du Souich P, Erill S
Clin Pharmacol Ther. 1977 Nov;22(5 Pt 1):588-95. doi: 10.1002/cpt1977225part1588.
Procainamide acetylation and hydrolysis, procainamide-derived p-amino-benzoic acid acetylation, and plasma hydrolysis of procaine were studied in normal volunteers and in 20 patients with chronic liver disease, Impairment of procainamide acetylation was evident in the patients, but no correlations were demonstrable between the degree of impairment and the severity of the disease. On the other hand, procainamide hydroylsis was diminished in liver disease, and as indicated by depression of serum albumin levels and plasma prothrombin activity this alteration did correlate with the degree of impairment of liver function. Procaine hydrolysis in plasma was also affected, the mean in vitro plasma half-life being prolonged in the patients with liver disease and correlating with the degree of hepatic impairment. A correlation of procainamide hydrolysis with procaine hydrolysis was also observed. Finally, acetylation of procainamide-derived p-aminobenzoic acid appeared to increase in patients with liver disease, the degree of acetylation increasing with decreasing procainamide hydrolysis capacity.
在正常志愿者和20例慢性肝病患者中研究了普鲁卡因酰胺的乙酰化和水解、普鲁卡因酰胺衍生的对氨基苯甲酸的乙酰化以及普鲁卡因的血浆水解。患者中普鲁卡因酰胺乙酰化明显受损,但受损程度与疾病严重程度之间无明显相关性。另一方面,肝病患者中普鲁卡因酰胺水解减少,血清白蛋白水平降低和血浆凝血酶原活性降低表明这种改变确实与肝功能损害程度相关。血浆中普鲁卡因水解也受到影响,肝病患者体外血浆平均半衰期延长,且与肝损害程度相关。还观察到普鲁卡因酰胺水解与普鲁卡因水解之间的相关性。最后,肝病患者中普鲁卡因酰胺衍生的对氨基苯甲酸的乙酰化似乎增加,乙酰化程度随普鲁卡因酰胺水解能力降低而增加。