Functional residual capacity and airway resistance in rats of COPD model induced by systemic hyaluronidase.

UNLABELLED: Chronic obstructive pulmonary disease (COPD) is characterized by obstructive bronchiolitis and parenchymal destruction. In animal models, air space enlargement induced by intratracheal elastase is augmented by prior depletion of lung hyaluronan by hyaluronisase. Recently our colleagues reported that intravenous hyaluronisaein in the absence of elastase produced emphysema-like alveolar dilation [1]. In this study we measured functional residual capacity (FRC) and airway resistance (Raw) in the rats with hyaluronidaseinduced experimental COPD.

MATERIALS AND METHODS: Hyaruonidase (20 mg/kg) was administered from the caudal vein of 19 male Wistar rats (COPD rats). Two weeks after the injection, FRC and Raw were measured with bodyplethysmogarph.

RESULTS: Thickness or inflammatory cell infiltrations were not apparent in the bronchus of the COPD rat while alveolar distension was obvious. The mean FRC of the COPD rats (6.22 ± 1.00 ml, mean ± SD) was significantly larger than that of Control rats (5.48 ± 0.85 ml). There was no statistical significance between the mean Raw of the COPD rats (0.28 ± 0.08 cmH2O/ml/s) and that of the control rats (0.28 ± 0.13 cmH2O/ml/s).

CONCLUSION: Systemic administration of hyaluronidase produced pulmonary overinflation but did not bronchial constriction. We speculate that hyaluonidase-induced COPD simulates panlobular emphysema.