ABSTRACT
To study the effect of ischemia preconditioning (IP) on renal ischemia/reperfusion (I/R)-associated functional injury and expression of renal adhesion molecules in rats. The ischemia preconditioning plan adopted in this experiment involved renal warm ischemia for 6 min. and blood flow for 4 min., repeated four times. The Wistar rat kidneys used for warm ischemia preconditioning were subjected to 60 min of renal warm ischemia followed by reperfusion. The rat kidneys with ischemia/reperfusion were compared with the ischemia preconditioning group to observe rat renal function and changes in the expression of renal adhesion molecules ICAM-1, P--Selectin, and E-Selectin. The expression of rat renal adhesion molecules (ICAM-1, P-Selectin, and E-Selectin) with ischemia preconditioning was significantly lower than that of the ischemia/reperfusion group. Serum creatinine was significantly lower than that in the ischemia/reperfusion group after 48 hours. Ischemia preconditioning has a protective effect on renal function. Reduced expression of renal adhesion molecules is likely a mechanism involved in the observed protection.
Subject(s)
Animals , Female , Male , Rats , Ischemic Preconditioning/methods , Kidney/blood supply , Reperfusion Injury/prevention & control , Cell Adhesion Molecules/analysis , Creatinine/blood , Disease Models, Animal , E-Selectin/analysis , Immunohistochemistry , Kidney/pathology , P-Selectin/analysis , Rats, Wistar , Reperfusion Injury/pathology , Time FactorsABSTRACT
OBJECTIVE: To study the effect of ischemia preconditioning (IP) on renal ischemia/reperfusion (I/R)-associated functional injury and expression of renal adhesion molecules in rats. MATERIALS AND METHODS: The ischemia preconditioning plan adopted in this experiment involved renal warm ischemia for 6 min. and blood flow for 4 min., repeated four times. The Wistar rat kidneys used for warm ischemia preconditioning were subjected to 60 min of renal warm ischemia followed by reperfusion. The rat kidneys with ischemia/reperfusion were compared with the ischemia preconditioning group to observe rat renal function and changes in the expression of renal adhesion molecules ICAM-1, P-Selectin, and E-Selectin. RESULTS: The expression of rat renal adhesion molecules (ICAM-1, P-Selectin, and E-Selectin) with ischemia preconditioning was significantly lower than that of the ischemia/reperfusion group. Serum creatinine was significantly lower than that in the ischemia/reperfusion group after 48 hours. CONCLUSIONS: Ischemia preconditioning has a protective effect on renal function. Reduced expression of renal adhesion molecules is likely a mechanism involved in the observed protection.
Subject(s)
Ischemic Preconditioning/methods , Kidney/blood supply , Reperfusion Injury/prevention & control , Animals , Cell Adhesion Molecules/analysis , Creatinine/blood , Disease Models, Animal , E-Selectin/analysis , Female , Immunohistochemistry , Kidney/pathology , Male , P-Selectin/analysis , Rats , Rats, Wistar , Reperfusion Injury/pathology , Time FactorsABSTRACT
Cigarette smoking produces peripheral airway inflammation in all smokers, and chronic airways obstruction in approximately 20% of heavy smokers. The present study was designed to test the hypothesis that airways obstruction is related to changes in the expression of adhesion molecules involved in the recruitment of cells to sites of inflammation in the lung. Freshly resected lungs from heavy smokers with airways obstruction (n = 10) and from heavy smokers with normal lung function (n = 10) were collected in the operating room, inflated with optimal cutting temperature (OCT) medium and frozen over liquid nitrogen. Six micrometres thick cryostat sections cut from random samples of this tissue were stained, using immunohistochemistry, with monoclonal antibodies to the adhesion molecules on leucocytes: L-selectin, very late activation antigen-4 (VLA-4), CD11a/CD18, CD11b/CD18, CD11c/CD18; and on endothelial and epithelial surfaces: E-selectin, P-selectin, vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM)-1 and ICAM-2 using the alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. The slides were coded and the expression of each molecule scored by three observers using a semiquantitative grading system. Two inducible adhesion molecules, E-selectin on endothelium and CD11b on leucocytes, were also evaluated using quantitative morphometric analysis. The results showed a distribution of adhesion molecules that was consistent with the inflammatory response in the airways and parenchyma of all subjects but failed to show any differences between those with or without airways obstruction. We conclude that development of airways obstruction in heavy smokers cannot be explained by differences in the expression of adhesion molecules known to be involved in the control of cell traffic in the lung.