Cardiotonic and sedative effects of Cecropia pachystachya Mart. (ambay) on isolated rat hearts and conscious mice

ALICIA E. CONSOLINI, MARÍA INÉS RAGONE, GRACIELA N. MIGLIORI, PAULA CONFORTI AND MARÍA G. VOLONTÉ

JOURNAL OF ETHNOPHARMACOLOGY

ELSEVIER IRELAND LTD

Año: 2006 vol. 106 p. 90 - 96

0378-8741

Cecropia pachystachya Mart. is popularly called “ambay” and extensively used in herbal medicine of South America for cough and asthma. In Argentina it grows in neotropical rainforest (Ntr C.p.) and in a temperate region (Tp C.p.). In a previous work we showed their hypotensive properties with different potency and toxicity, and now we studied the Tp C.p. effects in isolated heart from rats and central effects of both plants on the open-field test for mice. TpC.p. produced a positive inotropic effect on isolated rat hearts, wich was not affetced by 1 µM propranolol, suggesting that is not due to a β-adrenergic  effect. In contrast, it was prevented by pretreatmnet with high [K]o media, wich stimulate the Na,K-ATPase pump, suggesting an inhibition of the pump by “ambay”, as digital do. In the open-field test, both Ntr C.p. and Tp C.p. similarly decreased the spontaneus locomotion and exploratory behaviour of mice at doses between 180 and 600 mg/kg. Ntr C.p. potentiated the effect of 3 mg/kg diazepam to one similar to 10 mg/kg diazepam, but was not antagonized by 0.5 mg/kg flumazenil. Amphetamine at 5 mg/kg prevented the sedative effect of Ntr C.p. Chromatographic analysis showed that both plants have a qualitatively similar fingerprint but quantitatively differed in at least three components. Although the purpose was not to identify them, both plants have at least 10 compounds. Two of them  were in higher amount in Tp C.p than in Ntr C.p., and then, they could be responsible for the cardiovascular toxicity of Tp C.p. In conclusion, the results suggest that ambay has cardiotonic and sedative properties. The sedative effect could be useful in cough treatment. The extract resulted additive to benzodiazepines but it did not bind to the same site on GABA-A receptor, and it was interfered with by the dopamine release produced with amphetamine.