Chen C F, Chen H T, Wang D, Li J P, Fong Y
Department of Internal Medicine, Cheng Hsin General Hospital and Department of Healthcare Information, School of Health, Ming Chuan University, Taipei, Taiwan.
Transplant Proc. 2008 Sep;40(7):2185-7. doi: 10.1016/j.transproceed.2008.07.093.
Ischemia/reperfusion injury (I/R) of the rat pancreas induces acute pancreatitis with a systemic inflammatory response syndrome. Activated inflammatory cells sequestered in the lung and the proteases released from the inflammatory pancreas both induce acute lung injury.
Ischemia was induced by clamping the gastroduodenal artery and the splenic artery for 2 hours to induce ischemia of the pancreas, followed by reperfusion for 6 hours. We then observed lung function parameters, such as weight changes, compliance, functional residual capacity (FRC), and respiratory work.
This protocol resulted in elevation in the blood concentrations of nitric oxide (P < .05), hydroxyl radicals (P < .01), amylase (P < .05), and white blood cells (P < .001) among the I/R group. Pulmonary function data showed that I/R of the pancreas induced significant decreases in the FRC and lung compliance (Cchord), but significant increases in respiratory work. The lung weight/body weight ratio also increased significantly.
I/R of the pancreas induced lung injury and restrictive ventilatory insufficiency. Inflammatory responses in the lung tissues induced by oxidative stress and nitrosative stress may be major factors inducing lung injury and a restrictive type of ventilatory insufficiency.