Jiang-Mei Wang1, Zhi-Yong Hu, Wei-Zhong Gu. 1. Department of Anesthesiology, Children's Hospital of Zhejiang University School of Medicine, Hangzhou 310003, China.
Abstract
OBJECTIVE: To investigate the protective effects of postconditioning with different concentrations of sevoflurane on renal ischemia-reperfusion (I/R) injury. METHODS: The following procedures were performed on 48 male SD rats to establish I/R models: the right kidney and ureter were resected, and the left renal arteries and veins were occluded by atraumatic clamps for 45 min and then the clamps were removed to provide reperfusion for 24 h. And the rats were randomly divided into 4 equal groups; I/R Group, S(1.2) Group inbreathing 1.2% sevoflurane simultaneously since the beginning of reperfusion for 2 h, S(1.8) Group inbreathing 1.8% sevoflurane simultaneously since the beginning of reperfusion for 2 h, and S(2.2) Group inbreathing 2.2% sevoflurane simultaneously since the beginning of reperfusion for 2 h. Another 12 rats underwent resection of the right kidney and ureter and exposure of the left renal arteries and veins only for 45 min. The rates were killed at the end of 24h reperfusion. Blood samples were taken for determination of serum creatinine (Cr) and blood urea nitrogen (BUN). The left kidneys were harvested to undergo microscopy to observe the percentage of pyknotic nuclei in cortical tubular cells. Immunohistochemistry was used to detect the expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in the kidney. RESULTS: The necrotic rate of renal tubule of the Sham Group was significantly lower than those of the other 4 groups (all P < 0.01), and the necrotic rates of renal tubule of the S(1.2), S(1.8), and S(2.2) Groups were all significantly lower than that of I/R Group (all P < 0.05). The levels of blood Cr and BUN, and the percentage of pyknotic nuclei in cortical tuber cells of I/R, S(1.2), S(1.8), and S(2.2) Groups were all significantly higher than those of Sham Group (all P < 0.05) and these indexes listed above of S(1.2), S(1.8), and S(2.2) Groups were all significantly lower than those of I/R Group (all P < 0.05). However, there were not significant differences in these indexes among S(1.2), S(1.8), and S(2.2) Groups (all P > 0.05). The kidney eNOS and iNOS expression levels of I/R Group were both significantly higher than those of Sham Group (both P < 0.05), and the kidney eNOS and iNOS expression levels of S(1.8) Group were both significantly lower than those of I/R Group (both P < 0.05). CONCLUSION: Sevoflurane postconditioning attenuates the renal damage induced by I/R and down-regulates the eNOS and iNOS expression in kidney.Different concentrations do not show different effects.
OBJECTIVE: To investigate the protective effects of postconditioning with different concentrations of sevoflurane on renal ischemia-reperfusion (I/R) injury. METHODS: The following procedures were performed on 48 male SD rats to establish I/R models: the right kidney and ureter were resected, and the left renal arteries and veins were occluded by atraumatic clamps for 45 min and then the clamps were removed to provide reperfusion for 24 h. And the rats were randomly divided into 4 equal groups; I/R Group, S(1.2) Group inbreathing 1.2% sevoflurane simultaneously since the beginning of reperfusion for 2 h, S(1.8) Group inbreathing 1.8% sevoflurane simultaneously since the beginning of reperfusion for 2 h, and S(2.2) Group inbreathing 2.2% sevoflurane simultaneously since the beginning of reperfusion for 2 h. Another 12 rats underwent resection of the right kidney and ureter and exposure of the left renal arteries and veins only for 45 min. The rates were killed at the end of 24h reperfusion. Blood samples were taken for determination of serum creatinine (Cr) and blood ureanitrogen (BUN). The left kidneys were harvested to undergo microscopy to observe the percentage of pyknotic nuclei in cortical tubular cells. Immunohistochemistry was used to detect the expression of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in the kidney. RESULTS: The necrotic rate of renal tubule of the Sham Group was significantly lower than those of the other 4 groups (all P < 0.01), and the necrotic rates of renal tubule of the S(1.2), S(1.8), and S(2.2) Groups were all significantly lower than that of I/R Group (all P < 0.05). The levels of blood Cr and BUN, and the percentage of pyknotic nuclei in cortical tuber cells of I/R, S(1.2), S(1.8), and S(2.2) Groups were all significantly higher than those of Sham Group (all P < 0.05) and these indexes listed above of S(1.2), S(1.8), and S(2.2) Groups were all significantly lower than those of I/R Group (all P < 0.05). However, there were not significant differences in these indexes among S(1.2), S(1.8), and S(2.2) Groups (all P > 0.05). The kidney eNOS and iNOS expression levels of I/R Group were both significantly higher than those of Sham Group (both P < 0.05), and the kidney eNOS and iNOS expression levels of S(1.8) Group were both significantly lower than those of I/R Group (both P < 0.05). CONCLUSION:Sevoflurane postconditioning attenuates the renal damage induced by I/R and down-regulates the eNOS and iNOS expression in kidney.Different concentrations do not show different effects.