Interactive CardioVascular and Thoracic Surgery
ABSTRACTS - 28th EACTS
Sunday
Objectives: Levosimendan (LS) mitigates myocardial insufficiency. The impact
of LS on myocardial-mitochondrial function is unknown. Hence, we
analysed for subsarcolemmal mitochondrial (SSM) function dependent from LS
of rat hearts undergoing Langendorff perfusion with or without global
ischaemia.
Methods: Rat hearts divided into 4 study-groups were subjected to 30 min of
reperfusion without (IR0/30) or with application of 8 mg LS over 20 min (LSIR0/30). Experiments were repeated with hearts being subjected to 40 min of
warm global ischaemia without (IR40/30) or with application of LS (LS-IR40/
30). Myocardial function was determined by left-ventricular pressure (mean,
max, dP/dT max), contractility and coronary flow. SSM were isolated and analysed regarding electron transport chain (ETC) function, ATP production,
Ca2+-induced swelling and Ca2+ fluxes.
Results: Ischaemia significantly suppressed (P < 0.04) and LS insignificantly
improved myocardial function (LVPmax). Both ischaemia (P < 0.03) and LS
(P < 0.02) inhibited ETC function at complexes I–V, II–V and IV resulting in a
reduced ATP content and production (P < 0.003) (see Fig. 1). SSM demonstrated
an increased susceptibility towards Ca2+-induced swelling after ischaemia
(P < 0.005), an effect insignificantly ameliorated by LS. Interestingly, SSM Ca2+-re2+
tention capacity declined after ischaemia (P < 0.002) and LS (P <0.008). Ca flux
2+
2+
2+
demonstrated delayed Ca uptake and increased Ca -induced Ca liberation in
presence of ischaemia but predominantly after LS and IR (P < 0.004).
Conclusion: LS improved myocardial function at the expense of ETC function and
ATP production. Loss of ATP might explain limited Ca2+-retention capacity and
increased Ca2+-liberation of SSM. However, limitation of Ca2+-induced SSM swelling in presence of LS suggests cardioprotection due to reduction of IRdependent cell death.
Abstracts 001–006
009
LEVOSIMENDAN IMPAIRS ATP PRODUCTION BY LIMITATION OF ELECTRON
TRANSPORT CHAIN FUNCTION FOLLOWED BY LOSS OF CA2+ RETENTION
CAPACITY IN HEALTHY MYOCARDIAL MITOCHONDRIA AND DURING
ISCHAEMIA REPERFUSION INJURY
S. Sommer, M. Leistner, I. Aleksic, C. Schimmer, K. Alhussini, R.G. Leyh,
S. Sommer
Thoracic and Cardiovascular Surgery, University Hospital Würzburg,
Würzburg, Germany