INTRODUCTION: Hypomagnesemia and ischemia followed by reperfusion often occur in cardiac surgery. Both of them are associated with endothelial dysfunction which interfers negatively with patient evolution. Phisiopatology of these disturbances is similar and involves G-proteins dysfunction. OBJECTIVE: The present study focuses on the endothelial dysfunction consequent to the lesion resulting from global ischemia followed by reperfusion and the potential protective influence of magnesium on the endothelium functional integrity in isolated coronaries of dogs. METHOD: Segments of canine coronary arteries were suspended in organ chambers to measure isometric force. Endothelial dysfunction was evaluated by the ability of these segments to produce nitric oxide changing the initial isometric force. Four groups with six dogs in each one were selected: SEM CEC (control), CEC (110 minutes of perfusion without ischemia), ISQ (45 minutes of ischemia), ISQ/REP (45 minutes of ischemia followed by 60 minutes of reperfusion). The magnesium action was evaluated in three different phases: I (organ chambers with magnesium), II (organ chambers without magnesium) and III (organ chambers with restored magnesium). Three pharmacological agonists were used which represented the main steps involved in the nitric oxide production: the membrane receptor of the endothelial cell - acetylcholine (ACh); transduction of the signal between the receptor and the intracellular processes through the G-protein - sodium fluoride (NaF); liberation of intracellular stocks of calcium - calcium ionophore (A23187). The study of endothelial function was combined with the evaluation of smooth muscle activity dependent on GMPc - sodium nitroprusside (NPS). RESULTS: The major findings of this investigation were as follows: 1) presence of magnesium in priming seemed to attenuate the endothelial dysfunction caused by global ischemia followed by reperfusion; 2) presence of magnesium in the organ chamber (phase I) was associated with the greatest relaxation in response to agonists of the nitric oxide production; 3) removal of magnesium in the organ chamber (phase II) was linked to the reduction in the relaxation intensity in response to agonists of the nitric oxide production; 4) the magnesium restoration to the organ chamber (phase III) allowed restoration of the relaxation observed in the phase I, only in response to the direct stimulation of the G-proteins. For the rest of the remaining agonists, the restoration was associated with the additional reduction in the relaxation intensity; 5) the smooth muscle received the influence of the magnesium concentration in the organ chamber. CONCLUSION: It was concluded that magnesium favorably influences the nitric oxide production by the coronary endothelium attenuating the endothelial dysfunction caused by global ischemia followed by reperfusion.
Magnesium; Endothelium; Ischemia; Coronary Reperfusion
