Adenosine as an important mediator of post-ischaemic neuronal stunning

See article by Burgdorf et al. [11] (pages 713–720) in this issue. A brief period of ischaemia is known to induce a prolonged period of reversible myocardial dysfunction despite normalized electrocardiogram and absence of histological signs of necrosis. This was first described by Heyndrickx and co-workers [1] who found that myocardial function was depressed for several hours following a 15-min period of coronary artery occlusion in dogs. Braunwald and Kloner [2] subsequently named this phenomenon ‘myocardial stunning’. Although the exact mechanism underlying myocardial stunning is not fully understood, results from several studies indicate that it can be mediated by increased myocyte calcium levels and oxygen-derived free radicals during ischaemia and the initial part of reperfusion [3–5]. In addition to the reduced myocardial contractility, there is also evidence of a long-lasting impairment of neurotransmission in the post-ischaemic heart, a phenomenon known as ‘neuronal stunning’. Martins et al. [6] demonstrated that myocardial contractile function induced by sympathetic nerve stimulation was depressed in ischaemic myocardium. It was later described that the myocardial segment shortening evoked by sympathetic nerve stimulation in dogs was markedly reduced following coronary artery occlusion [7,8]. On the other hand, the response to administration of exogenous noradrenaline was unaffected by ischaemia, which indicates that the sympathetic neurotransmission but not the post-junctional response to noradrenaline was impaired. Neuronal stunning affects not only myocardial contractile function but also regulation of the coronary vasculature. … * Tel.: +46-8-5177-5876; fax: +46-8-311-044 john.pernow{at}ks.se