PURPOSE: Histochemical and immunohistochemical changes were observed in hepatocytes to study the developing and recovery processes of halothane-induced hepatic injury from 0 to 7 days after halothane exposure. METHODS: A total of 330 7-week-old male Sprague-Dawley rats, with or without phenobarbital preteatment, were exposed to halothane in 100%, 21%, 10% oxygen or oxygen alone for 2 h. RESULTS: In the phenobarbital group, degenerated hepatocytes were observed immediately after exposure to 10% oxygen, both with and without halothane: glycogen and ribosomal ribonucleic acid (rRNA) disappeared immediately and 6 h after exposure, respectively, and necrosis developed in zones 3 to 2 at 6 h after exposure. From 12 h to day 1, the necrosis was more marked and more widely observed in the cells with halothane than those without halothane. However, all tissues returned to normal by day 7. CONCLUSION: Disappearance of glycogen at 0 h and rRNA at 6 h after exposure to halothane under 10% oxygen is considered to be one of the factors inducing necrosis around the central vein. Recovery of the hepatolobular structure was attributed to the rearrangement of the remaining hepatocytes in the portal vein area.
PURPOSE: Histochemical and immunohistochemical changes were observed in hepatocytes to study the developing and recovery processes of halothane-induced hepatic injury from 0 to 7 days after halothane exposure. METHODS: A total of 330 7-week-old male Sprague-Dawley rats, with or without phenobarbital preteatment, were exposed to halothane in 100%, 21%, 10% oxygen or oxygen alone for 2 h. RESULTS: In the phenobarbital group, degenerated hepatocytes were observed immediately after exposure to 10% oxygen, both with and without halothane: glycogen and ribosomal ribonucleic acid (rRNA) disappeared immediately and 6 h after exposure, respectively, and necrosis developed in zones 3 to 2 at 6 h after exposure. From 12 h to day 1, the necrosis was more marked and more widely observed in the cells with halothane than those without halothane. However, all tissues returned to normal by day 7. CONCLUSION: Disappearance of glycogen at 0 h and rRNA at 6 h after exposure to halothane under 10% oxygen is considered to be one of the factors inducing necrosis around the central vein. Recovery of the hepatolobular structure was attributed to the rearrangement of the remaining hepatocytes in the portal vein area.