Zhihua Xu1,2, Dong Wang3,2, Zhumei Zhou1, Qiu Chen4, Dan Zhang1, Shuo Chen1, Han Jiang1, Chao Jia1, Xusen Liu1. 1. Department of Critical Care Medicine, Mianyang Central Hospital, Mianyang, China. 2. Southwest Medical University of Clinical Medicine, China. 3. Department of Critical Care Medicine, Mianyang Central Hospital, Mianyang, China wangdong804@aliyun.com. 4. Department of Endocrinology, Teaching Hospital of Chengdu University of Traditional Chinese Medicine, China.
Abstract
OBJECTIVE: To investigate the effect of dexmedetomidine (DEX) against renal and myocardial ischemia/reperfusion (I/R) injury induced by renal I/R and explore its potential mechanism. METHODS: Male Wistar rats were randomly allocated to sham, I/R, D1, D2 and D3 group. The sham group received laparotomy without a renal ischemia. I/R injury model was induced by bilateral renal pedicle clamping for 120 min followed by 3 h of reperfusion in I/R, D1, D2 and D3 group. Then D1, D2 and D3 group received DEX of 25 μg/kg, 50 μg/kg and 100 μg/kg by intraperitoneal injection at 30 min from ischemia onset, respectively, and I/R group received normal saline. Renal histopathology, myocardial histopathology and inflammatory cytokines were assessed. RESULTS: Renal and myocardial tissues were normal in the sham group. Pathological damage showed a trend of I/R>D1>D2>D3 group in renal and myocardial tissue, and the damage was negatively correlated with the dose of DEX. The concentration of creatinine and blood urea nitrogen in serum showed a trend of I/R>D1>D2>D3>sham group. The concentration of tumor necrosis factor α in renal and myocardial tissue showed a trend of I/R>D1>D2>D3>sham group. The concentration of interleukin-10 in renal and myocardial tissue showed a trend of D3>D2>D1>I/R>sham group. CONCLUSION: DEX could attenuate renal and myocardial I/R injury induced by renal I/R in a dose-dependent manner, at least in part, through its inhibitory effects on inflammatory response.
OBJECTIVE: To investigate the effect of dexmedetomidine (DEX) against renal and myocardial ischemia/reperfusion (I/R) injury induced by renal I/R and explore its potential mechanism. METHODS: Male Wistar rats were randomly allocated to sham, I/R, D1, D2 and D3 group. The sham group received laparotomy without a renal ischemia. I/R injury model was induced by bilateral renal pedicle clamping for 120 min followed by 3 h of reperfusion in I/R, D1, D2 and D3 group. Then D1, D2 and D3 group received DEX of 25 μg/kg, 50 μg/kg and 100 μg/kg by intraperitoneal injection at 30 min from ischemia onset, respectively, and I/R group received normal saline. Renal histopathology, myocardial histopathology and inflammatory cytokines were assessed. RESULTS: Renal and myocardial tissues were normal in the sham group. Pathological damage showed a trend of I/R>D1>D2>D3 group in renal and myocardial tissue, and the damage was negatively correlated with the dose of DEX. The concentration of creatinine and blood ureanitrogen in serum showed a trend of I/R>D1>D2>D3>sham group. The concentration of tumor necrosis factor α in renal and myocardial tissue showed a trend of I/R>D1>D2>D3>sham group. The concentration of interleukin-10 in renal and myocardial tissue showed a trend of D3>D2>D1>I/R>sham group. CONCLUSION:DEX could attenuate renal and myocardial I/R injury induced by renal I/R in a dose-dependent manner, at least in part, through its inhibitory effects on inflammatory response.
Authors: Necmiye Şengel; Zeynep Köksal; Ali Doğan Dursun; Ömer Kurtipek; Şaban Cem Sezen; Mustafa Arslan; Mustafa Kavutçu Journal: Drug Des Devel Ther Date: 2022-07-13 Impact factor: 4.319