Brief Article
Copyright ©2014 Baishideng Publishing Group Co.
World J Hepatol. Apr 27, 2014; 6(4): 243-250
Published online Apr 27, 2014. doi: 10.4254/wjh.v6.i4.243
Figure 2
Figure 2 Thioacetamide caused severe liver necrosis and inflammation, which may explain mice metabolic encephalopathy, coagulopathy and remote lung injury. A: Liver intravital microscopy showing crescent number of necrotic cells (in red, propidium iodide) with concomitant neutrophil infiltration (in green, Lysm-eGFP mice); B: Liver sections stained by hematoxylin and eosin (4 × increase). Arrows indicate necrotic areas; C, D: Liver macroscopic analysis confirmed extensive and diffuse necrosis, which is also reflected by elevated serum transaminase activity (D); E, F: Liver failure was confirmed by prolonged prothrombin and partial thromboplastin times; G, H: Also, significant drop in mean arterial pressure (MAP; G) and increased heart rate (H), as assessed by tail cuff method, suggested that TAA-treated mice also evolved to hemodynamic shock; I: After TAA treatment hours, lungs from mice had increased cellularity in lung parenchyma, alveolar edema and hemorrhage in comparison to controls (arrows, 4 x increase) aIndicates statistical significance in comparison to controls. aP < 0.05, ANOVA (Tukey’s post test). N ≥ 5 for each group. TAA: Thioacetamide.