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. 2003 Dec;163(6):2555–2563. doi: 10.1016/S0002-9440(10)63610-3

Figure 1.

Figure 1.

A: Effects of CO on survival following exposure to lethal hyperoxia. Mice in groups of 6 to 8 were exposed to >98% O2 or >98% O2 plus 250 ppm CO continuously and monitored for survival. Mice exposed to only O2 succumbed to O2 toxicity by 90 to 100 hours while >95% of those mice exposed in identical chambers to O2 in the presence of CO (250 ppm) were alive at 100 hours, with >50% alive at 128 hours of exposure. Data represent 20 to 25 animals per treatment group. B: Effects of CO on hyperoxia-induced PMN influx into the airways of mice. C: Effects of CO on hyperoxia-induced protein in the BAL. Mice were exposed continuously to either >98% O2 or >98% O2 plus 250 ppm CO. At 84 hours, a BAL was performed and PMN differential counts was determined. Total protein in the BAL was determined by Bradford assay. Data represent mean ± SEM of 8 to 10 mice per group. * P < 0.001 vs. air and CO. # P < 0.05 vs. CO/O2. D: Effects of CO (250 ppm) on hyperoxia-induced cytokine mRNA expression. Mice were exposed to >98% O2 in the presence or absence of CO (250 ppm). At 84 hours of exposure, the lungs were harvested and analyzed by RNase protection using the cytokine templates containing the above listed cytokines. L32 and GAPDH were used as loading controls. The blots are representative of three separate experiments in which the lungs from three mice were pooled for RNA extraction.