Premium
Lidocaine diminishes arrhythmia by Leiurus quinquestriatus quinquestriatus venom in rats
Author(s) -
Purali Nuhan,
Yagcioglu Suha
Publication year - 2002
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1046/j.1472-8206.2002.00071.x
Subject(s) - medicine , lidocaine , sinus rhythm , contraction (grammar) , papillary muscle , endocrinology , atropine , cardiac muscle , venom , anesthesia , chemistry , atrial fibrillation , biochemistry
The venom from the scorpion Leiurus quinquestriatus quinquestriatus has previously been shown to alter the excitability of the neural and skeletal muscle preparations. The present study was undertaken to explore the effects of the venom in cardiac potential signals at the animal, tissue and the cell level in rats hearts. In anaesthetised animals Leiurus quinquestriatus quinquestriatus venom (LqV) 100 μg applied intravenously reduced the heart rate by 13%, and evoked some abnormal waveforms in the electrocardiogram (ECG). Lidocaine injection (0.02 μg) restored the waveform of the ECG. However, the sinus rhythm resumed only when Atropine (2.5 μg) was applied in addition to previously administered Lidocaine. In isolated atria, LqV (10 –2 mg/mL) exposure abolished the sinus rhythm and decreased the spontaneous rate by 38%, and increased the contraction amplitude by 85%, and duration of the contractions by 17%. The gross electrical activity of the preparation and the duration of the individual atrial muscle action potential were prolonged by 150% and 186%, respectively. In isolated papillary muscle, LqV evoked irregular contractions, and the duration of the action potential was increased about 15‐fold. The effects by LqV in the action potential were present when calcium channels were blocked but not when extracellular sodium was substituted. Lidocaine (75 n M ) antagonised the effects by LqV in isolated atria and papillary muscle. It was concluded that the lethal cardio‐toxic effects by LqV were mainly due to its direct action in myocardial cells, and partly to an alteration in the autonomous nervous activity.