Hughes J M, Allison D J, Goatcher A, Tripathi A
Eur J Respir Dis Suppl. 1983;126:215-24.
The effects of almitrine bismesylate on the pulmonary circulation have been investigated in anaesthetized dogs, paralysed and artificially ventilated. An i.v. bolus of almitrine bismesylate (10 micrograms X Kg-1) caused a 35% increase in specific pulmonary vascular resistance under normoxic or hyperoxic conditions but only a 2% increase when pulmonary vessels were constricted by hypoxia (13% inspired O2). With local hypoxia, confined to the retrocardiac lobe, almitrine bismesylate caused lobar vasodilation (specific vascular conductance increased by 10%) while at the same time conductance fell by 38% in the rest of the lung which was hyperoxic. The almitrine-induced vasoconstriction was not abolished by alpha- or beta blockade, indomethacin, vagotomy or bilateral clamping of both common carotids in the neck. With constant ventilation, no rise of arterial PO2 occurred following almitrine bismesylate . In the presence of local hypoxia, the drug by virtue of its inhibition of local hypoxic vasoconstriction caused PaO2 to fall slightly. In conclusion, almitrine bismesylate constricts pulmonary vessels in normoxia and dilates them when they are constricted by hypoxia. The mechanism is unknown but it is likely to be an intra-rather than an extrapulmonary site of action.
