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The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium
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Abstract
Background: Ischemic preconditioning (IPC) and postconditioning (POC) are well documented to trigger cardioprotection against ischemia/reperfusion (I/R) injury, but the effect oftheir both co-application remains unclear in human heart. The present study sought to assessthe co-application of IPC and POC on fragments of human myocardium in vitro.
Methods: Muscular trabeculae of the human right atrial were electrically driven in the organbath and subjected to simulated I/R injury – hypoxia/re-oxygenation injury in vitro. To achieveIPC of trabeculae the single brief hypoxia period preceded the applied lethal hypoxia, and to achieve POC triple brief hypoxia periods followed the lethal hypoxia. Additional muscular trabeculae were exposed only to the hypoxic stimulation (Control) or were subjected to the non-hypoxic stimulation (Sham). 10 μM norepinephrine (NE) application ended every experiment to assess viability of trabeculae. The contraction force of the myocardium assessed as a maximal amplitude of systolic peak (%Amax) was obtained during the whole experiment’s period.
Results: Co-application of IPC and POC resulted in decrease in %Amax during the re-oxygentaionperiod and after NE application, as compared to Control (30.35 ± 2.25 vs. 41.89 ± 2.25, 56.26 ± 7.73 vs. 65.98 ± 5.39, respectively). This was in contrary to the effects observed when IPC and POC were applied separately.
Conclusions: The co-application of IPC and POC abolishes the cardioprotection of either intervention alone against simulated I/R injury in fragments of the human right heart atria.
Abstract
Background: Ischemic preconditioning (IPC) and postconditioning (POC) are well documented to trigger cardioprotection against ischemia/reperfusion (I/R) injury, but the effect oftheir both co-application remains unclear in human heart. The present study sought to assessthe co-application of IPC and POC on fragments of human myocardium in vitro.
Methods: Muscular trabeculae of the human right atrial were electrically driven in the organbath and subjected to simulated I/R injury – hypoxia/re-oxygenation injury in vitro. To achieveIPC of trabeculae the single brief hypoxia period preceded the applied lethal hypoxia, and to achieve POC triple brief hypoxia periods followed the lethal hypoxia. Additional muscular trabeculae were exposed only to the hypoxic stimulation (Control) or were subjected to the non-hypoxic stimulation (Sham). 10 μM norepinephrine (NE) application ended every experiment to assess viability of trabeculae. The contraction force of the myocardium assessed as a maximal amplitude of systolic peak (%Amax) was obtained during the whole experiment’s period.
Results: Co-application of IPC and POC resulted in decrease in %Amax during the re-oxygentaionperiod and after NE application, as compared to Control (30.35 ± 2.25 vs. 41.89 ± 2.25, 56.26 ± 7.73 vs. 65.98 ± 5.39, respectively). This was in contrary to the effects observed when IPC and POC were applied separately.
Conclusions: The co-application of IPC and POC abolishes the cardioprotection of either intervention alone against simulated I/R injury in fragments of the human right heart atria.
Keywords
ischemia, reperfusion, preconditioning, postconditioning
About this articleTitle
The co-application of hypoxic preconditioning and postconditioning abolishes their own protective effect on systolic function in human myocardium
Journal
Issue
Pages
472-477
Published online
2013-09-30
Page views
1452
Article views/downloads
1652
DOI
10.5603/CJ.2013.0131
Bibliographic record
Cardiol J 2013;20(5):472-477.
Keywords
ischemia
reperfusion
preconditioning
postconditioning
Authors
Tomasz Roleder
Krzysztof S. Gołba
Marcin Kunecki
Marcin Malinowski
Jolanta Biernat
Grzegorz Smolka
Marek A. Deja
