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Brief femoral artery ischaemia provides protection against myocardial ischaemia-reperfusion injury in rats: the possible mechanisms.
Exp Physiol. 2008 Aug; 93(8):954-68.EP

Abstract

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.

Authors+Show Affiliations

Department of Physiology, Vallabhbhai Patel Chest Institute, University of Delhi, PO Box 2101, Delhi 110007, India.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18356557

Citation

Shahid, Mohd, et al. "Brief Femoral Artery Ischaemia Provides Protection Against Myocardial Ischaemia-reperfusion Injury in Rats: the Possible Mechanisms." Experimental Physiology, vol. 93, no. 8, 2008, pp. 954-68.
Shahid M, Tauseef M, Sharma KK, et al. Brief femoral artery ischaemia provides protection against myocardial ischaemia-reperfusion injury in rats: the possible mechanisms. Exp Physiol. 2008;93(8):954-68.
Shahid, M., Tauseef, M., Sharma, K. K., & Fahim, M. (2008). Brief femoral artery ischaemia provides protection against myocardial ischaemia-reperfusion injury in rats: the possible mechanisms. Experimental Physiology, 93(8), 954-68. https://doi.org/10.1113/expphysiol.2007.041442
Shahid M, et al. Brief Femoral Artery Ischaemia Provides Protection Against Myocardial Ischaemia-reperfusion Injury in Rats: the Possible Mechanisms. Exp Physiol. 2008;93(8):954-68. PubMed PMID: 18356557.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brief femoral artery ischaemia provides protection against myocardial ischaemia-reperfusion injury in rats: the possible mechanisms. AU - Shahid,Mohd, AU - Tauseef,Mohammad, AU - Sharma,K K, AU - Fahim,M, Y1 - 2008/03/20/ PY - 2008/3/22/pubmed PY - 2008/9/26/medline PY - 2008/3/22/entrez SP - 954 EP - 68 JF - Experimental physiology JO - Exp Physiol VL - 93 IS - 8 N2 - 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. SN - 0958-0670 UR - https://www.unboundmedicine.com/medline/citation/18356557/Brief_femoral_artery_ischaemia_provides_protection_against_myocardial_ischaemia_reperfusion_injury_in_rats:_the_possible_mechanisms_ L2 - https://doi.org/10.1113/expphysiol.2007.041442 DB - PRIME DP - Unbound Medicine ER -