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Vol. 62. Issue 8.
Pages 953-954 (August 2009)
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Vol. 62. Issue 8.
Pages 953-954 (August 2009)
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DOI: 10.1016/S1885-5857(09)72670-2
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Marisol Ruiz-Meanaa, David García-Doradoa
a Laboratorio de Cardiología Experimental, Área del Corazón, Hospital Universitario Vall d’Hebron, Barcelona. Spain.
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To the Editor:

We are very honoured by the interest that Drs Domínguez and Abreu have shown in our article on the physiopathology of myocardial reperfusion.1 In their letter, the authors describe the possible cardioprotective effects of melatonin, which is a treatment approach that was not mentioned in our article. The reason for this omission was that given limited space, it was simply impossible to list all of the cardioprotective treatments that have been shown to be effective in experimental models; we only included those for which the experience is more solid, or the cardioprotective mechanism better-known. We do recognize, however, that melatonin is of special interest due to being an endogenous molecule that can be used in humans, and which is probably safe. Regarding its action mechanism, we feel that it is not completely clear. In their letter, Domínguez and Abreu attribute the mechanism to melatonin's antioxidant and anti-inflammatory properties. We would like to make 2 comments on this topic. Firstly, we feel that most important protective effect that can be expected in preventing damage by free radicals is the prevention of mitochondrial permeability transition.1,2 Some studies show that this could be true for melatonin.3 However, recent data indicate that these cardioprotective effects of melatonin could be mediated by receptors and could depend on the cyclic guanosine monophosphate channel, which is a signal channel shown to be very important for different cardioprotective strategies.4,5

We wish Drs Dominguez and Abreu success with their phase II study, and we will await their results with great interest.

Bibliography
[1]
Ruiz-Meana M, García-Dorado D..
Fisiopatología del daño miocárdico por isquemia-reperfusión: nuevas oportunidades terapéuticas en el infarto agudo de miocardio..
Rev Esp Cardiol, 62 (2009), pp. 199-209
[2]
Ruiz-Meana M, Abellán A, Miró-Casas E, García-Dorado D..
Opening of mitochondrial permeability transition pore induces hypercontracture in Ca2+ overloaded cardiac myocytes..
Basic Res Cardiol, 102 (2007), pp. 542-52
[3]
Jou MJ, Peng TI, Reiter RJ, Jou SB, Wu HY, Wen ST..
Visualization of the antioxidative effects of melatonin at the mitochondrial level during oxidative stress-induced apoptosis of rat brain astrocytes..
J Pineal Res, 37 (2004), pp. 55-70
[4]
García-Dorado D, Agulló L, Sartorio CL, Ruiz-Meana M..
Myocardial protection against reperfusion injury: The cGMP pathway..
Thromb Haemost, 101 (2009), pp. 635-42
[5]
Genade S, Genis A, Ytrehus K, Huisamen B, Lochner AJ..
Melatonin receptor-mediated protection against myocardial ischaemia/reperfusion injury: role of its anti-adrenergic actions..
Pineal Res, 45 (2008), pp. 449-58
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Revista Española de Cardiología (English Edition)

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