Changes in lung function in a rodent model of diabetes mellitus

Diabetes mellitus (DM) deteriorates various organ functions involving smooth muscle cells and interstitial matrix proteins including collagen and elastin. Since the lung contains high amount of collagen and airway smooth muscle cells, diabetes may affect the lung function. Thus, we investigated the potential impact of DM on lung function in a rat model. Rats (n=42) were randomized into group Control (C), and Type-I (DM1) and Type-II DM (DM2) induced by low and high dose of streptozotocin. Respiratory mechanics was determined by forced oscillations and intrapulmonary shunt fraction (Qs/Qt) was calculated from arterial and central venous blood gas samples at end-expiratory pressures (PEEP) of 3, 0 and 6 cmH2O. Lung responsiveness to iv. Methacholine (MCh) (2-32 μg/kg/min) was also assessed. Respiratory tissue damping and elastance were significantly higher at PEEP0 in the DM1 (1147±155[SE] and 5647±613 cmH 2 O/L) and DM2 (889±44 and 3826±311 cmH 2 O/L) groups as compared to group C (749±40 and 2813±191 cmH 2 O/L, p In this model of DM, the respiratory tissue viscoelasticity is compromised, but can be compensated by PEEP elevations. DM also deteriorates gas exchange and leads to airway hyporeactivity to MCh. These findings indicate that alveolar collapsibility in DM is associated with alveolo-capillary dysfunction and abnormal adaptation ability of the airways to exogenous constrictor stimuli. Grant supports: OTKA-NKFI K115253, GINOP-2.3.2-15-2016-00006, UNKP-17-3