Somatostatin peptides prevent increased human colonic epithelial permeability induced by hypoxia

• DOI: 10.1152/ajpgi.00057.2024
• Publication Date: 2024-09-03T20:59:36Z
• Authors: Ibrahim Rajput; Vazhaikkurichi M....; Andrew J. Nickerson; J. Peter A. Lodge; Geoffrey I. Sandle
• Keywords: Hypoxia; Paracellular transport; Intestinal mucosa

Mesenteric ischemia increases gut permeability and bacterial translocation. In human colon, chemical hypoxia induced by 2,4-dinitrophenol (DNP) activates basolateral intermediate conductance K + (IK) channels (designated KCa3.1 or KCNN4) paracellular shunt conductance/permeability (G S ), but whether this leads to increased macromolecule is unclear. Somatostatin (SOM) inhibits IK prevents hypoxia-induced in G . Thus, we examined octreotide (OCT), a synthetic SOM analogue, colon total epithelial T ) FITC-dextran 4000 (FITC) rat colon. The effects of serosal OCT on 100 µM DNP were compared isolated DNP-induced transepithelial FITC movement evaluated distal DNP-treated was 52% greater than controls ( P = 0.003). similar when 2 added after before treatment, both cases being less <0.05) with alone. 0.2 equally effective preventing , treatment. significantly 18% 0.016) mucosa-to-serosa 43% 0.01), pre-treatment completely prevented these changes. We conclude that paracellular/macromolecule speculate it may limit ischemia-induced hyperpermeability during abdominal surgery, thereby reducing bacterial/bacterial toxin translocation sepsis.