Key result
Intravenous colchicine administration in rats induced electrocardiographic changes indicating decreased myocardial excitability and conductivity, alongside histopathological and blood chemical evidence of cardiac injury.
Why the study?
Does colchicine intoxication induce electrocardiographic, histopathological, and blood chemical changes in rats?
Does colchicine intoxication induce electrocardiographic, histopathological, and blood chemical changes in rats?
Colchicine intoxication in rats induces significant cardiotoxicity characterized by ECG conduction delays, myocardial degeneration, and elevated cardiac biomarkers, potentially linked to increased parasympathetic activity and hypocalcemia.
Supports cardiac monitoring in colchicine overdose; leaves open human translation of rat ECG and injury findings.
The microtubule inhibitor colchicine is cardiotoxic and is suggested to impair impulse formation and conduction. However, little is known about the electrocardiographic (ECG) changes induced by colchicine in experimental animals and the detailed pathogenesis of its cardiotoxicity. Therefore, we analyzed cardiotoxicity in colchicine-treated rats using electrocardiographic, histopathological and blood-chemistry approaches. A telemetry device for transmitting ECG data was implanted into male Crl:CD(SD) rats, and ECG tracings were obtained. At 6 weeks of age, 1.25 mg/kg colchicine was injected intravenously once daily for 2 consecutive days, and ECG waveforms and heart rate variability were analyzed. Furthermore, 1.25 mg/kg colchicine or vehicle was injected for 1 or 2 consecutive days in other rats at 6 weeks of age. One day after the final dosing, heart and blood samples were taken for histopathological and bloodchemical examination. ECG analysis revealed a prolonged RR interval, QRS duration, PR interval and QT interval. Heart rate variability analysis showed an increase in high frequency (HF) components as an index of parasympathetic nervous activity. In blood chemical examinations, colchicine induced high levels of parameters of cardiac injury and low levels and/or variations in Ca, inorganic phosphorus, potassium and chloride. Histopathologically, colchicine-treated rats showed eosinophilic granular degeneration and cytoplasmic vacuolation of ventricular myocardial cells but no remarkable change in the atrioventricular node. Not only blood chemical and histopathological changes but also ECG changes were induced in colchicine-treated rats, which indicated a decrease in myocardium excitability and conductivity, and these changes might be related to increased parasympathetic nervous activity and low blood Ca levels.
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Tochinai et al. (2014) studied Colchicine cardiotoxicity (n=12). Colchicine vs. 5% glucose (vehicle) was evaluated on Electrocardiographic, histopathological, and blood chemical changes. Intravenous colchicine administration in rats induced electrocardiographic changes indicating decreased myocardial excitability and conductivity, alongside histopathological and blood chemical evidence of cardiac injury.
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