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Objective: To examine critical interactions between the nervous system and the immune system during experimental African trypanosomiasis. Methods and Results: Inoculation of Trypanosoma brucei brucei resulted in early interferon (IFN)-γ production, elevated corticosterone and prostaglandin E₂ (PGE₂) levels and increased splenocyte proliferation, as measured by enzyme-linked immunospot assay, radioimmunoassay and thymidine incorporation assay, respectively. Splenic denervation suppressed IFN-γ, corticosterone and PGE₂ production, enhanced splenocyte proliferation, and significantly reduced parasitemia and prolonged rat survival. Conclusions: Our data show substantial effects of the nervous system on early immune responses that may influence the outcome of this disease. These effects were not dependent on cytokine inhibitory mediators such as prostaglandins or stress hormones. More investigations are required to understand the evident neural control over the immune system during infectious challenges, which may assist in novel therapeutic approaches.

Digoxin was infused intravenously 27.5 μg/min. to guinea pigs. By means of the ECG doses of digoxin needed to cause ventricular extrasystoles (VES), ventricular fibrillation (VF), and asystole (AS) were determined in a control group without any premedication. Three groups were given a pre‐treatment with desipramine, phenytoin and reserpine. After AS digoxin concentrations in the heart muscle and in the kidneys were determined by radioimmunoassay. The concentrations of adrenaline and noradrenaline were also determined in these tissues. After reserpine and phenytoin the doses of digoxin needed to induce VF and AS were increased. Desipramine had no effect on digitalis‐induced arrhythmias. The relative uptake of digoxin in the heart muscle was decreased after all of the three premedications; there was no change in the kidney. The tissue catecholamine concentrations were decreased after reserpine and desipramine, but remained unchanged after phenytoin. The lethal dose of digoxin seemed not to correlate to the myocardial digoxin concentration after different premedications. The mechanism of the uptake in the heart muscle seemed to be different from that in the kidney. There was no correlation between the catecholamine concentration in myocardium and the ar‐rhythmogenic effect of digoxin in the different groups.

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