PMID- 27830025
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220409
IS  - 1943-8141 (Print)
IS  - 1943-8141 (Electronic)
IS  - 1943-8141 (Linking)
VI  - 8
IP  - 10
DP  - 2016
TI  - Sevoflurane postconditioning improves myocardial mitochondrial respiratory 
      function and reduces myocardial ischemia-reperfusion injury by up-regulating 
      HIF-1.
PG  - 4415-4424
AB  - BACKGROUND: Sevoflurane postconditioning (SPostC) can exert myocardial protective 
      effects similar to ischemic preconditioning. However, the exact myocardial 
      protection mechanism by SPostC is unclear. Studies indicate that 
      hypoxia-inducible factor-1 (HIF-1) maintains cellular respiration homeostasis by 
      regulating mitochondrial respiratory chain enzyme activity under hypoxic 
      conditions. This study investigated whether SPostC could regulate the expression 
      of myocardial HIF-1alpha and to improve mitochondrial respiratory function, thereby 
      relieving myocardial ischemia-reperfusion injury in rats. METHODS: The myocardial 
      ischemia-reperfusion rat model was established using the Langendorff isolated 
      heart perfusion apparatus. Additionally, postconditioning was performed using 
      sevoflurane alone or in combination with the HIF-1alpha inhibitor 2-methoxyestradiol 
      (2ME2). The changes in hemodynamic parameters, HIF-1alpha protein expression levels, 
      mitochondrial respiratory function and enzyme activity, mitochondrial reactive 
      oxygen species (ROS) production rates, and mitochondrial ultrastructure were 
      measured or observed. RESULTS: Compared to the ischemia-reperfusion (I/R) group, 
      HIF-1alpha expression in the SPostC group was significantly up-regulated. 
      Additionally, cardiac function indicators, mitochondrial state 3 respiratory 
      rate, respiratory control ratio (RCR), cytochrome C oxidase (CcO), NADH oxidase 
      (NADHO), and succinate oxidase (SUCO) activities, mitochondrial ROS production 
      rate, and mitochondrial ultrastructure were significantly better than those in 
      the I/R group. However, these advantages were completely reversed by the HIF-1alpha 
      specific inhibitor 2ME2 (P<0.05). CONCLUSION: The myocardial protective function 
      of SPostC might be associated with the improvement of mitochondrial respiratory 
      function after up-regulation of HIF-1alpha expression.
FAU - Yang, Long
AU  - Yang L
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
FAU - Xie, Peng
AU  - Xie P
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
FAU - Wu, Jianjiang
AU  - Wu J
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
FAU - Yu, Jin
AU  - Yu J
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
FAU - Yu, Tian
AU  - Yu T
AD  - Guizhou Key Laboratory of Anesthesia and Organ Protection, Department of 
      Anesthesiology, Zunyi Medical College Zunyi, Guizhou, China.
FAU - Wang, Haiying
AU  - Wang H
AD  - Guizhou Key Laboratory of Anesthesia and Organ Protection, Department of 
      Anesthesiology, Zunyi Medical College Zunyi, Guizhou, China.
FAU - Wang, Jiang
AU  - Wang J
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
FAU - Xia, Zhengyuan
AU  - Xia Z
AD  - Department of Anesthesiology, The University of Hong Kong Pokfulam, Hong Kong, 
      China.
FAU - Zheng, Hong
AU  - Zheng H
AD  - Department of Anesthesiology, The First Affiliated Hospital of Xinjiang Medical 
      University Urumqi, Xinjiang, China.
LA  - eng
PT  - Journal Article
DEP - 20161015
PL  - United States
TA  - Am J Transl Res
JT  - American journal of translational research
JID - 101493030
PMC - PMC5095334
OTO - NOTNLM
OT  - Sevoflurane postconditioning
OT  - hypoxia-inducible factor-1
OT  - mitochondrial respiratory function
OT  - myocardial protective effect
OT  - respiratory enzyme activity
EDAT- 2016/11/11 06:00
MHDA- 2016/11/11 06:01
PMCR- 2016/10/15
CRDT- 2016/11/11 06:00
PHST- 2016/05/06 00:00 [received]
PHST- 2016/09/19 00:00 [accepted]
PHST- 2016/11/11 06:00 [entrez]
PHST- 2016/11/11 06:00 [pubmed]
PHST- 2016/11/11 06:01 [medline]
PHST- 2016/10/15 00:00 [pmc-release]
PST - epublish
SO  - Am J Transl Res. 2016 Oct 15;8(10):4415-4424. eCollection 2016.