Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning

Title

Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning

Creator

Cai M; Li Y J; Xu Y; Swartz H M; Chen C L; Chen Y R; He G L

Publisher

American Journal of Physiology-Heart and Circulatory Physiology

Date

2011
2011-03

Description

Cai M, Li Y, Xu Y, Swartz HM, Chen C, Chen Y, He G. Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning. Am J Physiol Heart Circ Physiol 300: H1069-H1077, 2011. First published January 7, 2011; doi: 10.1152/ajpheart.00694.2010.-Ischemic postconditioning (IPOC) could be ineffective or even detrimental if the index ischemic duration is either too short or too long. The present study is to demonstrate that oxygen supply and metabolism defines a salvageable ischemic time window of IPOC in mice. C57BL/6 mice underwent coronary artery occlusion followed by reperfusion (I/R), with or without IPOC by three cycles of 10 s/10 s R/I. In vivo myocardial tissue oxygenation was monitored with electron paramagnetic resonance oximetry. Regional blood flow (RBF) was measured with a laser Doppler monitor. At the end of 60 min reperfusion, tissue from the risk area was collected, and mitochondrial enzyme activities were assayed. Tissue oximetry demonstrated that I/R induced a reperfusion hyperoxygenation state in the 30- and 45-min but not 15- and 60-min ischemia groups. IPOC attenuated the hyperoxygenation with 45 but not 30 min ischemia. RBF, eNOS phosphorylation, and mitochondrial enzyme activities were suppressed after I/R with different ischemic time, and IPOC afforded protection with 30 and 45 but not 60 min ischemia. Infarct size measurement indicated that IPOC reduced infarction with 30 and 45 min but not 60 min ischemia. Clearly, IPOC protected mouse heart with a defined ischemic time window between 30 and 45 min. This salvageable time window was accompanied by the improvement of RBF due to increased phosphorylated eNOS and the preservation of mitochondrial oxygen consumption due to conserved mitochondrial enzyme activities. Interestingly, this salvageable ischemic time window was mirrored by tissue hyperoxygenation status in the postischemic heart.

Subject

cardioprotection; mice; inhibition; Physiology; Cardiovascular System & Cardiology; activation; dysfunction; reperfusion injury; tissue oxygenation; consumption; blood flow; electron paramagnetic resonance; infarct size; ischemia and reperfusion; mitochondrial enzyme activity; mitochondrial permeability transition; rabbit hearts; regional

Format

Journal Article or Conference Abstract Publication

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Rights

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

Pages

H1069-H1077

Issue

3

Volume

300

Citation

Cai M; Li Y J; Xu Y; Swartz H M; Chen C L; Chen Y R; He G L, “Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning,” NEOMED Bibliography Database, accessed September 23, 2021, https://neomed.omeka.net/items/show/8782.

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