Related Experiment Videos
Cyanide-induced increases in plasma catecholamines: relationship to acute toxicity
A G Kanthasamy1, J L Borowitz, G E Isom
1Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana 47907-1334.
Neurotoxicology
|January 1, 1991
Summary
Cyanide (KCN) significantly elevates plasma catecholamines, including norepinephrine and epinephrine, in mice. Adrenalectomy prevents epinephrine increase, indicating direct action on the adrenal medulla.
Area of Science:
- Pharmacology
- Neuroscience
- Endocrinology
Background:
- Cyanide is known to stimulate catecholamine release from chromaffin cells and isolated adrenal glands.
- The impact of cyanide on *in vivo* plasma catecholamine levels remains largely unreported.
Purpose of the Study:
- To investigate the effect of cyanide on plasma catecholamine levels in mice.
- To elucidate the mechanism of cyanide-induced catecholamine release.
Main Methods:
- Administration of potassium cyanide (KCN) at varying doses (subcutaneous and intracerebroventricular).
- Measurement of plasma norepinephrine (NE) and epinephrine (EPI) levels.
- Assessment of KCN effects following adrenalectomy and pargyline pretreatment.
Main Results:
- Sublethal KCN doses (5 and 10 mg/kg) caused significant, dose-dependent increases in plasma NE and EPI.
- Repeated KCN administration led to sustained elevations in plasma catecholamines.
- Intracerebroventricular KCN induced convulsions but did not alter plasma catecholamine levels.
- Adrenalectomy abolished KCN-induced EPI elevation, while NE levels remained unaffected, suggesting direct adrenal stimulation for EPI release.
Conclusions:
- Cyanide directly stimulates the sympathoadrenal axis, leading to increased plasma catecholamine levels.
- The adrenal medulla is a primary site for cyanide-induced epinephrine release.
- Central administration of cyanide does not significantly impact peripheral catecholamine levels.