Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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Advances in Clinical and Experimental Medicine

2009, vol. 18, nr 2, March-April, p. 115–120

Publication type: original article

Language: English

Intestinal Ischemia, Bacterial Translocation, and Oxygen Free−Radical Production in Abdominal Compartment Syndrome

Niedokrwienie jelit, translokacja bakteryjna i wydzielanie wolnych rodników tlenowych w zespole ciasnoty wewnątrzbrzusznej

Yusuf Yagmur1,, Hayrettin Ozturk2,, Cafer Guloglu3,, Mehmet Faruk Geyik4,, Hulya Ozturk5,, Fatih Mete6,

1 Department of General Surgery, Dicle University Medical School, Diyarbakir, Turkey

2 Department of Pediatric Surgery, Abant Izzet Baysal University Medical School, Bolu, Turkey

3 Department of Emergency Medicine, Dicle University Medical School, Diyarbakir, Turkey

4 Department of Infection Disease, Duzce University Medical School, Duzce, Turkey

5 Department of Pediatric Surgery, Duzce University Medical School, Duzce, Turkey

6 Department of Pediatry, Vakif Gureba Educational Hospital, Istanbul, Turkey

Abstract

Objectives. The aim of this experimental study was to evaluate the consequences of increased intra−abdominal pressure on the small bowel and whether this pressure creates intestinal ischemia leading to oxygen free−radical production and bacterial translocation.
Material and Methods. Twenty Sprague−Dawley rats weighing 275–300 g were used. Group 1 rats (n = 10) were subjected to 20−mm Hg pneumoperitoneum pressure for 60 minutes. In group 2 rats (n = 10, controls) the intraabdominal pressure was not increased. In all rats the following parameters were investigated: mean arterial pressure after carotid catheterization, histopathological examination of the intestinal mucosa evaluated with a scoring system, malondialdehyde production in the liver and small bowel, and bacterial translocation towards the mesenteric lymph nodes, liver, and spleen 24 hours after pneumoperitoneum deflation.
Results. The mean arterial pressure exhibited no alterations. Histological analysis mainly showed extensive epithelial separations from the lamina propria down the sides of the villi and ulceration at the villus tips in the rats with increased intra−abdominal pressure. Bacterial translocation occurred to the mesenteric lymph nodes, spleen, and liver after 60 minutes of increased intra−abdominal pressure of 20 mm Hg (p < 0.05). Malondialdehyde increased in the liver and small bowel mucosa (p < 0.05 for both).
Conclusion. Increased intra−abdominal pressure in rats leads to intestinal ischemia and mild histological changes in the small bowel and to oxygen free−radical production and bacterial translocation.

Streszczenie

Cel pracy. Ocena wpływu zwiększonego ciśnienia wewnątrz jamy brzusznej na jelito cienkie. Zbadano ponadto, czy zwiększone ciśnienie wewnątrz jamy brzusznej wywołuje niedokrwienie jelit prowadzące do wydzielania wolnych rodników tlenowych i translokacji bakteryjnej.
Materiał i metody. Badanie doświadczalne przeprowadzono w grupie 20 szczurów Sprague−Dawley o masie 275–300 g. U szczurów w grupie 1 (n = 10) wytworzono na 60 minut odmę otrzewnową (20 mm Hg) i badano wpływ zwiększonego ciśnienia wewnątrz jamy brzusznej na błonę śluzową jelita cienkiego, wytwarzanie wolnych rodników tlenowych i translokację bakteryjną. W grupie 2 (n = 10, grupa kontrolna) ciśnienie wewnątrz jamy brzusznej nie było zwiększone. U wszystkich szczurów oceniano średnie ciśnienie tętnicze; wykonano badanie histopatologiczne błony śluzowej jelita cienkiego z zastosowaniem systemu punktowego; badano wydzielanie aldehydu dimalonowego w wątrobie i jelicie cienkim; translokację bakteryjną do krezkowych węzłów chłonnych, wątroby i śledziony 24 godziny po odmie otrzewnowej.
Wyniki. Nie wykazano różnic w średnim ciśnieniu tętniczym. Badanie histologiczne wykazywało przede wszystkim obfite oddzielanie komórek nabłonka od blaszki właściwej, owrzodzenia na szczytach kosmków u szczurów poddawanych zwiększonemu ciśnieniu wewnątrz jamy brzusznej. Translokacja bakteryjna do krezkowych węzłów chłonnych, śledziony i wątroby pojawiała się po 60 minutach działania ciśnienia 20 mm Hg (p < 0,05). Wydzielanie aldehydu dimalonowego zwiększało się w wątrobie i błonie śluzowej jelita cienkiego (p < 0,05 dla obu).
Wnioski. Zwiększone ciśnienie wewnątrz jamy brzusznej u szczurów prowadzi do niedokrwienia jelit, łagodnych zmian histologicznych w jelicie cienkim, wydzielania wolnych rodników tlenowych oraz translokacji bakteryjnej.

Key words

abdominal compartment syndrome, intestinal ischemia, bacterial translocation, rat

Słowa kluczowe

zespół ciasnoty wewnątrzbrzusznej, niedokrwienie jelit, translokacja bakteryjna, szczur

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