PMID- 20207813
OWN - NLM
STAT- MEDLINE
DCOM- 20100623
LR  - 20220330
IS  - 1522-1539 (Electronic)
IS  - 0363-6135 (Linking)
VI  - 298
IP  - 6
DP  - 2010 Jun
TI  - Combined local ischemic postconditioning and remote perconditioning recapitulate 
      cardioprotective effects of local ischemic preconditioning.
PG  - H1819-31
LID - 10.1152/ajpheart.01102.2009 [doi]
AB  - Ischemic postconditioning (PostC) and perconditioning (PerC) provide practical 
      methods for protecting the heart against ischemia-reperfusion (I/R) injury, but 
      their combined effects have not been studied in detail. Using an in vivo rat I/R 
      model, we tested 1) whether additive effects were produced when local PostC was 
      preceded by varying doses of remote PerC, and whether the optimal PostC+PerC 
      regime is additive to local ischemic preconditioning (IPC), and 2) how combined 
      PostC+PerC alters the activity of the reperfusion injury salvage kinase pathway. 
      The optimal combination of PerC and PostC therapy was produced by PerC delivered 
      with four cycles of 5 min of limb ischemia followed by 5-min reperfusion. This 
      resulted in lower infarct size (22.56 +/- 4.45%) compared with rats with PostC 
      alone (29.39 +/- 3.66%) and PerC alone (33.49 +/- 5.81%) and complementary 
      differences in the generation of reactive oxygen species and apoptotic signaling. 
      However, this optimal combination of PostC+PerC resulted in protection similar to 
      local IPC alone (18.8 +/- 2.54%, P = 0.13), and when added to IPC there was no 
      additional protection (19.62 +/- 2.89%, P = 0.675). Akt and ERK1/2 
      phosphorylation was induced by PostC and PerC and maximally by combined 
      PostC+PerC treatment, and protection was abolished by phosphatidylinositol 
      3-kinase or ERK1/2 inhibitors. This study shows that neither PostC nor a 
      maximized "dose" of PerC leads to optimal kinase signaling or cardioprotection 
      compared with IPC alone. However, combined PostC+PerC may result in complementary 
      effects on kinase signaling to recapitulate the effects of local IPC. Finally, 
      combined PostC+PerC is not additive to IPC, suggesting that each works via a 
      common pathway.
FAU - Xin, Ping
AU  - Xin P
AD  - Division of Cardiology, Shanghai Sixth Hospital, Shanghai Jiao Tong University 
      School of Medicine, Shanghai, People's Republic of China.
FAU - Zhu, Wei
AU  - Zhu W
FAU - Li, Jing
AU  - Li J
FAU - Ma, Shixin
AU  - Ma S
FAU - Wang, Lixing
AU  - Wang L
FAU - Liu, Mingya
AU  - Liu M
FAU - Li, Jingbo
AU  - Li J
FAU - Wei, Meng
AU  - Wei M
FAU - Redington, Andrew N
AU  - Redington AN
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100305
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  - 11062-77-4 (Superoxides)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
EIN - Am J Physiol Heart Circ Physiol. 2010 Sep;299(3):H957
MH  - Animals
MH  - Apoptosis/physiology
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - *Ischemic Preconditioning, Myocardial
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - Models, Animal
MH  - Myocardial Reperfusion Injury/metabolism/*physiopathology/*prevention & control
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction/physiology
MH  - Superoxides/metabolism
EDAT- 2010/03/09 06:00
MHDA- 2010/06/24 06:00
CRDT- 2010/03/09 06:00
PHST- 2010/03/09 06:00 [entrez]
PHST- 2010/03/09 06:00 [pubmed]
PHST- 2010/06/24 06:00 [medline]
AID - 01102.2009 [pii]
AID - 10.1152/ajpheart.01102.2009 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2010 Jun;298(6):H1819-31. doi: 
      10.1152/ajpheart.01102.2009. Epub 2010 Mar 5.