/dl arasında olanlar olmak üzere iki gruba ayrıldı. Şok belirtileri saptandıktan sonra ölen ratlardan, doku örnekleri (Mezenter lenf nodu, karaciğer, dalak) alındı. Polymerase Chain Reaction (PCR) ve kültür yöntemi ile bakteriyel translokasyon Araştırıldı. Bulgular: Diyabetik gruptaki ratlara LPS uyguladıktan sonra 5 gün içinde tamamı, kontrol grubunda ise 12 gün içinde tamamı kaybedildi. Mortalite hızı diabetik grupta, kontrol grubuna göre yüksek olarak bulundu (p<0.05). Sonuç: Bu çalışmada sepsis oluşturulan ratlarda sadece kan glukoz düzeyi değişken tutulup mortaliteye bakıldı. Sonuç olarak, sepsis oluşturulan ratlarda kan glukoz düzeyinin 80-110 mg/dl aralığında tutulduğunda mortalite hızının düştüğü kanısına vardık. ©2007, Fırat Üniversitesi, Tıp Fakültesi
FULL TEXT (PDF): 
PDF icon arastirmax-sepsis-olusturulan-ratlarda-kan-glukoz-duzeyinin-mortaliteye-etkisi.pdf
  • 1
1-4
  • Turkish

REFERENCES

References: 

1. Angus DC,
Lind
e WT, Lidicker J, et al. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome and associated costs of care. Crit Care Med 2001; 29: 1303-1310.
2. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill. N Engl J Med 2001 345: 1359-1367.
3. Baker WJ, Edwin AD, Berg RD, et al. Hemorrhagic Shock Induces Bacterial Translocation from the Gut. The Journal of
Trauma 1988: 28; 896-904.
4. Sambrook J, Fritsch E, Maniatis T. Moleculer Cloning: A Laboratory Manuel, Ed. 2. Cold Spring Harbor Laboratory Pres:
New York, 1989.
5. Kane TD, Johnson SR, Alexander JW, et al. Detection of intestinal bacterial translocation using PCR. J Surg Res 1996; 63:
59-63.
6. Kazez A, Saglam M, Doymaz MZ, et al. Detection of bacterial translocation during intestinal distension in rats using the polymerase chain reaction. Pediatr Surg Int 2001; 17: 624-627.
3
Fırat Tıp Dergisi 2007;12(1):01-04
7. Mizrock BA: Alterations in carbohydrate metabolism during
stress
: a review of the literature. Am J Med, 1995: 98:75-107
8. Inzucchi SE, Goldberg PA, Dziura JD,et al. Risk factors for poor glycemic control in a medical intensive care unit (ICU) (Abstract). Diabetes 52 (Suppl. 1):A96, 2003
9. Preiser J-C, Devos P, Van den Berghe G. Tight control of glycaemia in critically ill patients. Curr Opin Clin Nutr Metab
Care 2002; 5: 533-537.
10. Oliver MF, Opie LH. Effects of glucose and fatty acids on myocardial ischaemia and arrythmias. Lancet 1994; 343:155-158
11. Undurti ND. Current advances in sepsis and septic shock with particular emphasis on the role of insulin.Med Sci Monit 2003;
9:181-192.
12. Losser MR, Bernard C, Beaudeux JL, et al. Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits. J Appl Physiol 1997; 83: 1566¬1574.
13. Ling PR, Lydon E, Frederich RC, et al. Metabolic effects of insulin and insulin-like growth factor-1 in endotoxemic rats during total parenteral nutrition feeding. Metabolism 2000; 49:
611-615.
Yaşar
v
e Ark
14. Ljungqvist O, Nygren J, Thorell A. Insulin resistance and elective surgery. Surgery 2000; 128: 757-760.
15. Gore DC, Chinkes D, Heggers J, et al.. Association of hyperglycemia with increased mortality after severe burn injury. J Trauma 2001; 51: 540-544.
16. Chambrier C, Laville M, Rhzioual Berrada K, et al: Insulin sensitivity of glucose and fat metabolism in severe sepsis. Clin
Sci (Colch) 2000; 99: 321-328.
17. Dahn MS, Lange MP, Mitchell RA, et al: Insulin production following injury and sepsis. J Trauma 1987; 27: 1031-1038.
18. Raymond RM, Harkema JM, Emerson TE. In vivo skeletal muscle insulin resistance during E Coli endotoxin shock in the dog. Circ Shock 1981; 8: 425-433.
19. Maitra SR, Wang S, Baithwaite CE, et al. Alterations in glucose-6-phosphatase gene expression in sepsis. J Trauma 2000; 49: 38¬42.

Thank you for copying data from http://www.arastirmax.com