Myocardial noradrenaline uptake after coronary occlusion in the rat.
Coronary ligation produced a marked increase in labelled noradrenaline uptake by the myocardial tissue of rats. The peri-ischemic zones showed an elevated accumulation of noradrenaline on the 4th day but the intact zone had returned to normal values. At the 14th day of observation, both the ischemic and per-ischemic tissue exhibited a subnormal accumulation of radioactivity. The role of the acidotic state in the changes of noradrenaline uptake was studied in vitro. Noradrenaline accumulation in the myocardial tissue was higher at pH 6.8 than at 7.4 or 7.1 Competition studies revealed that unlabelled noradrenaline had occupied the binding sites in the same quantity at pH 6.8 and at 7.4. It is assumed that intracellular acidosis was involved in the enhanced accumulation of noradrenaline in the damaged myocardium, and that an increase of noradrenaline concentration in the myocardium may be considered a risk factor in supporting heart function.
Myocardial noradrenaline uptake after coronary occlusion in the rat. Coronary ligation produced a marked increase in labelled noradrenaline uptake by the myocardial tissue of rats. The peri-ischemic zones showed an elevated accumulation of noradrenaline on the 4th day but the intact zone had returned to normal values. At the 14th day of observation, both the ischemic and per-ischemic tissue exhibited a subnormal accumulation of radioactivity. The role of the acidotic state in the changes of noradrenaline uptake was studied in vitro. Noradrenaline accumulation in the myocardial tissue was higher at pH 6.8 than at 7.4 or 7.1 Competition studies revealed that unlabelled noradrenaline had occupied the binding sites in the same quantity at pH 6.8 and at 7.4. It is assumed that intracellular acidosis was involved in the enhanced accumulation of noradrenaline in the damaged myocardium, and that an increase of noradrenaline concentration in the myocardium may be considered a risk factor in supporting heart function.