Protective effects of treprostinil and ischemic preconditioning on hepatic ischemia-reperfusion injury and biomarkers in experimental studies in rats

Figure 4 Histopathological findings of liver samples in sham group, hepatic ischemia-reperfusion injury group, treprostinil-treated group, and ischemic preconditioning group. A: Sham group; histological section from a rat of the sham group shows normal architecture. Hematoxylin and eosin (HE), original magnification 100 ×; B: Hepatic ischemia-reperfusion injury (HIRI) group; rat subjected to HIRI presents sinusoidal dilatation and portal spaces with inflammatory cell infiltration (mostly neutrophilic). HE, original magnification 100 ×; C: HIRI group; hepatic hemorrhages and sinusoidal hyperemia accompanied by hepatocyte necrosis, primarily characterized by pyknotic nuclei. Intracytoplasmic eosinophilic bodies are present in numerous hepatocytes while in lower center, there is vacuolar degeneration. Inset shows Mallory-like hyaline bodies. HE, original magnification 100 ×, inset 400 ×; D: HIRI group, hyperhemia and microhemorrhages and multiple necrotic hepatocytes characterized by homogenous eosinophilic cytoplasm and pyknotic or absent nucleus, are detectable. HE, original magnification 200 ×; E: Treprostinil treated group; treatment with treprostinil shows less disturbed/normal lobular architecture, mild sinusoidal hyperhemia and sparse inflammatory cells in portal spaces (upper right) and central vein dilatation (lower left), C × 100; F: Ischemic preconditioning group; rats pre-treated with IP preserve hepatic lobular architecture. However sparse hepatocyte necrosis and mild periportal neutrophilic infiltration are observed. HE, original magnification 100 ×.