du Souich P, Erill S
Eur J Clin Pharmacol. 1978 Nov 9;14(1):21-7. doi: 10.1007/BF00560254.
Fractional hydrolysis and acetylation of procainamide, acetylation of procainamide-derived p-aminobenzoic acid and plasma hydrolysis of procaine were studied in 20 patients with chronic heart failure (CHF), 20 patients with chronic respiratory insufficiency (CRI) and 20 patients with chronic renal failure (RF). The results were compared with those obtained in a group of 20 normal volunteers. Hydrolysis of procainamide and procaine were reduced in patients with CHF and CRI, but not in patients with RF. Moreover, more marked decreases in procainamide and procaine hydrolysis were seen in subgroups with secondary hepatic dysfunction. The diminution of hydrolysis of procainamide was not paralleled by changes in acetylation of procainamide or p-aminobenzoic acid. It is concluded that in patients with hepatic involvement secondary to advanced CHF or CRI, hepatic and plasmatic hydrolysis activity is decreased to a degree equivalent to primary liver failure.
在20例慢性心力衰竭(CHF)患者、20例慢性呼吸功能不全(CRI)患者和20例慢性肾衰竭(RF)患者中,研究了普鲁卡因酰胺的部分水解和乙酰化、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。将结果与一组20名正常志愿者的结果进行比较。CHF和CRI患者中普鲁卡因酰胺和普鲁卡因的水解减少,但RF患者中未减少。此外,在继发肝功能不全的亚组中,普鲁卡因酰胺和普鲁卡因水解的降低更为明显。普鲁卡因酰胺水解的减少与普鲁卡因酰胺或对氨基苯甲酸乙酰化的变化并不平行。结论是,在继发于晚期CHF或CRI的肝脏受累患者中,肝脏和血浆水解活性降低到与原发性肝衰竭相当的程度。