Objective: In type 1 diabetes, lung diffusing capacity for carbon monoxide (DL(CO)) may be impaired, and insulin has been shown to be beneficial in cases in which near-normal metabolic control is achieved. An influence of insulin, per se, on the alveolar-capillary membrane conductance is unexplored. We aimed at testing this possibility.
Research design and methods: We studied 19 life-long nonsmoking, asymptomatic patients with type 2 diabetes and normal cardiac function, whose GHb averaged 6.2 +/- 0.3% with diet and hypoglycemic drugs. DL(CO) and its subcomponents (alveolar capillary membrane conductance [D(M)] and pulmonary capillary blood volume available for gas exchange [Vc]), vital capacity (VC), forced expiratory volume 1 s (FEV(1)), cardiac output (CO), ejection fraction (EF), pulmonary wedge pressure (WPP), and pulmonary arteriolar resistance (PAR) were determined before and within 60 min after infusion of 50 ml saline + 10 IU of regular insulin or after saline alone on 2 consecutive days (random block design). Glycemia was kept at baseline levels during experiments by dextrose infusion.
Results: Percent of normal predicted DL(CO) averaged 84.2 +/- 7.9% and in 14 patients was <100%. Insulin infusion, not saline alone, improved (P < 0.01) DL(CO) (12%) and D(M) (14%) and raised DL(CO) to 98% of the normal predicted value. There were no variations in VC, FEV(1,) CO, EF, WPP, or PAR, suggesting that the influences of the hormone on gas transfer were not mediated by changes in spirometry, volumes, and hemodynamics of the lung.
Conclusions: Several cases of type 2 diabetes present with increased impedance to gas transfer across the alveolar-capillary membrane, and hypoglycemic drugs do not prevent this inconvenience. Insulin, independently of the metabolic effects, acutely improves gas exchange, possibly through a facilitation of the alveolar-capillary interface conductance.