3 | RESULTS
Table 1 shows the physiological conditions at pre- and post-injury (before intratracheal treatment). Severe acidosis with a concomitant increase in PaCO2 and a notable drop in PaO2 were found for all animals the after induction of ALI by lavage and LPS (P < 0.05). All animal groups also presented significant increases in peak inspiratory pressure, AaDO2, and oxygen index after ALI. Except for the IT-DS-BUD group, all other groups showed a significant drop in the mean arterial blood pressure after ALI. However, these cardiopulmonary parameters at post-injury (before intratracheal treatment) showed no statistical difference among the five study groups.
After intratracheal treatments, the post-injury deteriorations of PaO2 and AaDO2 significantly improved over time in the IT-FS-BUD and IT-FS groups (Figures 1A and 1C). By contrast, these improvements were not observed in the Control, IT-NS-BUD, and IT-DS-BUD groups (Figures 1A and 1C). The base excess remained in the normal range during the study period in the IT-FS-BUD and IT-FS groups but worsened in the Control, IT-NS-BUD, and IT-DS-BUD groups (Figure 1D). The post-injury deteriorations of PaCO2 significantly improved over time in all the study groups (Figure 1B). The IT-FS-BUD and IT-FS groups also had a lower oxygen index (Figure 2A), higher mean arterial pressure (Figure 2B), and lower peak inspiratory pressure (Figure 2C) compared with the other three groups throughout the whole study period. Heart rate changed variedly over time among the five study groups, and no significance can be detected between any two groups at almost all time points (Figure 2D).
A histological evaluation of the lung sections from the Control and IT-NS-BUD groups revealed extensive inflammatory cell infiltration, hemorrhage, edema, and atelectasis, and all of these pathohistological changes were lessened in lung sections from the IT-DS-BUD, IT-FS-BUD, and IT-FS groups (Figure 3). These observations were confirmed by comparison of the group data in terms of lung injury scores for each pathohistological characteristic or total lung injury scores (Table 2). Numerically, the total injury scores in the five study groups followed the order IT-FS-BUD < IT-DS-BUD or IT-FS < IT-NS-BUD < Control (Table 2). Further immunohistochemical staining of the lung sections from the Control and IT-FS groups revealed marked signals of myeloperoxidase and TNF-α in the alveoli space and interstitials of the alveoli (Figure 4). These signals were reduced in the lung sections from the IT-NS-BUD, IT-DS-BUD, and IT-FS-BUD groups (Figure 4). Comparisons of group data revealed that the immunostaining intensity of myeloperoxidase in the IT-NS-BUD, IT-DS-BUD, and IT-FS-BUD groups was significantly smaller than that in the Control and IT-FS groups (Figure 5). Additionally, the immunostaining intensity of TNF-α in the IT-FS-BUD group was significantly smaller than that in the other four groups (Figure 5).