Role of prostaglandins in lipopolysaccharide effects on K+-induced contractions in rabbit small intestine
Autor: | M. P. Arruebo, M. A. Plaza, E. Rebollar, María Divina Murillo, E. Guerrero-Lindner |
---|---|
Rok vydání: | 2003 |
Předmět: |
medicine.medical_specialty
Lagomorpha Lipopolysaccharide Physiology medicine.medical_treatment digestive oral and skin physiology Ileum Biology biology.organism_classification digestive system Small intestine Jejunum chemistry.chemical_compound Endocrinology medicine.anatomical_structure chemistry Internal medicine medicine Duodenum lipids (amino acids peptides and proteins) Prostaglandin E2 Prostaglandin E medicine.drug |
Zdroj: | Acta Physiologica Scandinavica. 179:299-307 |
ISSN: | 0001-6772 |
Popis: | Aim: The mediators of the pathophysiologcal symptoms of septic shock are not completely understood. The aim of this work was to investigate the effect of lipopolysaccharide (LPS) on the K + -induced response of longitudinal segments of rabbit small intestine in vitro and the possible role of prostaglandins. Methods and results: Rabbits were treated with intravenously injected LPS. After 90 min animals were killed and intestinal segments were mounted in an organ bath. Lipopolysaccharide (0.2 μg kg -1 ) inhibited K + -induced contractions (60 mM) by 68% in duodenum, 58% in jejunum and 52% in ileum. Indomethacin antagonized LPS actions when injected 15 min before LPS. PGE 2 reduced K + -induced contractions, imitating LPS effects. In contrast, contractions induced by K + increased when intestinal segments were incubated in vitro with LPS for 90 min. The LPS (0.3 μg mL -1 ) increased K + -induced contractions (60 mM) by 46% in duodenum, 63% in jejunum and 85% in ileum. The LPS effect was antagonized by indomethacin at 10 -6 M in duodenum and jejunum and at 10 -8 M in ileum. PGE 2 evoked dose-dependent contractions when added to the bath in duodenum, jejunum and ileum. Conclusion: These results suggest that effect of LPS on K + -induced contractions in the rabbit small bowel may be mediated by prostaglandin E 2 . |
Databáze: | OpenAIRE |
Externí odkaz: |