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Eksperimental'naya i Klinicheskaya Farmakologiya

[Cardioprotective and antiarrhythmic properties of preparations from Leuzea carthamoides, Aralia mandshurica, and Eleutherococcus senticosus].

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L N Maslov
N V Guzarova

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It is established that pretreatment with Leuzea carthamoides extract (LCE) (1 ml/kg per os during 8 days) prevents the development of stress-induced (6-hr painful-emotional stress) damage of the rat heart. A chronic administration of LCE (1 ml/kg per os during 8 days) increased the cardiac tolerance to the cardiotoxic action of D, L-isoproterenol and the arrhythmogenic action of epinephrine. Pretreatment with naloxone (2 mg/kg) completely eliminated the cardioprotective effect LCE and attenuated but not abolished the antiarrhythmic effect of the phytoadaptogen. A chronic administration of LCE elevated the level of beta-endorphin levels in the rat blood plasma. It is suggested that the cardioprotective effect of LCE is related to an increase in the level of opioid peptides, which produce stimulation of the opioid receptors. It is also established that preliminary chronic administration of Aralia mandshurica extract (AME) increases the cardiac resistance to the arrhythmogenic action of a 45-min coronary artery occlusion, but has no effect on the necrosis/risk area ratio. A pretreatment with Eleutherococcus senticosus extract (ESE) (1 ml/kg per os during 8 days) prevented the stress-induced damages of the rat heart. A chronic administration of ESE increased the cardiac tolerance to the cardiotoxic action of D, L-isoproterenol and the arrhythmogenic action of epinephrine. The pretreatment with naloxone (2 mg/kg) completely eliminated both the cardioprotective action and the antiarrhythmic effect of the phytoadaptogen. A chronic administration of ESE increased the beta-endorphin level in the rat blood plasma. It is suggested that the cardioprotective and antiarrhythmic effects of ESE is also related to an increase in the endogenous opioid peptide levels. A chronic administration of ESE had no effect on the arrhythmogenic effect of a 45-min coronary artery occlusion and did not change the necrosis/risk area ratio in rats.

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