Characteristics and mechanism of secondary liver injury in pigs with traumatic hemorrhagic shock in dry heat environment

Objective　To document the dynamics of secondary liver injury in pigs with traumatic hemorrhagic shock (THS) induced by simulated desert dry heat environment and to explore its possible mechanism. Methods　Sixty male Landrace piglets were randomly divided into three groups: Dry heat trauma hemorrhagic shock group (DHS group, n=20), dry heat trauma hemorrhagic shock sham operation group (DHC group, n=20), normal temperature trauma hemorrhagic shock group (NTS group, n=20). DHS group and DHC group were exposed to a dry and hot environment [temperature (40.5±0.5) ℃, humidity 10%±2%]; while NTS group were exposed to normal temperature environment [temperature (25.0±0.5) ℃, humidity 35%±5%] for 3 h. Then the model of blood pressure controlled hemorrhagic shock was established. Animals were euthanized at 0 min (T0), 50 min (T1), 100 min (T2) or 150 min (T3) after the successful establishment of the hemorrhagic shock model, blood and live tissue were collected. The pathological changes of liver tissue were observed by HE staining; the levels of TNF-α and IL-1β in liver tissue were detected by ELISA; the expressions of HMGB-1 and ICAM-1 in liver tissue were detected by Western blotting; the contents of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were determined. Results　HE staining results showed that the DHS group had different degrees of injury at each time point, and gradually aggravated with time, and gradually appeared different degrees of hepatic sinusoidal expansion, congestion, hepatic lobule, portal area structure disorder, inflammatory cell infiltration, liver cell degeneration, necrosis and so on. In the NTS group, the injury began to appear at T2 and gradually worsened. In the DHC group, there was no obvious pathological change at each time point (P>0.05). In the DHS group, ALT and AST showed dynamic changes, and the changing trend was the same, compared with the DHC group, it began to rise at T0, the difference was statistically significant (P 0.05). As time went on, the expression of ICAM-1 and HMGB-1 in the DHS group was higher than that in the previous time point (P<0.05 or P<0.01). Conclusion　In desert dry and hot environment, the secondary liver injury of THS occurs early and progresses seriously. This can activate more Kupffer cells in the liver to promote the release of TNF-α and IL-1β leading to elevated expression of HMGB-1 and ICAM-1 resulting in further liver injury. DOI: 10.11855/j.issn.0577-7402.2021.03.05