Inflammation and Edema in the Lung and Kidney of Hemorrhagic Shock Rats Are Alleviated by Biliary Tract External Drainage via the Heme Oxygenase-1 Pathway

Inflammation. 2015 Dec;38(6):2242-51. doi: 10.1007/s10753-015-0208-z.

Abstract

The lung and kidney are two organs that are easily affected by hemorrhagic shock (HS). We investigated roles of biliary tract external drainage (BTED) in inflammation and edema of the lung and kidney in HS and its relationship with the heme oxygenase-1 (HO-1) pathway. Rat models of HS were induced by drawing blood from the femoral artery until a mean arterial pressure (MAP) of 40 ± 5 mmHg was achieved. A MAP of 40 ± 5 mmHg was maintained for 60 min. Thirty-six Sprague-Dawley rats were randomized to the following groups: sham group; HS group; HS + zinc protoporphyrin IX (ZnPP), a specific HO-1 inhibitor, group; HS + BTED group; HS + BTED + ZnPP group; and HS + BTED + bile infusion (BI) group. HO-1 levels, aquaporin-1 levels, and ratios of dry/wet in the lung and kidney increased markedly after BTED, but tumor necrosis factor-α and myeloperoxidase levels in the lung and kidney decreased significantly after BTED under HS conditions. Under the condition that HO-1 was inhibited by ZnPP, all these effects induced by BTED disappeared in the lung and kidney. These results demonstrated that inflammation and edema of the lung and kidney of HS rats are alleviated by BTED via the HO-1 pathway.

Keywords: aquaporin-1; biliary tract external drainage; heme oxygenase-1; hemorrhagic shock; tumor necrosis factor-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aquaporin 1 / genetics
  • Aquaporin 1 / metabolism
  • Biliary Tract Surgical Procedures / methods*
  • Disease Models, Animal
  • Drainage / methods*
  • Enzyme Inhibitors / pharmacology
  • Heme Oxygenase (Decyclizing) / antagonists & inhibitors
  • Heme Oxygenase (Decyclizing) / metabolism*
  • Kidney / drug effects*
  • Kidney / enzymology
  • Kidney / pathology
  • Lung / drug effects*
  • Lung / enzymology
  • Lung / pathology
  • Male
  • Nephritis / enzymology
  • Nephritis / genetics
  • Nephritis / pathology
  • Nephritis / prevention & control*
  • Peroxidase / metabolism
  • Pneumonia / enzymology
  • Pneumonia / genetics
  • Pneumonia / pathology
  • Pneumonia / prevention & control*
  • Protoporphyrins / pharmacology
  • Pulmonary Edema / enzymology
  • Pulmonary Edema / genetics
  • Pulmonary Edema / pathology
  • Pulmonary Edema / prevention & control*
  • Rats, Sprague-Dawley
  • Shock, Hemorrhagic / enzymology
  • Shock, Hemorrhagic / genetics
  • Shock, Hemorrhagic / pathology
  • Shock, Hemorrhagic / therapy*
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation

Substances

  • Aqp1 protein, rat
  • Enzyme Inhibitors
  • Protoporphyrins
  • Tumor Necrosis Factor-alpha
  • Aquaporin 1
  • zinc protoporphyrin
  • Peroxidase
  • Heme Oxygenase (Decyclizing)
  • Hmox1 protein, rat