Determinants of intestinal barrier failure in critical illness
| Autor: | J S Aranow, M P Fink |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Critical Illness Multiple Organ Failure Nitric Oxide Gastroenterology Intestinal absorption Proinflammatory cytokine Sepsis Adenosine Triphosphate Immune system Intestinal mucosa Internal medicine medicine Humans Intestinal Mucosa Hypoxia Barrier function Lamina propria business.industry Organ dysfunction medicine.disease Oxidative Stress Anesthesiology and Pain Medicine medicine.anatomical_structure Intestinal Absorption Immunology Cytokines medicine.symptom Acidosis business |
| Zdroj: | British Journal of Anaesthesia. 77:71-81 |
| ISSN: | 0007-0912 |
| DOI: | 10.1093/bja/77.1.71 |
| Popis: | The gut serves not only as a physiological portal for the entry of water and nutrients into the body, but also as a barrier limiting the systemic absorption of intraluminal microbes, microbial products, or both. Evidence exists to support the view that trauma, sepsis or other critical illnesses lead to derangements in the barrier function of the gut. One potential consequence of deranged barrier function is bloodstream invasion by gut-derived pathogens, leading to “primary” bacteraemias or fungaemias, or even metastatic infections. Another consequence of gut barrier dysfunction might be a several step process leading to a poorly controlled systemic inflammatory response and organ system failure. In the first step of this postulated pathophysiological process, microbes or toxins passively diffuse or are actively transported out of the lumen of the gut into submucosal tissues. In step two, these microbes or toxins activate immune cells in tissues or organs, which are “downstream” from the mucosa (e.g. Kuppfer cells in the liver; macrophages in the lamina propria of the gut, Peyer’s patches or mesenteric lymph nodes). In the third step, the activated immune cells release various inflammatory mediators (cytokines, nitric oxide, eicosanoids, platelet activating factor), which have been implicated as being important in the pathogenesis of multiple organ dysfunction. The hypothesis that the gut is an endogenous source of proinflammatory agents is attractive because it might explain why signs and symptoms of sepsis, such as fever, leucocytosis, hypermetabolism and organ system dysfunction, frequently are present in critically ill patients, even in the absence of a welldefined focus of infection [42, 91, 92]. |
| Databáze: | OpenAIRE |
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