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Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice.

Abstract

Myocardial dysfunction accompanied by severe sepsis could significantly increase the mortality rate of septic patients. This study investigated the effects and the potential mechanisms of sevoflurane preconditioning on septic myocardial dysfunction which was induced by lipopolysaccharide (LPS; from Escherichia coli O55:B5; 18 mg/kg) in mice. Results indicated that one hour after the administration, LPS induced a significant increase in cell-surface Toll-like receptor 4 (TLR4), cytoplasmic IKKα protein expression and nuclear translocation of nuclear factor kappa-B (NF-κB) protein (P<0.05), which was attenuated by preconditioning with sevoflurane. Two hours after the administration, inhalation of sevoflurane significantly reduced the serum levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-10 (P < 0.05). Twelve hours after administration, LPS caused pathological damage to the heart and elevated the serum levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB; P < 0.05). Echocardiography indicated that sevoflurane preconditioning significantly improved systolic and diastolic function. The inhalation of sevoflurane inhibited increases in myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2), TNF-α and IL-1β levels (P < 0.05) induced by endotoxemia, whereas IL-6 release was facilitated. Sevoflurane attenuated the myocardial levels of nitric oxide (NO; P < 0.05) without an apparent influence on malondialdehyde (MDA), or superoxide dismutase (SOD; P > 0.05). In conclusion, our study indicates that exposure to 2% sevoflurane prior to LPS challenge is protective against myocardial dysfunction. Sevoflurane preconditioning may attenuate neutrophil infiltration and the release of inflammatory mediators during endotoxemia.

Authors+Show Affiliations

Department of Anesthesiology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China.Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, China. Department of Pathophysiology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China.Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Anesthesiology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China.Department of Pathophysiology, Key Laboratory of State Administration of Traditional Chinese Medicine of the People's Republic of China, School of Medicine, Jinan University, Guangzhou 510632, China.Department of Anesthesiology, First Affiliated Hospital of Jinan University, Guangzhou 510630, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31425341

Citation

Li, Jianling, et al. "Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice." Journal of Cardiovascular Pharmacology, 2019.
Li J, Liu P, Li H, et al. Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice. J Cardiovasc Pharmacol. 2019.
Li, J., Liu, P., Li, H., Wang, Y., Chen, Y., Qi, R., & Li, Y. (2019). Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice. Journal of Cardiovascular Pharmacology, doi:10.1097/FJC.0000000000000734.
Li J, et al. Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice. J Cardiovasc Pharmacol. 2019 Aug 13; PubMed PMID: 31425341.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sevoflurane Preconditioning Prevents Septic Myocardial Dysfunction in Lipopolysaccharide-Challenged Mice. AU - Li,Jianling, AU - Liu,Panhong, AU - Li,Hongmei, AU - Wang,Yanping, AU - Chen,Yifei, AU - Qi,Renbin, AU - Li,Yalan, Y1 - 2019/08/13/ PY - 2019/8/20/entrez PY - 2019/8/20/pubmed PY - 2019/8/20/medline JF - Journal of cardiovascular pharmacology JO - J. Cardiovasc. Pharmacol. N2 - Myocardial dysfunction accompanied by severe sepsis could significantly increase the mortality rate of septic patients. This study investigated the effects and the potential mechanisms of sevoflurane preconditioning on septic myocardial dysfunction which was induced by lipopolysaccharide (LPS; from Escherichia coli O55:B5; 18 mg/kg) in mice. Results indicated that one hour after the administration, LPS induced a significant increase in cell-surface Toll-like receptor 4 (TLR4), cytoplasmic IKKα protein expression and nuclear translocation of nuclear factor kappa-B (NF-κB) protein (P<0.05), which was attenuated by preconditioning with sevoflurane. Two hours after the administration, inhalation of sevoflurane significantly reduced the serum levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-10 (P < 0.05). Twelve hours after administration, LPS caused pathological damage to the heart and elevated the serum levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB; P < 0.05). Echocardiography indicated that sevoflurane preconditioning significantly improved systolic and diastolic function. The inhalation of sevoflurane inhibited increases in myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2), TNF-α and IL-1β levels (P < 0.05) induced by endotoxemia, whereas IL-6 release was facilitated. Sevoflurane attenuated the myocardial levels of nitric oxide (NO; P < 0.05) without an apparent influence on malondialdehyde (MDA), or superoxide dismutase (SOD; P > 0.05). In conclusion, our study indicates that exposure to 2% sevoflurane prior to LPS challenge is protective against myocardial dysfunction. Sevoflurane preconditioning may attenuate neutrophil infiltration and the release of inflammatory mediators during endotoxemia. SN - 1533-4023 UR - https://www.unboundmedicine.com/medline/citation/31425341/Sevoflurane_Preconditioning_Prevents_Septic_Myocardial_Dysfunction_in_Lipopolysaccharide-Challenged_Mice L2 - http://dx.doi.org/10.1097/FJC.0000000000000734 DB - PRIME DP - Unbound Medicine ER -