PMU-Autor/inn/en
Ritter MarkusAbstract
Mucosal hypoxia is a common endpoint for many pathological processes including ischemic colitis, colonic obstruction and anastomotic failure. Previous studies suggest that hypoxia modulates colonic mucosal function through inhibition of chloride secretion. However, the molecular mechanisms underlying this observation are poorly understood. AMP-activated protein kinase (AMPK) is a metabolic energy regulator found in a wide variety of cells and has been linked to cystic fibrosis transmembrane conductance regulator (CFTR) mediated chloride secretion in several different tissues. We hypothesized that AMPK mediates many of the acute effects of hypoxia on human and rat colonic electrolyte transport.
Useful keywords (using NLM MeSH Indexing)
AMP-Activated Protein Kinases/physiology*
Animals
Cell Hypoxia/physiology*
Chloride Channels/physiology*
Chlorides/metabolism*
Colon/blood supply*
Cystic Fibrosis Transmembrane Conductance Regulator/antagonists*
inhibitors*
Humans
Intestinal Mucosa/blood supply*
Ischemia/physiopathology*
Male
Membrane Potentials/physiology
Microscopy, Fluorescence
Rats
Rats, Sprague-Dawley