Key result
Levosimendan treatment in isolated rat hearts subjected to ischaemia-reperfusion significantly reduced tissue malondialdehyde levels (P=0.019) and myeloperoxidase activity (P=0.004) compared to control.
Why the study?
Does levosimendan reduce myocardial damage during hypothermic ischemia and reperfusion in isolated rat hearts?
Does levosimendan reduce myocardial damage during hypothermic ischemia and reperfusion in isolated rat hearts?
p-value: p=0.019
In a preclinical model, levosimendan provided cardioprotection against ischemia-reperfusion injury during cold cardioplegic arrest.
May attenuate oxidative stress in preclinical ischemia-reperfusion; leaves open translation to clinical cardioplegic arrest.
BACKGROUND AND OBJECTIVE: Levosimendan has a cardioprotective action by inducing coronary vasodilatation and preconditioning by opening KATP channels. The aim of this study was to determine whether levosimendan enhances myocardial damage during hypothermic ischaemia and reperfusion in isolated rat hearts. METHODS: Twenty-one male Wistar rats were divided into three groups. After surgical preparation, coronary circulation was started by retrograde aortic perfusion using Krebs-Henseleit buffer solution and lasted 15 min. After perfusion Group 1 (control; n = 7) received no further treatment. In Group 2 (non-treated; n = 7), hearts were arrested with cold cardioplegic solution after perfusion and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. In Group 3 (levosimendan treated; n = 7), levosimendan was added to the buffer solution during perfusion and the hearts were arrested with cold cardioplegic solution and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. At the end of the reperfusion period, the hearts were prepared for biochemical assays and for histological analysis. RESULTS: Tissue malondialdehyde levels were significantly lower in the levosimendan-treated group than in the non-treated group (P = 0.019). The tissue Na+-K+ ATPase activity was significantly decreased in the non-treated group than in the levosimendan-treated group (P = 0.027). Tissue myeloperoxidase (MPO) enzyme activity was significantly higher in the non-treated group than in the levosimendan-treated group (P = 0.004). Electron microscopic examination of the hearts showed cardiomyocytic degeneration at the myofibril, mitochondria and sarcoplasmic reticulum in both non-treated and levosimendan-treated groups. The severity of these findings was more extensive in the non-treated group. CONCLUSIONS: Treatment with levosimendan provided better cardioprotection with cold cardioplegic arrest followed by global hypothermic ischaemia in isolated rat hearts.
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Yapıcı et al. (2007) studied Myocardial ischaemia-reperfusion injury (n=21). Levosimendan vs. Non-treated (cold cardioplegic solution only) was evaluated on Tissue malondialdehyde levels, Na+-K+ ATPase activity, and myeloperoxidase (MPO) enzyme activity (p=0.019). Levosimendan treatment in isolated rat hearts subjected to ischaemia-reperfusion significantly reduced tissue malondialdehyde levels (P=0.019) and myeloperoxidase activity (P=0.004) compared to control.
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