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. Author manuscript; available in PMC: 2010 Aug 9.
Published in final edited form as: Shock. 2009 Apr;31(4):376–381. doi: 10.1097/SHK.0b013e3181862279

Figure 1. Lung dysfunction after pulmonary contusion is dependent on the TLR4 pathway.

Figure 1

Figure 1

Figure 1

Arterial blood from uninjured (open) and injured animals (closed) was isolated and blood gas analysis performed as described in the methods. (A) PaO2:FiO2 ratios were calculated and are shown for WT animals at 3, 6 and 24 hours after injury (n=5/time). There is a significant decrease in PaO2:FiO2 in WT animals after injury (*p≤0.01), with the most significant decrease at 24H (**p<0.01 relative to other injury times). (B) Blood gas analysis on injured TLR4 and MyD88 deficient animals (gray) at 24H shows significantly increased PaO2:FiO2 ratios when compared to WT injured animals (#p≤0.05, n=7/genotype). (C) WT (black) and TLR4 and MyD88 deficient (gray) injured lungs were isolated at 24H after injury and weighed before (wet wt.) and after drying (dry wt.) as described in the methods (n=5/genotype). Pulmonary edema (wet wt/dry wt) is significant (*p≤.05) in all animals and is significantly decreased in MyD88 deficient mice (**p<.05 compared to WT).