In anaesthetised open-chest pigs, sequential myocardial samples were obtained before and after occlusion of the distal half of the LAD. These samples were analysed histofluorimetrically to determine the density of catecholamine containing neurones in each sample (quantified morphometrically), and radioenzymatically for total tissue noradrenaline content. Following coronary artery occlusion, 75% of the animals (24 out of 32) died in ventricular fibrillation in the first 30 min, the other 25% (8/32) survived the first 60 min of myocardial ischaemia. Coronary artery occlusion led to a significant reduction in the density of fluorescing fibres in the ischaemic myocardium of animals which fibrillated (from 1.25 +/- 0.2% to 0.67 +/- 0.10% at 15 min) whereas in the survivors there was no significant change in fluorescing area during the course of the experiment. Animals which fibrillated had a significant reduction in tissue noradrenaline concentration of the ischaemic myocardium (from an initial concentration of 612 +/- 72 to 402 +/- 64 ng/g ww) within the first 5 min of ischaemia. It is concluded that in this model of myocardial ischaemia, the development of ventricular fibrillation in the early phase seems to be related to the release of noradrenaline from the sympathetic neurones after the onset of myocardial ischaemia.
1 The effects of morphine (10mgkg-' i.p.) on haemodynamics, arrhythmias and plasma and myocardial catecholamines (CA) were studied after coronary artery occlusion in anaesthetized rats. Myocardial intraneuronal CA were assessed histofluorimetrically and CA concentrations measured by high performance liquid chromatography. 2 Morphine increased blood pressure, presumably due to higher plasma noradrenaline (NA) concentrations found in morphine-treated rats. 3 Morphine increased the area ofcatecholamine-containing fluorescing neurones in the myocardium (as a percentage of total field area) 60 min after sham-operation (0.87 ± 0.07%) or occlusion (0.57 ± 0.05%) compared to untreated animals (0.67 ± 0.06 and 0.38 ± 0.03% respectively). Tissue NA content was not significantly affected by coronary occlusion and/or morphine within the first 60 min. 4 Morphine had no effect on ischaemia-induced arrhythmias. 5 Whether the higher intraneuronal NA content following morphine resulted from reduced central sympathetic outflow to the heart, presynaptic inhibition of NA release, or increased uptake due to higher plasma concentrations is unclear. Ischaemia-induced local NA release appears independent of these mechanisms, as it was unaffected by morphine.
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