Regev A, Drori R, Fraser G M, Niv Y
Department of Gastroenterology, Rabin Medical Center (Beilinson Campus), Petah Tiqva, Israel.
Isr Med Assoc J. 2001 Apr;3(4):247-50.
Alkaline tide is the transient increase in blood and urine pH following stimulation of gastric acid secretion. It is attributed to HCO3- release from parietal cells in parallel with H+ secretion. The enzyme carbonic anhydrase is thought to be responsible for HCO3- production from CO2 and OH- in the parietal cell.
To examine the effect of pretreatment with the carbonic anhydrase inhibitor, acetazolamide, on the alkaline tide phenomenon.
Ten patients with dyspepsia and demonstrable alkaline tide were tested on three separate days. The pH and base excess were determined in arterialized venous blood before and 45 minutes after an intramuscular injection of pentagastrin. The pH of the urine was measured before and 120 min after pentagastrin injection. Measurements were performed after pentagastrin alone on day 1, following pretreatment with acetazolamide 60 min before pentagastrin on day 2, and after the administration of acetazolamide alone on day 3.
Following the administration of pentagastrin alone, the blood base excess increased by 1.61 +/- 0.2 mEq/L (mean +/- standard deviation) and the calculated alkaline tide at 45 min was 33.99 +/- 4.49 mEq. On day 2 with prior administration of acetazolamide, base excess decreased by 0.21 +/- 0.39 mEq/L, and the calculated alkaline tide was -3.28 +/- 7.57 mEq, which was significantly lower than on day 1 (P = 0.0001). On day 3, following acetazolamide alone, the base excess values decreased by 0.53 +/- 0.2 mEq/L and the alkaline tide was -10.05 +/- 3.33 mEq; there was no significant difference compared with day 2 (P = 0.44).
Pretreatment with acetazolamide abolished the alkaline tide induced by pentagastrin. This finding supports the view that carbonic anhydrase has a major role in the alkaline tide phenomenon.
碱潮是胃酸分泌受刺激后血液和尿液pH值的短暂升高。它归因于壁细胞在分泌H⁺的同时释放HCO₃⁻。碳酸酐酶被认为负责壁细胞中由CO₂和OH⁻生成HCO₃⁻。
研究碳酸酐酶抑制剂乙酰唑胺预处理对碱潮现象的影响。
10例有消化不良且证实存在碱潮的患者在三个不同日期接受测试。在肌肉注射五肽胃泌素前及注射后45分钟测定动脉化静脉血的pH值和碱剩余。在五肽胃泌素注射前及注射后120分钟测量尿液pH值。第1天仅注射五肽胃泌素后进行测量，第2天在五肽胃泌素注射前60分钟用乙酰唑胺预处理后进行测量，第3天仅给予乙酰唑胺后进行测量。
仅给予五肽胃泌素后，血液碱剩余增加1.61±0.2 mEq/L（均值±标准差），45分钟时计算出的碱潮为33.99±4.49 mEq。在第2天预先给予乙酰唑胺后，碱剩余降低0.21±0.39 mEq/L，计算出的碱潮为 -3.28±7.57 mEq，显著低于第1天（P = 0.0001）。第3天，仅给予乙酰唑胺后，碱剩余值降低0.53±0.2 mEq/L，碱潮为 -10.05±3.33 mEq；与第2天相比无显著差异（P = 0.44）。
乙酰唑胺预处理消除了五肽胃泌素诱导的碱潮。这一发现支持碳酸酐酶在碱潮现象中起主要作用的观点。
