Kancirova 2014 Cardiovascular Research Supplements

Kancirova I, Jasova M, Murarikova M, Carnicka S, Sumbalova Z, Ulicna O, Vancova O, Waczulikova I. Ziegelhoffer A, Ferko M (2014) Adaptivechangesofratheartmitochondrialrespiration:responseofremoteischemic preconditioning. Cardiovascular Research Supplements 103:57–94.

Kancirova I, Jasova M, Murarikova M, Carnicka S, Sumbalova Z, Ulicna O, Vancova O, Waczulikova I. Ziegelhoffer A, Ferko M (2014) Cardiovascular Research Supplements

Abstract: POSTER SESSION 2 Session held on 5 July 2014 doi:10.1093/cvr/cvu091 P406 Adaptivechangesofratheartmitochondrialrespiration:responseofremoteischemic preconditioning I. Kancirova 1

M. Jasova

1

M. Murarikova

1

S. Carnicka

1

Z. Sumbalova

2

O. Ulicna

2

O. Vancova

2

I. Waczulikova; A. Ziegelhoffer 1

M. Ferko

1 1 Institute for Heart Research, Slovak Academy of Science, Bratislava, Slovak Republic; 2 Comenius University, Laboratory of Pharmacobiochemistry, Third Department of Internal Medicine, Faculty of Medicine, Bratislava, Slovak Republic Introduction: Myocardium heavily depends on the oxidative generation of energy that requires in- volvement of functional mitochondria. These organelles were recently shown to participate also in the mechanisms of cardioprotection induced by ischemic preconditioning. Based on the previous find- ings of increased myocardial resistance to ischemia, it could be assumed that mitochondria and func- tional alterations in the respiratory chain might also be involved in the mechanisms of remote ischemic preconditioning (RIP). In RIP, the increased cardiac resistance to ischemia is achieved by brief episodes of ischemia with subsequent reperfusion performed in distant organs or places. Hence, on the contrary to ischemic preconditioning, a direct restriction of oxygen supply to cardiac mitochondria is missing. The aim of this pilot study was to reveal whether, and in what way are cardiac mitochondria and respiratory chain involved in the mechanism of cardioprotection. Methods: For this purpose, 13-week-old male Wistar rats were divided into 2 groups: control group withoutRIP(n=21)andthegroupwithRIP(n=21).ProtocolofRIPconsistedof3cyclesofischemiaand reperfusion,5minofdurationeach.Not-preconditionedandpreconditionedheartsweresubjectedto the testing of ischemia-reperfusion injury (T-IRI): 30 minute ischemia followed by 40 minutes of reper- fusion according to Langendorff. Parameters of oxidative phosphorylation (OXPHOS) in the isolated cardiac mitochondria were determined by the method of high resolution respirometry using Oxygraph-2k (Oroboros Instruments, Austria). Results: Mitochondrial respiration was stimulated by ADP (state III) using glutamate + malate and malate + octanoylcarnitineassubstrates.AfterischemicphaseofT-IRItheheartswithoutRIPexhibited a decrease by 26.7% whereas the hearts with RIP showed an increase by 40.4% in the rate of O2-consumption in comparison with the hearts in baseline preischemic phase of T-IRI. Reperfusion phase of T-IRI was characterized by a decrease in state III respiration in the group of hearts without RIP(65.9 %)andwithRIP(35.6%).Interestingly,adecreaseinO2-consumptioninducedbyreperfusion was less pronounced when malate + octanoylcarnitine as a substrate was used instead of glutamate + malate. Conclusion: Ourresultsrevealedthatthepositiveeffectofremotepreconditioningi.e.,theincreased or better preserved state III O2 consumption, became manifested only during the ischemic and reper- fusion phase of T-IRI. Grants: VEGA 2/0101/12, APVV 0102-11, KEGA 003 UK-4/2012.

Labels: