The acute effects were compared of selected flavonoids on the pulmonary vascular circuit in two experimental models of pulmonary hypertension, produced by hypoxia and by prostaglandin F2α (PGF2α) in anaesthetized dogs. In all dogs, haemodynamic variables (pulmonary artery pressure, pulmonary artery wedge and aortic pressure, pulmonary vascular resistance, cardiac output) were recorded in the control state, during hypoxia or PGF2α-induced pulmonary vasoconstriction, and after equimolar doses (5 mM/kg/i.v.) of luteolin, apiin and rhoifolin. The effects observed after flavonoid administration were compared with those of equimolar doses of nifedipine. The results obtained have shown that luteolin and apiin caused a decrease of hypoxic pulmonary vascular resistance to normoxic values and of the pulmonary arterial pressure while cardiac output remained unchanged. Rhoifolin produced no change in hypoxic pulmonary vasoconstriction, but decreased cardiac output and aortic pressure. The response of the pulmonary hypertension induced by PGF2α to flavonoids and nifedipine was nearly identical to that of hypoxia-induced pulmonary hypertension. The mechanism of action of these flavonoids is discussed.

COMPARATIVE EFFECTS OF THE FLAVONOIDS LUTEOLIN, APIIN AND RHOIFOLIN ON EXPERIMENTAL PULMONARY-HYPERTENSION IN THE DOG

OCCHIUTO, Francesco;
1994

Abstract

The acute effects were compared of selected flavonoids on the pulmonary vascular circuit in two experimental models of pulmonary hypertension, produced by hypoxia and by prostaglandin F2α (PGF2α) in anaesthetized dogs. In all dogs, haemodynamic variables (pulmonary artery pressure, pulmonary artery wedge and aortic pressure, pulmonary vascular resistance, cardiac output) were recorded in the control state, during hypoxia or PGF2α-induced pulmonary vasoconstriction, and after equimolar doses (5 mM/kg/i.v.) of luteolin, apiin and rhoifolin. The effects observed after flavonoid administration were compared with those of equimolar doses of nifedipine. The results obtained have shown that luteolin and apiin caused a decrease of hypoxic pulmonary vascular resistance to normoxic values and of the pulmonary arterial pressure while cardiac output remained unchanged. Rhoifolin produced no change in hypoxic pulmonary vasoconstriction, but decreased cardiac output and aortic pressure. The response of the pulmonary hypertension induced by PGF2α to flavonoids and nifedipine was nearly identical to that of hypoxia-induced pulmonary hypertension. The mechanism of action of these flavonoids is discussed.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11570/13626
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