[Catecholamine metabolism. Physiopathology and pathobiochemistry]

Metabolic studies on isolated rat organs showed that vanillyl mandelic acid (VMA) is dehydrogenated by liver homogenate and suspension of pseudomonas fluorescens. In the 100000 g supernatant fraction of homogenated rat kidneys enzymatic activity was sufficient for kinetic studies and the examination of substrate specificity, pH dependence and changes with age and sex of rats. Norepinephrine secretion and resorption may be influenced by antiarrhythmic drugs in vivo: after lidocaine, there was no change of the tyramine dependend norepinephrine depletion of rat hearts, Verapamil inhibited the uptake of norepinephrine by rat hearts. Immobilisation of the animals led to a significant decrease in the myocardial levels for norepinephrine and epinephrine, which was antagonised by recreation of 24 hours. Adumbran prevented the catecholamine depletion, so that the influence of the limbic system may be important for the mediation of sympathetic stimuli.

Emotional stress was shown to lead to an elevated plasma level of norepinephrine, cortisole and free fatty acids. In patients undergoing surgery, the application of Valium and Fortral inhibited these stress reactions. After physical stress, which did not lead to significant changes of the catecholamine level in plasma of healthy volunteers, there was an elevated norepinephrine plasma level in patients with cardiac failure, which could be prevented by different antiarrhythmic drugs. The excretion of norepinephrine and VMA of these patients was also increased. It was shown, that sinus rate rose according to norepinephrine levels in plasma in this group, which was contrary to the behaviour of healthy volunteers, showing neither a norepinephrine overflow nor increased heart rate. In patients with atrial fibrillation, AV-conduction also increased with elevated norepinephrine levels in plasma. There was, however, no direct correlation. Determination of the cardiac AV-difference of plasma-norepinephrine levels showed a cardiac catecholamine overflow, which could be inhibited by specific and nonspecific antiarrhythmic drugs (Verapamil, Practolol). In studies of catecholamine and glucocorticoid metabolism, no significant difference of catecholamine and VMA could be determined in patients with normal blood pressure and arterial hypertension. There was, however, a tendency to increased values in patients of the last group. In postural hypotension, plasma levels and urinary excretion of catecholamines were decreased and showed no variation after physical stress in orthostasis and after nicotine. In patients with tumors of the adrenal cortex and medulla, a close relation of the disturbance in catecholamine and corticoid metabolism was revealed.