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Signalling pathways of cardiac ischaemic preconditioning (PC) and the final effector mechanisms involved in the process remain as yet unknown. The most likely mechanisms of “classic” preconditioning involve the release of endogenous substances from the ischaemic myocardium. Stimuli other than ischaemia of the myocardial risk territory may create cardioprotection against damage resulting from subsequent coronary artery occlusion. Gho et al. [1] demonstrated that brief renal or mesenteric ischaemia led to protection against coronary artery occlusion and suggested that a neuronal mechanism was involved. The important metabolic feature of preconditioned myocardium is decreased utilisation of ATP during ischaemia. Our previous data suggest that in the rat, histamine (H) partially contributes to ischaemiareperfusion cardiac damage [2]. The aim of our study was to examine whether intestinal preconditioning (IPC) causes changes in the intracellular ATP level of cardiomyocytes during ischaemia-reperfusion injury and to determine whether H receptors are involved in this process. Materials and methods