Pulmonary vasodilation in the rat by insulin in vitro could indicate potential hazard for inhaled insulin

Aims/hypothesis. Hypoxic pulmonary vasoconstriction is an essential mechanism to prevent hypoxaemia in lung diseases. Insulin is known to be a systemic vasodilator but its effect on the pulmonary circulation is not known. Inhaled particulate insulin can generate locally high concentrations in the lung which could be physiologically important. Methods. We therefore studied the effects of insulin in vitro on isolated rat pulmonary artery in a small vessel myograph. Results. We have shown that pulmonary artery vasodilatation with insulin occurs in a dose-dependent manner. Pre-constriction with PGF(2alpha) can be abolished (105.7+/-2.9%, mean+/-SEM) and pre-constriction with hypoxia reduced (68.9+/-6.5%) by pharmacologically relevant concentrations of insulin. The characteristic phasic vasoconstriction by pulmonary vessel to hypoxia is substantially modified, resulting in sustained vasodilatation. Conclusions/interpretation. These effects could be clinically important for patients using inhaled insulins who have acute or occult chronic lung disease.