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Brief periods of ischaemia, are known to induce a reversible deficit in myocardial function despite the maintenance of histological and metabolic integrity, a phenomenon initially described by Heyndrickx et al. in 1975, and called stunning several years after [1]. In that first study it was reported that several hours were required for complete recovery of regional contractility following a 5 min occlusion of the left anterior descending coronary artery in conscious dogs and up to 24 h were needed for complete recovery following a 15 min occlusion [1]. Therefore, myocardial stunning is considered to represent reversible injury contrasting the irreversible injury of myocardial infarction. The phenomenon has been described in every species studied so far, does occur in several clinical settings and likely plays an important role in the morbidity of patients with coronary artery disease [2]. Although the principal cause of the reversible contractile dysfunction is not fully understood, there is now consensus that loss of Ca2+ responsiveness of the myofilaments represents a major underlying mechanism as first proposed by Kusuoka et al. in 1987 on basis of experiments with isolated perfused ferret hearts [3]. Initially some studies suggested an additional role of failing sarcoplasmic reticulum Ca2+ pump, but this could not be substantiated [4]. There is evidence that abnormalities in myofilaments also underly stunning induced in clinically relevant large animal models. For instance, it was shown in the in situ porcine model that the potent Ca2+ sensitizer (EMD 60263), without phosphodiesterase inhibitory properties, increased segment length shortening to a greater extent in stunned than in non-stunned myocardium [5]. These findings were consistent with the left-and upward shifts of the p[Ca2+]/Mg2+-ATPase curves induced by Ca2+ sensitizer as observed with isolated myofibrils from stunned pig myocardium … * Corresponding author. Tel.: +31-10-408-7335; fax: +31-10-4089472

Preconditioning and limitation of stunning one step closer to the protected protein(s)?