Key result
Continuous noradrenaline infusion damages sympathetic nerve endings in dogs, preventable by desipramine and superoxide dismutase.
Why the study?
The neurotoxic effects of continuous intravenous noradrenaline infusion and potential prevention by desipramine or superoxide dismutase were investigated.
Does desipramine or superoxide dismutase prevent sympathetic denervation caused by long-term noradrenaline infusions in normal dogs?
Population
Normal dogs
Comparison
Noradrenaline infusion vs saline vs noradrenaline + desipramine vs noradrenaline + superoxide dismutase
Design
Preclinical study using Alzet osmotic minipumps
Follow-up
5 days
Authors
Loading...
Animal data link prolonged noradrenaline exposure to venous sympathectomy preventable by desipramine or SOD; leaves open relevance to clinical infusions.
Does desipramine or superoxide dismutase prevent sympathetic denervation caused by long-term noradrenaline infusions in normal dogs?
Long-term noradrenaline infusion causes chemical sympathectomy in dogs, which can be prevented by desipramine or superoxide dismutase, suggesting the involvement of free oxygen radicals.
Albino‐Teixeira et al. (1989) studied Normal dogs. Noradrenaline infusion (with or without desipramine or superoxide dismutase) vs. Saline was evaluated on Morphological and biochemical parameters (sympathetic nerve ending damage, extraneuronal structure/function changes). Continuous intravenous infusion of noradrenaline caused dose-dependent damage to sympathetic nerve endings in normal dogs, which was prevented or reduced by desipramine and superoxide dismutase.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: