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. 2018 Oct 31;316(1):H212–H223. doi: 10.1152/ajpheart.00652.2017

Fig. 1.

Fig. 1.

Bromine (Br2) inhalation increases mortality and causes respiratory distress and acute cardiopulmonary injury in survivors. Rats were exposed to Br2 (600 ppm, 30 or 45 min) and returned to room air. Rats were observed for clinical symptoms for 48 h, and Kaplan-Meier curves were generated for survival data (dotted line, 600 ppm for 30 min; solid line, 600 ppm for 45 min dose) (A). B−D: deterioration in clinical scores (B), decrease in O2 saturation (C) and heart rate (D). Lung injury was determined by increased bronchoalveolar lavage fluid (BALF) protein (E) and lung wet-to-dry weight ratios (F). Cardiac injury was indicated by increased troponin (G) and heart-type fatty acid-binding protein (hFABP) (H). Increased NH2-terminal pro-brain natriuretic peptide (NT-proBNP; I) in plasma and increases in heart-to-body weight ratios (HW/BW; J) also indicated heart damage. Data are means ± SE; n = 8 for each group. *P < 0.05 vs. 0 ppm.