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).