European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes · 1999
Endotoxin and cytokine release in strangulation obstruction and in partial occlusion of the mesenteric artery in pigs.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Fevang J, Ovrebo K, Svanes K, Røkke O
Аннотация
BACKGROUND: The study was performed to determine if endotoxin or the cytokines interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor (TNF) are liberated from strangulated or partially ischemic small bowel.
METHODS: Strangulation obstruction was induced by elevating pressure in a gasket placed around a loop of ileum until venous pressure reached 50 mm Hg. Low arterial flow in a loop of ileum was produced by arterial clamping reducing blood flow by 70%. A proximal bowel loop was used for control. Arterial blood flow was measured by transit time flowmetry. Blood samples were collected before and after 30, 90 and 180 min of strangulation or clamping. Plasma levels of endotoxin and cytokines (TNF, IL-1 and IL-6) were measured by limulus amebocyte lysate test and bioassays, respectively.
RESULTS: Strangulation obstruction caused more extensive mucosal damage than arterial clamping. Strangulation was followed by markedly increased venous concentration and release of IL-6 in the strangulated loop. Partial arterial occlusion did not cause increased release of IL-6. Strangulation or partial clamping did not influence the concentration of endotoxin, IL-1 or TNF in intestinal venous blood.
CONCLUSIONS: Strangulation obstruction causes increased release of IL-6 to intestinal venous blood. IL-6 levels did not increase after 70% reduction of arterial blood flow. The early IL-6 increase was not detected in systemic blood. Strangulation did not cause early changes in plasma levels of endotoxin, TNF or IL-1.
METHODS: Strangulation obstruction was induced by elevating pressure in a gasket placed around a loop of ileum until venous pressure reached 50 mm Hg. Low arterial flow in a loop of ileum was produced by arterial clamping reducing blood flow by 70%. A proximal bowel loop was used for control. Arterial blood flow was measured by transit time flowmetry. Blood samples were collected before and after 30, 90 and 180 min of strangulation or clamping. Plasma levels of endotoxin and cytokines (TNF, IL-1 and IL-6) were measured by limulus amebocyte lysate test and bioassays, respectively.
RESULTS: Strangulation obstruction caused more extensive mucosal damage than arterial clamping. Strangulation was followed by markedly increased venous concentration and release of IL-6 in the strangulated loop. Partial arterial occlusion did not cause increased release of IL-6. Strangulation or partial clamping did not influence the concentration of endotoxin, IL-1 or TNF in intestinal venous blood.
CONCLUSIONS: Strangulation obstruction causes increased release of IL-6 to intestinal venous blood. IL-6 levels did not increase after 70% reduction of arterial blood flow. The early IL-6 increase was not detected in systemic blood. Strangulation did not cause early changes in plasma levels of endotoxin, TNF or IL-1.