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  • The responses to mg mL MCh in the

    2020-07-27

    The responses to 50mg/mL MCh in the control and elastase-induced A 61603 hydrobromide mg groups did not significantly differ. However, the Raw response to 100mg/mL MCh in the 0.6U elastase-induced emphysema group (0.80±0.07cmH2Os/mL) was reduced when compared to that of A 61603 hydrobromide mg the control group (1.51±0.33cmH2Os/mL; p<0.005) in the closed thorax condition, but no significant response was found in the opened thorax condition. G was significantly reduced in the 0.6U elastase-induced emphysema group (9.26±0.80cmH2O/mL) relative to that of the control group (15.34±1.54cmH2O/mL; p<0.005) in the closed thorax condition. However, in the opened thorax condition, the 0.3U group exhibited a significant increase in G (17.51±2.19cmH2O/mL) compared to control group (10.26±1.59cmH2O/mL; p<0.005). The H response to 100mg/mL MCh was significantly lower in the 0.6U elastase-induced emphysema group (25.40±2.60, closed thorax; 37.52±7.40cmH2O/mL, opened thorax) than in the control group (40.30±4.84; 56.27±3.63cmH2O/mL, respectively; p<0.005). The η response to the high dose of MCh was elevated in the 0.3U opened thorax group (0.42±0.05) compared to the control group (0.35±0.05). All elastase-induced emphysema groups showed significant reductions in the normal areas. Hyper-inflation was only significant increase in 0.6U group and Lm was only significant increase in 0.3U group than in control. However, the 0.6U elastase-induced emphysema group exhibited more alveolar collapse (Table 2) than the control group. The morphological changes in each group are shown in Fig. 2; note, in particular, the hyperinflated area in the 0.6U group.
    Discussion The present study revealed attenuated Raw (closed thorax), H and G (closed and opened thorax) responses in mice with elastase-induced emphysema after MCh challenge. These results may be associated with the collapsed and/or hyperinflated areas in the 0.6U mice with elastase-induced emphysema. These changes were studied with closed thorax to measure the mechanics of the intact respiratory system and in opened thorax to measure the mechanics without the influence of the rib cage and adjacent muscles. The attenuated response to MCh in the elastase group shown in the present study contributes new information about the behaviour of airways after MCh challenge and the respiratory system in COPD. The elastase-induced injury model has been shown to produce airspace enlargement, and increases in lung volume and compliance that are similar to those observed in human patients (Hantos et al., 2008, Hamakawa et al., 2011). Thus, this model, which has been used to study emphysema, should be adequate for a first-order evaluation of structure–function relationships during disease progression (Luthje et al., 2009, Snider, 2000, Kasahara et al., 2000). This method of emphysema induction yielded lengthy and progressive inflammation and remodelling of the lung tissue in addition to alveolar destruction. Elastase caused structural lung changes, including enlargement of the air spaces and alveoli destruction while simultaneously causing increases in the following: mean linear intercepts, fractions of collapsed and hyperinflated alveolar areas and alveolar-capillary membrane damage (Tomioka et al., 2002, Antunes and Rocco, 2011). In this study, two PPE doses were used to illustrate the magnitudes of functional changes after MCh challenge in Swiss mice; we used the same animal model and elastase-induced emphysema model used by Otto-Verberne et al. (1992).