Squarzoni G, Bariani L, Ughi M, Squerzanti R, Bariani M C, Fersini C, Castaldi G
Istituto di Semeiotica Medica, Università di Ferrara.
Riv Eur Sci Med Farmacol. 1990 Aug-Oct;12(4-5):253-8.
Red cell carbonic anhydrase isoenzymes I and II have been measured by means of cellulose acetate membrane electrophoresis in patients with chronic renal failure and dependent on periodic hemodialysis; these patients showed a chronic anemia due to many factors. Carbonic anhydrase isoenzymes were higher in uremic and anemic patients than in the controls. Since hemoglobin can act as a protons acceptor from the active site of carbonic anhydrase during the hydratation of CO2 (and vice-versa), the increase of carbonic anhydrase can facilitate, via the Bohr effect, the transfer of the oxygen to the peripheral tissues. Therefore an increase of red cell carbonic anhydrase can constitute a compensating mechanism of anemic hypoxia in uremic patients.
采用醋酸纤维素膜电泳法测定了慢性肾功能衰竭且依赖定期血液透析患者的红细胞碳酸酐酶同工酶I和II；这些患者因多种因素呈现慢性贫血。尿毒症和贫血患者的碳酸酐酶同工酶高于对照组。由于在二氧化碳水合过程中血红蛋白可作为碳酸酐酶活性位点的质子受体（反之亦然），碳酸酐酶的增加可通过玻尔效应促进氧气向周围组织的转移。因此，红细胞碳酸酐酶增加可构成尿毒症患者贫血性缺氧的一种代偿机制。
