[Effects of sevoflurane preconditioning on cardiomyocyte apoptosis and myocardial inflammation in rats with sepsis]

Nan Fang Yi Ke Da Xue Xue Bao. 2014 Nov;34(11):1680-3.
[Article in Chinese]

Abstract

Objective: To observe the effects of preconditioning with different concentrations of sevoflurane on cariomyocyte apoptosis and myocardial inflammation in rats with sepsis and explore the possible mechanism of sevoflurane for myocardial protection.

Methods: Forty adult male Sprague-Dawley rats were randomly divided into 4 groups (n=10), namely the control group, LPS group, low-concentration sevoflurane group and high-concentration sevoflurane group. Following sevoflurane pretreatment for 30 min and a washout period for 10 min, all the rats received intraperitoneal injection of LPS or normal saline (NS) and were sacrificed 12 h later to observe the myocardial histopathology. Apoptosis of the ardiomyocytes was detected with TUNEL assay, and enzyme-linked immunosorbent assay was used to detect serum cTnI level and myocardial TNF-α level.

Results: Compared with the control group, the rats in the other 3 groups showed significantly increased serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes (P<0.05). Compared with those in LPS group, serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes were significantly decreased in the two sevoflurane preconditioning groups (P<0.05), and the effect was more obvious with a high dose of sevoflurane (P<0.05 CONCLUSION: Sevoflurane preconditioning can concentration-dependently reduce LPS-induced myocardial injury in rats possibly by decreasing cardiomyocyte apoptosis and alleviating myocardial inflammations.

MeSH terms

  • Animals
  • Apoptosis*
  • Male
  • Methyl Ethers / pharmacology*
  • Myocarditis / drug therapy*
  • Myocardium / pathology
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / drug effects*
  • Rats
  • Rats, Sprague-Dawley
  • Sepsis*
  • Sevoflurane
  • Troponin I / blood
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Methyl Ethers
  • Troponin I
  • Tumor Necrosis Factor-alpha
  • Sevoflurane