Figure 3.

Sham-treated animals show no significant congestion at low power (a ×100). Vacuolization and cellular necrosis are not evident in periportal hepatocytes (b ×200) or in centrizonal areas. Hepatic architecture is unremarkable. In contrast, control animals following 45 min of ischemia and 4 h of reperfusion show diffuse, moderate sinusoidal congestion, with numerous sinusoidal channels distended by red blood cells in several areas of the liver section (c ×200). Two dying hepatocytes (likely evolving into Councilman bodies) are visible in the center of the field (c). Mild parenchymal vacuolization is visible in some hepatocytes, with several hepatocytes in this field showing irregular nuclear contours, chromatin condensation, pyknosis, and nuclear dust, histologic evidence of cell damage, and evolving cell death (d ×400). Moderate sinusoidal congestion also is seen in hyperglycemic animals treated with high levels of dextrose before ischemia (e ×200). This particular animal showed both zones of necrosis and patchy single-cell necrosis. Cell damage is seen in several adjacent hepatocytes containing vacuolated cytoplasm, pyknotic nuclei, and nuclear dust. These dying hepatocytes also show paler cytoplasm than their undamaged counterparts nearby (f ×400).