Chang-Tsui Y Y, Ho I K
Clin Toxicol. 1980 Mar;16(1):41-50. doi: 10.3109/15563658008989922.
The results demonstrated that both acute and continuous administration of pentobarbital enhanced the CCl4-induced elevation of SGOT and SGPT activities. The potentiation of pentobarbital on CCl4-elevated SGOT and SGPT activities showed both time- and dose-dependent actions. The CCl4-induced elevation of both serum enzyme activities after continuous exposure of pentobarbital was still significant 6 days after the termination of pentobarbital. The CCl4-elevated SGOT and SGPT activities were also affected by various doses of Na-pentobarbital, although the degree of potentiation was less than the results obtained by pentobarbital pellet implantation. The present results further support the contention that proliferation of hepatic cells by barbiturates enhances CCl4-induced toxicity.
结果表明，戊巴比妥的急性给药和持续给药均增强了四氯化碳诱导的血清谷草转氨酶（SGOT）和谷丙转氨酶（SGPT）活性的升高。戊巴比妥对四氯化碳升高的SGOT和SGPT活性的增强作用呈现出时间和剂量依赖性。在戊巴比妥终止给药6天后，持续暴露于戊巴比妥后四氯化碳诱导的两种血清酶活性升高仍很显著。不同剂量的戊巴比妥钠也影响四氯化碳升高的SGOT和SGPT活性，尽管增强程度小于戊巴比妥植入小球所获得的结果。目前的结果进一步支持了巴比妥类药物引起的肝细胞增殖会增强四氯化碳诱导的毒性这一观点。
