PCO2 measurements in surface proximal tubules and peritubular capillaries of the rat kidney.

PCO2 measurements in surface proximal tubules and peritubular capillaries of the rat kidney.
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大鼠肾脏表面近端肾小管和肾小管周围毛细血管的 PCO2 测量。

DOI:
10.1152/ajprenal.1982.242.1.f78
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发表时间:
1982
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Cohen,JJ
Cohen,JJ
中科院分区:
--
文献类型:
--
作者:
Gennari,FJ;Caflisch,CR;Johns,C;Maddox,DA;Cohen,JJ

文献摘要

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在正常酸碱条件下和三种HCO3(-)再吸收减少的情况下,分别测量大鼠表面近端小管和小管周围毛细血管的PCO2浓度:苯并胺给药、呼吸性碱中毒和代谢性酸中毒。正常情况下,早期近端小管(EP)的PCO2比PaCO2高10.5 mmHg (P < 0.001),比晚期近端(LP)和小管周围毛细血管(PC)的PCO2高3-4 mmHg (P < 0.001)。LP和PC的PCO2比PaCO2高7 mmHg (P < 0.001)。苯并胺(3mg /kg)对动脉血PCO2和EP与动脉血PCO2的差异无影响。将苯甲酰胺增加到8 mg/kg时,相对于动脉PCO2,表面结构中的PCO2增加了3 ~ 5 mmHg (P < 0.01)。代谢性酸中毒没有改变皮质和动脉PCO2之间的关系。相比之下,呼吸性碱中毒使皮质PCO2相对于PaCO2降低了50%以上。EP PCO2仍高于LP和PC PCO2 (P < 0.01)。因此,减少HCO3(-)重吸收并不能消除EP与LP或PC PCO2之间的差异,也不能降低肾脏表面结构中相对于动脉PCO2的PCO2。
PCO2 was measured in surface proximal tubules and peritubular capillaries in the rat under normal acid-base conditions and in three settings with decreased HCO3(-) reabsorption: benzolamide administration, respiratory alkalosis, and metabolic acidosis. Under normal conditions, PCO2 in the early proximal tubule (EP) was 10.5 mmHg higher than PaCO2 (P less than 0.001) and 3-4 mmHg higher than late proximal (LP) and peritubular capillary (PC) PCO2 (P less than 0.001). PCO2 in LP and PC was 7 mmHg higher than PaCO2 (P less than 0.001). Benzolamide (3 mg/kg) had no effect on the difference between PC and arterial PCO2 or between EP and PC PCO2. Increasing benzolamide to 8 mg/kg increased PCO2 in the surface structures relative to arterial PCO2 by 3-5 mmHg (P less than 0.01). Metabolic acidosis did not alter the relationships between cortical and arterial PCO2. By contrast, respiratory alkalosis decreased cortical PCO2 relative to PaCO2 by over 50%. Nonetheless, EP PCO2 was still higher than LP or PC PCO2 (P less than 0.01). Thus, reducing HCO3(-) reabsorption does not obliterate the difference between EP and LP or PC PCO2 nor does it invariably reduce PCO2 in the surface structures of the kidney relative to arterial PCO2.