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 PGF2alpha 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.