Baba T, Murabayashi S, Tomiyama T, Takebe K
Third Department of Internal Medicine, Hirosaki University School of Medicine, Japan.
Br J Clin Pharmacol. 1990 Jun;29(6):766-9. doi: 10.1111/j.1365-2125.1990.tb03700.x.
The possibility of an impaired hepatic de-esterification of enalapril to enalaprilat due to hepatic dysfunction was assessed in seven patients with compensated liver cirrhosis and 10 normal control subjects. The peak serum concentration and time to the peak serum concentration of enalaprilat, as well as the suppression of serum angiotensin converting enzyme activity, following a single oral dose of enalapril maleate (10 mg) were not different in the two groups. The elimination half-life of enalaprilat was related to renal function. The results suggest that hepatic biotransformation of the drug may not be disturbed in a clinically significant manner in patients with moderate hepatic dysfunction due to compensated liver cirrhosis.
在7例代偿期肝硬化患者和10名正常对照者中评估了因肝功能障碍导致依那普利肝去酯化生成依那普利拉受损的可能性。两组单次口服马来酸依那普利（10毫克）后，依那普利拉的血清峰值浓度、达到血清峰值浓度的时间以及血清血管紧张素转换酶活性的抑制情况均无差异。依那普利拉的消除半衰期与肾功能有关。结果表明，对于因代偿期肝硬化导致中度肝功能障碍的患者，该药物的肝生物转化可能不会受到具有临床意义的干扰。
