endothelin-1 and Intestinal-Obstruction

Topics: Animals; Biomarkers; Early Diagnosis; Endothelin-1; Intestinal Obstruction; Rabbits

Large intestinal obstruction (LIO) in farm animals can cause a ischaemic necrosis of intestinal tissue, eventually leading to death. The roles of endothelin-1 (ET-1) and nitric oxide (NO) are not well understood in the process of LIO, but evidence suggests that endothelial-derived mediators may participate. In the present study, ET-1 concentration and total nitric oxide synthase (NOS) activity were measured in heart, liver, pancreas, lung and kidney in a model of LIO in sheep. Our data demonstrated that ET-1 concentration and NOS activity were altered, with significant increases of ET-1 in heart, lung and kidney and of NOS activity in pancreas and kidney, but a marked decline of NOS activity in liver (p < 0.05). It is postulated that these alterations in NOS activity and ET-1 concentration may contribute to the progressive loss of organ function, and finally lead to death in LIO in sheep.

Topics: Animals; Disease Models, Animal; Endothelin-1; Intestinal Obstruction; Intestine, Large; Nitric Oxide Synthase; Organ Specificity; Random Allocation; Sheep

Evidence has been provided that increased portal vein pressure results in increased release of endothelin-1 (ET-1). Strangulation obstruction is associated with increased venous pressure, and we wanted to determine if it is associated with increased local release of ET-1 and elevated concentration of ET-1 in systemic blood. Strangulation obstruction was induced by elevating pressure in a gasket placed around a loop of ileum until venous pressure reached 50 mm Hg. Ischemia in a bowel loop was induced by arterial clamping, reducing blood flow by 70%. Blood samples were collected before and after 30, 90, and 180 min of strangulation or ischemia. ET-1 was determined by radioimmunoassay following acidification and extraction on C18 columns. In strangulated loop the blood flow decreased by 70%. ET-1 concentration remained around 5 pg/ml in arterial blood, increased fourfold in strangulated venous blood, and remained unchanged in venous blood from control bowel. The release of ET-1 from the strangulated loop to blood increased twofold. Ischemia resulted in reduced release of ET-1. It is concluded that strangulation obstruction causes increased release of ET-1 to venous blood in the strangulated loop, but not increased ET-1 concentration in systemic blood. The increased ET-1 release was probably due to increased venous pressure, not to low blood flow.

Topics: Animals; Endothelin-1; Heart Rate; Intestinal Obstruction; Intestines; Ischemia; Regional Blood Flow; Swine; Venous Pressure