Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.
Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.
复制标题
大鼠慢性代谢性碱中毒中的近端肾小管碳酸氢盐重吸收和 PCO2。
DOI：
10.1172/jci111095
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Gennari,FJ
中科院分区：
文献类型：
--
作者：
Maddox,DA;Gennari,FJ
本研究旨在探讨慢性代谢性肺气肿（CMA）大鼠近端肾小管重吸收碳酸氢盐的模式及其与肾小管和毛细血管PCO 2的关系。采用低电解质饮食加碳酸氢钠和碳酸氢钾诱发大鼠肌萎缩。近端肾小管重吸收和PCO 2测定CMA大鼠呋塞米注射后4-7或11-14天，以研究广泛的过滤的碳酸氢盐负荷。一组9只年龄匹配的对照动物，喂食相同的饮食，但没有给予呋塞米，进行了比较研究。在第三组对照中，通过血浆输注和主动脉收缩，碳酸氢盐的过滤负荷在与CMA大鼠相同的范围内变化。CMA大鼠有明显的碱血症和低钾血症（4-7 d：pH 7.58，HCO 3 38.3 meq/L，K+ 2.1 meq/L; 11-14 d：pH 7.54，HCO 3 38.1 meq/L，K+ 2.5 meq/L）。尽管如此，在任何给定的过滤碳酸氢盐负荷（250至1，300 pmol/min）下，近端碳酸氢盐重吸收与对照大鼠中观察到的无显著差异。在对照组和CMA大鼠中，83-85%的过滤的碳酸氢盐被近端小管末端重吸收。这些观察结果表明，近端重吸收的碳酸氢盐主要是由慢性代谢性肺水肿的过滤负荷。当单肾单位肾小球滤过率（SNGFR）在呋塞米治疗后早期因血容量不足而降低时，滤过负荷和近端重吸收率保持在或低于对照水平，维持代谢性肾小球疾病。然而，在呋塞米治疗后的后期，SNGFR在某些情况下恢复到对照水平。在这些动物中，滤过负荷和近端重吸收率均高于对照动物中观察到的最高水平。尽管近端碳酸氢盐重吸收率没有差异，但CMA组肾小管周围毛细血管和动脉血（PC-Art）之间的PCO 2梯度显著高于对照组。因此，近端碳酸氢盐重吸收似乎不是Pc-Art PCO 2的主要决定因素。PCO 2在早期近端（EP）小管显着高于在任何一个晚期近端（LP）小管或管周毛细血管在对照组和CMA大鼠。EP-LP PCO 2梯度与近端碳酸氢盐重吸收直接相关（P <0.05）。EP中PCO 2的小幅升高可能与碳酸氢盐重吸收过程中该部位产生的CO2有关。
Studies were undertaken to define the pattern of proximal tubular bicarbonate reabsorption and its relation to tubular and capillary PCO2 in rats with chronic metabolic alkalosis (CMA). CMA was induced by administering furosemide to rats ingesting a low electrolyte diet supplemented with NaHCO3 and KHCO3. Proximal tubular bicarbonate reabsorption and PCO2 were measured in CMA rats either 4-7 or 11-14 d after furosemide injection, in order to study a wide range of filtered bicarbonate loads. A group of nine age-matched control animals, fed the same diet but not given furosemide, was studied for comparison. In a third group of controls, the filtered load of bicarbonate was varied over the same range as in the CMA rats by plasma infusion and aortic constriction. The CMA rats had significant alkalemia and hypokalemia (4-7 d: pH 7.58, HCO3 38.3 meq/liter, K+ 2.1 meq/liter; 11-14 d: pH 7.54, HCO3 38.1 meq/liter, K+ 2.5 meq/liter). Nonetheless, proximal bicarbonate reabsorption was not significantly different from that seen in control rats at any given load of filtered bicarbonate (from 250 to 1,300 pmol/min). In both control and CMA rats, 83-85% of the filtered bicarbonate was reabsorbed by the end of the accessible proximal tubule. These observations indicate that proximal bicarbonate reabsorption is determined primarily by the filtered load in chronic metabolic alkalosis. When single nephron glomerular filtration rate (SNGFR) is reduced by volume depletion in the early postfurosemide period, the filtered load and the rate of proximal bicarbonate reabsorption remain at or below control levels, maintaining metabolic alkalosis. In the late postfurosemide period, however, SNGFR returned to control levels in some instances. In these animals, both the filtered load and rate of proximal reabsorption were increased above the highest levels seen in control animals. The PCO2 gradient between the peritubular capillaries and arterial blood (Pc-Art) was significantly higher in CMA than in control, even though the rate of proximal bicarbonate reabsorption did not differ. Thus, proximal bicarbonate reabsorption did not appear to be the primary determinant of Pc-Art PCO2. PCO2 in the early proximal (EP) tubule was significantly higher than in either the late proximal (LP) tubule or peritubular capillaries in both control and CMA rats. The EP-LP PCO2 gradient correlated directly with proximal bicarbonate reabsorption (P less than 0.05). The small elevation in PCO2 in EP may be related to CO2 generated at this site in the process of bicarbonate reabsorption.