TY - JOUR
T1 - Effect of Dexmedetomidine Preconditioning on Hepatic Ischemia–Reperfusion Injury in Acute Hyperglycemic Rats
AU - Lee, Jeong Eun
AU - Jung, Hoon
AU - Byun, Sung Hye
AU - Park, Jun Mo
AU - Yeo, Jinseok
AU - Jeon, Younghoon
AU - Lee, See Woo
AU - Park, Sung Sik
AU - Lim, Dong Gun
AU - Kim, Si Oh
AU - Kwak, Kyung Hwa
N1 - Publisher Copyright:
© 2023 Elsevier Inc.
PY - 2023/12
Y1 - 2023/12
N2 - Background: Acute hyperglycemia frequently occurs in stressful situations, including liver transplantation or hepatic surgery, which may affect the protective effects of dexmedetomidine preconditioning and increase postoperative mortality. Therefore, this study aimed to investigate the effects of dexmedetomidine on hepatic ischemia–reperfusion injury in acute hyperglycemia. Methods: Thirty-six Sprague–Dawley rats were randomly assigned to 6 groups, including a combination between 2 glycemic (normo- and hyperglycemia) and 3 ischemia–reperfusion conditions (sham, ischemia–reperfusion only, and dexmedetomidine plus ischemia–reperfusion). Dexmedetomidine 70 μg/kg was preconditioned 30 minutes before ischemic injury. After 6 hours of reperfusion, serum aminotransferase levels were measured to confirm the hepatic tissue injury. Furthermore, inflammatory (nuclear factor-κb, tumor necrosis factor-α, and interleukin-6) and oxidative stress markers (malondialdehyde and superoxide dismutase) were detected. Results: Ischemia–reperfusion injury significantly increased the serum levels of aminotransferase and inflammatory and oxidative stress markers. These ischemia–reperfusion-induced changes were further exacerbated in hyperglycemia and were significantly attenuated by dexmedetomidine preconditioning. However, the effects of dexmedetomidine in hyperglycemia were lesser than those in normoglycemia (P <.05 for aminotransferases, inflammatory markers, malondialdehyde, and superoxide dismutase). Conclusions: These findings suggest that the protective effects of dexmedetomidine preconditioning may be intact against hepatic ischemia–reperfusion injury in acute hyperglycemia. Although its effects appeared to be relatively reduced, this may be because of the increase in oxidative stress and inflammatory response caused by acute hyperglycemia. To determine whether the effects of dexmedetomidine itself would be impaired in hyperglycemia, further study is needed.
AB - Background: Acute hyperglycemia frequently occurs in stressful situations, including liver transplantation or hepatic surgery, which may affect the protective effects of dexmedetomidine preconditioning and increase postoperative mortality. Therefore, this study aimed to investigate the effects of dexmedetomidine on hepatic ischemia–reperfusion injury in acute hyperglycemia. Methods: Thirty-six Sprague–Dawley rats were randomly assigned to 6 groups, including a combination between 2 glycemic (normo- and hyperglycemia) and 3 ischemia–reperfusion conditions (sham, ischemia–reperfusion only, and dexmedetomidine plus ischemia–reperfusion). Dexmedetomidine 70 μg/kg was preconditioned 30 minutes before ischemic injury. After 6 hours of reperfusion, serum aminotransferase levels were measured to confirm the hepatic tissue injury. Furthermore, inflammatory (nuclear factor-κb, tumor necrosis factor-α, and interleukin-6) and oxidative stress markers (malondialdehyde and superoxide dismutase) were detected. Results: Ischemia–reperfusion injury significantly increased the serum levels of aminotransferase and inflammatory and oxidative stress markers. These ischemia–reperfusion-induced changes were further exacerbated in hyperglycemia and were significantly attenuated by dexmedetomidine preconditioning. However, the effects of dexmedetomidine in hyperglycemia were lesser than those in normoglycemia (P <.05 for aminotransferases, inflammatory markers, malondialdehyde, and superoxide dismutase). Conclusions: These findings suggest that the protective effects of dexmedetomidine preconditioning may be intact against hepatic ischemia–reperfusion injury in acute hyperglycemia. Although its effects appeared to be relatively reduced, this may be because of the increase in oxidative stress and inflammatory response caused by acute hyperglycemia. To determine whether the effects of dexmedetomidine itself would be impaired in hyperglycemia, further study is needed.
UR - http://www.scopus.com/inward/record.url?scp=85174465015&partnerID=8YFLogxK
U2 - 10.1016/j.transproceed.2023.09.017
DO - 10.1016/j.transproceed.2023.09.017
M3 - Article
C2 - 37867004
AN - SCOPUS:85174465015
SN - 0041-1345
VL - 55
SP - 2478
EP - 2486
JO - Transplantation Proceedings
JF - Transplantation Proceedings
IS - 10
ER -