PMID- 17513495
OWN - NLM
STAT- MEDLINE
DCOM- 20071019
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 293
IP  - 3
DP  - 2007 Sep
TI  - Ischemic preconditioning prevents in vivo hyperoxygenation in postischemic 
      myocardium with preservation of mitochondrial oxygen consumption.
PG  - H1442-50
AB  - Ischemic preconditioning (IPC) strongly protects against ischemia-reperfusion 
      injury; however, its effect on subsequent myocardial oxygenation is unknown. 
      Therefore, we determine in an in vivo mouse model of regional ischemia and 
      reperfusion (I/R) if IPC attenuates postischemic myocardial hyperoxygenation and 
      decreases formation of reactive oxygen/nitrogen species (ROS/RNS), with 
      preservation of mitochondrial function. The following five groups of mice were 
      studied: sham, control (I/R), ischemic preconditioning (IPC + I/R, 3 cycles of 5 
      min coronary occlusion/5 min reperfusion) and IPC + I/R N(G)-nitro-L-arginine 
      methyl ester treated, and IPC + I/R eNOS knockout mice. I/R and IPC + I/R mice 
      were subjected to 30 min regional ischemia followed by 60 min reperfusion. 
      Myocardial Po(2) and redox state were monitored by electron paramagnetic 
      resonance spectroscopy. In the IPC + I/R, but not the I/R group, regional blood 
      flow was increased after reperfusion. Po(2) upon reperfusion increased 
      significantly above preischemic values in I/R but not in IPC + I/R mice. Tissue 
      redox state was measured from the reduction rate of a spin probe, and this rate 
      was 60% higher in IPC than in non-IPC hearts. Activities of NADH dehydrogenase 
      (NADH-DH) and cytochrome c oxidase (CcO) were reduced in I/R mice after 60 min 
      reperfusion but conserved in IPC + I/R mice compared with sham. There were no 
      differences in NADH-DH and CcO expression in I/R and IPC + I/R groups compared 
      with sham. After 60 min reperfusion, strong nitrotyrosine formation was observed 
      in I/R mice, but only weak staining was observed in IPC + I/R mice. Thus IPC 
      markedly attenuates postischemic myocardial hyperoxygenation with less ROS/RNS 
      generation and preservation of mitochondrial O(2) metabolism because of conserved 
      NADH-DH and CcO activities.
FAU - Zhu, Xuehai
AU  - Zhu X
AD  - Center for Biomedical Electron Paramagnetic Resonance Spectroscopy and Imaging, 
      Davis Heart and Lung Research Institute, The Ohio State University College of 
      Medicine, Columbus, Ohio, USA.
FAU - Liu, Bin
AU  - Liu B
FAU - Zhou, Shaotang
AU  - Zhou S
FAU - Chen, Yeong-Renn
AU  - Chen YR
FAU - Deng, Yuanmu
AU  - Deng Y
FAU - Zweier, Jay L
AU  - Zweier JL
FAU - He, Guanglong
AU  - He G
LA  - eng
GR  - HL-65608/HL/NHLBI NIH HHS/United States
GR  - HL-38324/HL/NHLBI NIH HHS/United States
GR  - HL-073087/HL/NHLBI NIH HHS/United States
GR  - R01 HL083237/HL/NHLBI NIH HHS/United States
GR  - HL-63744/HL/NHLBI NIH HHS/United States
GR  - R01 EB000890-04/EB/NIBIB NIH HHS/United States
GR  - HL-081630/HL/NHLBI NIH HHS/United States
GR  - R01 EB000890/EB/NIBIB NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20070518
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Reactive Oxygen Species)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - 9007-43-6 (Cytochromes c)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.6.99.3 (NADH Dehydrogenase)
SB  - IM
MH  - Animals
MH  - Coronary Vessels/physiology
MH  - Cytochromes c/metabolism
MH  - *Ischemic Preconditioning, Myocardial
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mitochondria, Heart/*metabolism
MH  - Myocardial Infarction/pathology
MH  - Myocardium/*metabolism
MH  - NADH Dehydrogenase/metabolism
MH  - Nitric Oxide Synthase Type III/genetics/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/physiology
MH  - Oxygen Consumption/*physiology
MH  - Random Allocation
MH  - Reactive Oxygen Species/metabolism
MH  - Regional Blood Flow/physiology
MH  - Tyrosine/analogs & derivatives/metabolism
EDAT- 2007/05/22 09:00
MHDA- 2007/10/20 09:00
CRDT- 2007/05/22 09:00
PHST- 2007/05/22 09:00 [pubmed]
PHST- 2007/10/20 09:00 [medline]
PHST- 2007/05/22 09:00 [entrez]
AID - 00256.2007 [pii]
AID - 10.1152/ajpheart.00256.2007 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1442-50. doi: 
      10.1152/ajpheart.00256.2007. Epub 2007 May 18.