PMID- 19455261
OWN - NLM
STAT- MEDLINE
DCOM- 20090811
LR  - 20181201
IS  - 0379-0355 (Print)
IS  - 0379-0355 (Linking)
VI  - 31
IP  - 2
DP  - 2009 Mar
TI  - Modulation of cardioprotective effect of ischemic pre- and postconditioning in 
      the hyperhomocysteinemic rat heart.
PG  - 71-9
LID - 10.1358/mf.2009.31.2.1357292 [doi]
AB  - The present study was designed to investigate the effect of hyperhomocysteinemia 
      (Hhcy) on cardioprotective potentials of ischemic preconditioning (IPC) and 
      postconditioning (IPost). Rats were administered L-methionine (1.7 g/kg/day 
      orally) for 4 weeks to produce Hhcy. Isolated Langendorff-perfused normal and 
      hyperhomocysteinemic rat hearts were subjected to global ischemia for 30 min 
      followed by reperfusion for 120 min. Myocardial infarct size was assessed 
      macroscopically by volume method using triphenyltetrazolium chloride staining. 
      Coronary effluent was analyzed for the release of lactate dehydrogenase (LDH) and 
      creatine kinase (CK) to assess the degree of cardiac injury. Moreover, oxidative 
      stress in the heart was assessed by measuring lipid peroxidation, superoxide 
      anion generation and reduced glutathione. Ischemia-reperfusion (I/R) was noted to 
      produce myocardial injury, as assessed in terms of increase in myocardial infarct 
      size, LDH and CK in coronary effluent and oxidative stress in normal and 
      hyperhomocysteinemic rat hearts. In addition, the hyperhomocysteinemic rat hearts 
      showed enhanced I/R-induced myocardial injury with a high degree of oxidative 
      stress in comparison with normal rat hearts subjected to I/R. Four episodes of 
      IPC (5 min each) and six episodes of IPost (10 s each) afforded cardioprotection 
      against I/R-induced myocardial injury in normal rat hearts, as assessed in terms 
      of reduction in myocardial infarct size, LDH, CK and oxidative stress. However, 
      surprisingly, IPC- and IPost-mediated myocardial protection against I/R injury 
      was abolished in the hyperhomocysteinemic rat heart. It may be concluded that 
      Hhcy may make the heart susceptible to oxidative stress induced by I/R, and that 
      the high degree of oxidative stress produced in the hyperhomocysteinemic rat 
      heart in response to reperfusion may be responsible for abolishing the 
      cardioprotective potential of IPC and IPost against I/R injury.
CI  - Copyright 2009 Prous Science, S.A.U. or its licensors. All rights reserved.
FAU - Balakumar, Pitchai
AU  - Balakumar P
AD  - Cardiovascular Pharmacology Division, ISF College of Pharmacy, Punjab, India. 
      pbala2002@rediffmail.com
FAU - Rohilla, Ankur
AU  - Rohilla A
FAU - Singh, Gurfateh
AU  - Singh G
FAU - Singh, Kulwinder
AU  - Singh K
FAU - Singh, Manjeet
AU  - Singh M
LA  - eng
PT  - Journal Article
PL  - Spain
TA  - Methods Find Exp Clin Pharmacol
JT  - Methods and findings in experimental and clinical pharmacology
JID - 7909595
RN  - 11062-77-4 (Superoxides)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.3.2 (Creatine Kinase)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Animals
MH  - Creatine Kinase/metabolism
MH  - Female
MH  - Glutathione/metabolism
MH  - Hyperhomocysteinemia/complications/*physiopathology
MH  - Ischemic Preconditioning, Myocardial/*methods
MH  - L-Lactate Dehydrogenase/metabolism
MH  - Lipid Peroxidation
MH  - Male
MH  - Myocardial Infarction/complications/physiopathology/*prevention & control
MH  - Myocardial Reperfusion Injury/complications/*physiopathology
MH  - Oxidative Stress
MH  - Rats
MH  - Rats, Wistar
MH  - Superoxides/metabolism
EDAT- 2009/05/21 09:00
MHDA- 2009/08/12 09:00
CRDT- 2009/05/21 09:00
PHST- 2009/05/21 09:00 [entrez]
PHST- 2009/05/21 09:00 [pubmed]
PHST- 2009/08/12 09:00 [medline]
AID - 1357292 [pii]
AID - 10.1358/mf.2009.31.2.1357292 [doi]
PST - ppublish
SO  - Methods Find Exp Clin Pharmacol. 2009 Mar;31(2):71-9. doi: 
      10.1358/mf.2009.31.2.1357292.