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目的 评估正常家猪肝动脉内给予３２ 磷玻璃微球（３２ＰＧＭＳ） 后的急性和亚急性毒性反应。方法 １０ 只健康家猪经皮肝动脉内接受人类治疗剂量的３２ＰＧＭＳ（５ 只猪）、惰性３１ＰＧＭＳ（５ 只猪） ；２ 只猪作全程空白对照。术后按第１ 、２、４ 、８ 或１６ 周分期处以安乐死，取不同部位的肝组织进行光镜、电镜检查和超微形态计量分析。结果 给药组１、２ 周肝细胞核异常率（Ｎａｂｎ） 和线粒体变异率（ Ｍｖａｒ） 与其他各组比较差异均有显著性（ Ｐ＜ ０．０１，Ｐ＜ ０ ．００１）；给药组第８ 周与第１６ 周比较Ｎａｂｎ 无统计学意义（ Ｐ＞０ ．２０）。给药后第１、２ 周异常肝细胞多见；第４ 周异常肝细胞减少，血窦内皮破坏明显；第８ 周异常肝细胞少见，血窦内皮修复；第１６ 周肝组织形态学表现正常。结论 ３２ＰＧＭＳ肝动脉给药正常肝组织宏观吸收剂量不超过１９０Ｇｙ 只是引起临床上允许的肝内变化，肝脏组织损伤修复的时间约８ 周以上。
Objective To assess the acute and subacute toxicity of 32P-GMS in hepatic artery of normal domestic pigs. Methods Ten healthy pigs received human therapeutic doses of 32P-GMS (five pigs) and inert 31P-GMS (five pigs) in the transdermal hepatic artery. Two pigs were used as control. Postoperative euthanasia was performed on the first, second, fourth, eighth, or sixteenth week postoperatively. Liver tissues from different sites were taken for light microscopy, electron microscopy, and ultrathromorphometric analysis. Results Compared with other groups, the abnormalities of hepatocyte nuclear abnormality (Nabn) and mitochondrial mutation (Mvar) were significantly different between the first and second week in the treatment group (P<0.01, P<0.001); Nabn was not statistically significant between weeks 8 and 16 (P>0. 20). Abnormal hepatocytes were more common at the 1st and 2nd week after administration. Abnormal hepatocytes were decreased at 4th week and the sinusoidal endothelium was destroyed. At the 8th week, abnormal hepatocytes were rare and the sinusoidal endothelium was repaired. At the 16th week, the morphological appearance of liver tissue was normal. . Conclusion The macroabsorbed dose of 32PGMS hepatic arterial normal hepatic tissue does not exceed 190 Gy. It only causes clinically acceptable intrahepatic changes. The time of hepatic tissue damage repair is approximately 8 weeks.