PMID- 18356557
OWN - NLM
STAT- MEDLINE
DCOM- 20080925
LR  - 20131121
IS  - 0958-0670 (Print)
IS  - 0958-0670 (Linking)
VI  - 93
IP  - 8
DP  - 2008 Aug
TI  - Brief femoral artery ischaemia provides protection against myocardial 
      ischaemia-reperfusion injury in rats: the possible mechanisms.
PG  - 954-68
LID - 10.1113/expphysiol.2007.041442 [doi]
AB  - The present study was conducted to examine the role of nitric oxide (NO), 
      mitochondrial ATP-sensitive K(+) channels (mito K(+)(ATP) channels) and reactive 
      oxygen species (ROS) and their interdependence in brief femoral artery 
      ischaemia-induced myocardial preconditioning. To assess myocardial injury, 
      myocardial infarction was induced by occlusion followed by reperfusion of the 
      left anterior descending (LAD) coronary artery in anaesthetized rats and was 
      assessed by triphenyl tetrazolium chloride (TTC) staining. Left ventricular 
      function was assessed by left ventricular end-diastolic pressure (LVEDP) and the 
      maximal rate of rise of left ventricular pressure [LV(dP/dt)(max)]. Serum 
      creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) were determined by 
      colorimetric kits. Remote preconditioning (RPC) was induced by 15 min occlusion 
      of femoral arteries followed by 10 min of reperfusion just before LAD coronary 
      artery occlusion. Brief femoral artery ischaemia led to a 61% reduction in 
      myocardial infarct size, 57% reduction in elevated serum LDH and 72% reduction in 
      elevated CK-MB activities, and a significant improvement in LVEDP and 
      LV(dP/dt)(max) compared with control animals. Pretreatment with 
      5-hydroxydecanoate (5-HD) or l-NAME or N-acetylcystein (NAC) blocked this 
      protective effect of femoral artery ischaemia. Moreover, infusion of l-arginine 
      or diazoxide before coronary artery occlusion markedly reduced the myocardial 
      infarction and improved the left ventricular function. This effect of l-arginine 
      was found to be abolished by the blockade of mito K(+)(ATP) channels with 5-HD 
      and, similarly, the effect of diazoxide was blocked in the presence of a ROS 
      scavenger, NAC. The results suggest that brief femoral artery ischaemia-induced 
      RPC is mediated by a combination of increased NO synthesis, opening of mito 
      K(+)(ATP) channels and increased ROS production. Moreover, it appears that NO is 
      working upstream and acts via activation of mito K(+)(ATP) channels, which 
      subsequently increases the production of ROS.
FAU - Shahid, Mohd
AU  - Shahid M
AD  - Department of Physiology, Vallabhbhai Patel Chest Institute, University of Delhi, 
      PO Box 2101, Delhi 110007, India.
FAU - Tauseef, Mohammad
AU  - Tauseef M
FAU - Sharma, K K
AU  - Sharma KK
FAU - Fahim, M
AU  - Fahim M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080320
PL  - England
TA  - Exp Physiol
JT  - Experimental physiology
JID - 9002940
RN  - 0 (KATP Channels)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Vasodilator Agents)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.3.2 (Creatine Kinase, MB Form)
RN  - O5CB12L4FN (Diazoxide)
SB  - IM
MH  - Animals
MH  - Arginine/pharmacology
MH  - Blood Pressure/physiology
MH  - Creatine Kinase, MB Form/blood
MH  - Diazoxide/pharmacology
MH  - Disease Models, Animal
MH  - Femoral Artery/*physiopathology
MH  - Heart Rate/physiology
MH  - Hindlimb/blood supply
MH  - Ischemia/metabolism/*physiopathology
MH  - Ischemic Preconditioning, Myocardial
MH  - KATP Channels/*metabolism
MH  - L-Lactate Dehydrogenase/blood
MH  - Male
MH  - Myocardial Infarction/pathology
MH  - Myocardial Reperfusion Injury/metabolism/*prevention & control
MH  - Nitric Oxide/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/*metabolism
MH  - Vasodilator Agents
EDAT- 2008/03/22 09:00
MHDA- 2008/09/26 09:00
CRDT- 2008/03/22 09:00
PHST- 2008/03/22 09:00 [pubmed]
PHST- 2008/09/26 09:00 [medline]
PHST- 2008/03/22 09:00 [entrez]
AID - expphysiol.2007.041442 [pii]
AID - 10.1113/expphysiol.2007.041442 [doi]
PST - ppublish
SO  - Exp Physiol. 2008 Aug;93(8):954-68. doi: 10.1113/expphysiol.2007.041442. Epub 
      2008 Mar 20.