Release of endogenous catecholamines in the ischemic myocardium of the rat. Part B: Effect of sympathetic nerve stimulation

The contribution of centrally originating sympathetic activity to the myocardial extracellular accumulation of noradrenaline during the early phase of ischemia has been assessed in a perfused (Langendorff) rat heart preparation isolated except for its sympathetic innervation. A 10-minute electrical stimulation (4 Hz, 5 V) of the left cervicothoracic ganglion during normal perfusion causes the overflow of 177.5 ± 13.7 pmol noradreanline/g heart, whereas such stimulation during ischemia liberates only 21.5 ± 3.6 pmol/g (collected during reperfusion). When neuronal reuptake is blocked by desipramine, corresponding values are 321.5 ± 22.5 pmol/g (normal flow) and 151.8 ± 22.4 pmol/g (ischemia). After combined blockade of neuronal uptake, extraneuronal uptake, and α₂-receptors, nerve stimulation liberates 674 ± 22 pmol/g during normal flow and 206 ± 24.3 pmol/g during ischemia. These results suggest that, in vivo, centrally originating neural activity would not lead to substantial accumulation of noradrenaline within the extracellular space of the ischemic myocardium. This failure of accumulation is due to both a functioning neuronal uptake of noradrenaline and a failure of neurotransmission.