Calvo R, Carlos R, Erill S
Eur J Clin Pharmacol. 1983;24(4):533-5. doi: 10.1007/BF00609899.
Procaine esterase activity in plasma from patients with renal failure is decreased by 40%. Since cyanate is formed from urea and readily carbamylates certain blood proteins, a possible role for cyanate in the depression of plasma esterase activity in uraemic patients was considered. However, in vitro carbamylation of normal plasma in a range similar to that detected in uraemic patients did not influence procaine esterase activity. Kinetic analysis of the reaction showed that the maximal hydrolyzing capacity but not the Km in uraemic plasma was diminished (5.0 +/- 0.3 X 10(-5) moles hydrolyzed per litre of plasma per minute and a Km of 3.9 +/- 0.2 X 10(-5) mol/l in plasma from normal volunteers as compared to 3.1 +/- 0.1 X 10(-5) mol/l/min and 3.5 +/- 0.2 X 10(-5) ml/l in plasma from patients with renal failure). Therefore, not carbamylation but rather a decrease in enzyme synthesis is the likely explanation for the lower rate of procaine hydrolysis in uraemic plasma.
肾衰竭患者血浆中的普鲁卡因酯酶活性降低了40%。由于氰酸盐由尿素形成并容易使某些血液蛋白发生氨甲酰化，因此人们考虑了氰酸盐在尿毒症患者血浆酯酶活性降低中可能发挥的作用。然而，在体外以与尿毒症患者中检测到的范围相似的程度对正常血浆进行氨甲酰化处理，并未影响普鲁卡因酯酶活性。对该反应的动力学分析表明，尿毒症血浆中的最大水解能力降低，但Km值未变（正常志愿者血浆中每分钟每升血浆水解5.0±0.3×10⁻⁵摩尔，Km为3.9±0.2×10⁻⁵摩尔/升，而肾衰竭患者血浆中为3.1±0.1×10⁻⁵摩尔/升/分钟和3.5±0.2×10⁻⁵毫升/升）。因此，对于尿毒症血浆中普鲁卡因水解速率较低的原因，可能的解释不是氨甲酰化，而是酶合成减少。
