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Bretylium caused a specific and lasting depression of many excitatory and inhibitory responses evoked by electrical stimulation of the peripheral sympathetic nervous system, probably by impairing conduction of impulses in adrenergic neurones with consequent failure of noradrenaline and adrenaline release. This effect, which will be referred to as the adrenergic neurone blocking action, was preceded by weak sympathomimetic effects. In the presence of bretylium the effects of adrenaline and noradrenaline were increased, as after sympathectomy. Concentrations producing blocking of adrenergic neurones did not prevent the release of adrenaline and noradrenaline from the adrenal medulla by splanchnic nerve stimulation or by the injection of dimethylphenylpiperazinium iodide, nor did they cause antiparasympathetic or parasympathomimetic effects. No action on the central nervous system has been detected. Curare-like neuromuscular block occurred with 10 to 30 times the amount required to block the response to adrenergic nerve stimulation alone and was accompanied by signs of temporary synaptic block in autonomic ganglia. Adrenergic nerve trunks and sensory nerves in the skin were readily blocked for long periods by topical application of bretylium, whereas the phrenic nerve of the rat was not. Bretylium had little effect on gastrointestinal propulsion or on the sensitivity of smooth muscle to acetylcholine, 5-hydroxytryptamine, adrenaline, or noradrenaline, but moderate amounts depressed the peristaltic reflex and the sensitivity of the guinea-pig ileum to histamine. Bretylium caused postural hypotension in the cat in doses which had little effect on the supine blood pressure. Experiments on the nictitating membrane indicated that compensation for the effects of bretylium on low rates of stimulation of postganglionic sympathetic nerves could be attained by a small increase in the rate of stimulation, whereas compensation for its effects on high rates required an increase in the rate of stimulation beyond physiological limits.
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By means of vital microscopy a possibility of histochemical detection of redox enzymes and of study of changes in their activity in intramural nerve plexuses of the small intestine on a live animal was demonstrated. Severe thermal trauma induced a disturbance of permeability of mitochondrial membranes of the Auerbach's plexus nerve cells; as a result, there was a change in the activity of redox enzymes localized within the mitochondria. Lumbar novocain block performed soon after the burn trauma normalized the state of the mitochondrial membranes of the nerve cells.
Careful clinical and experimental studies in well-diagnosed groups of selected patients can give valuable information concerning unknown mechanisms involved in certain disease states. In particular, microneurographic techniques can be applied to assess the underlying neural pathophysiology. It is anticipated that future studies performed along these guidelines will contribute to an improved diagnosis and/or therapy in a number of clinical conditions.
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The mechanism by which adenosine increases heart rate was investigated in 21 chronically catheterized fetal sheep (> 0.8 term). Intra-arterial infusion of adenosine (0.16 mg.min-1.kg fetal wt-1) for 1 h significantly increased fetal heart rate within 5 min with maximum values of approximately 68 beats/min above the control mean of 163 +/- 8 beats/min. The average diastolic blood pressure was reduced only during the first 10 min of infusion, and the average systolic and mean arterial pressures were not significantly affected. Mean venous pressure rose by approximately 48% after 20 min of adenosine infusion, but all other measurements did not differ significantly from the control value. The mean hemoglobin concentration during the last 30 min of infusion was increased by approximately 8%. Plasma concentrations of norepinephrine and epinephrine were elevated only during the first 30 min of adenosine administration, to values as high as 2.3 and 5 times the respective control mean. Adenosine significantly increased mean fetal heart rate by about 15-20 beats/min in fetuses with autonomic ganglion blockade or combined cholinergic, alpha-, and beta-adrenergic receptor blockade. Intra-arterial infusion of CGS 21680C, an A2-adenosine receptor agonist, also produced a fetal tachycardia of approximately 86 beats/min above the control mean and increased intrinsic fetal heart rate by approximately 38 beats/min. It is concluded that approximately 75% of the positive chronotropic effects of adenosine are produced by A2-receptor stimulation of the autonomic nervous system and that approximately 25% of the rise in heart rate induced by adenosine may be caused by activation of A2-receptors in myocardium.
This work was intended to analyze the sympathetic and parasympathetic factors affecting the hemodynamics of hyperthyroidism. Seven patients with hyperthyroidism, diagnosed based on the determinations of BMR, 131I-uptake, T3-resin sponge uptake (T3-RSU), and serum level of thyroxine (T4) were subjected to the study. The hemo-dynamic estimation was done (1) at rest, (2) after vagus blocking by the injection of 0.04 mg/Kg b.wt. atropine and 0.2 mg/Kg b.wt. propranolol before (hyperthyroid state=H) and after (euthyroid state=E) anti-thyroid drug therapy. Cardiac output was measured by the dye-dilution method, and the valve was calculated according to the standard Hamilton formula. The following results were obtained. (1) The vagal tone is lower in H than in E, on the other hand, sympathetic beta-receptor tone is higher in H than in E. (2) The sympathetic alpha-receptor tone in H may be equivalent to that in E. (3) There might exist inotropic factors which affect the hemo-dynamics, other than autonomic nervous system in H.
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