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本文引用的文献

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THE RESPONSE OF EXTRACELLULAR HYDROGEN ION CONCENTRATION TO GRADED DEGREES OF CHRONIC HYPERCAPNIA: THE PHYSIOLOGIC LIMITS OF THE DEFENSE OF PH.细胞外氢离子浓度对不同程度慢性高碳酸血症的反应:pH 防御的生理极限
J Clin Invest. 1965 Feb;44(2):291-301. doi: 10.1172/JCI105143.
2
Effects of chronic hypercapnia on electrolyte and acid-base equilibrium. I. Adaptation.慢性高碳酸血症对电解质及酸碱平衡的影响。I. 适应性
J Clin Invest. 1961 Jul;40(7):1223-37. doi: 10.1172/JCI104353.
3
Effect of luminal and peritubular HCO3(-) concentrations and PCO2 on HCO3(-) reabsorption in rabbit proximal convoluted tubules perfused in vitro.管腔和肾小管周围HCO3(-)浓度及PCO2对体外灌注的兔近端曲管中HCO3(-)重吸收的影响。
J Clin Invest. 1982 Sep;70(3):639-49. doi: 10.1172/jci110658.
4
Effects of CO2 and acetazolamide on bicarbonate and fluid transport in rabbit proximal tubules.二氧化碳和乙酰唑胺对兔近端小管中碳酸氢盐和液体转运的影响。
Am J Physiol. 1981 Jan;240(1):F54-62. doi: 10.1152/ajprenal.1981.240.1.F54.
5
Axial heterogeneity in the rat proximal convoluted tubule. I. Bicarbonate, chloride, and water transport.大鼠近端曲管的轴向异质性。I. 碳酸氢盐、氯和水的转运
Am J Physiol. 1984 Nov;247(5 Pt 2):F816-21. doi: 10.1152/ajprenal.1984.247.5.F816.
6
Chronic hypercapnia stimulates proximal bicarbonate reabsorption in the rat.慢性高碳酸血症刺激大鼠近端碳酸氢盐重吸收。
J Clin Invest. 1984 Dec;74(6):1942-7. doi: 10.1172/JCI111614.
7
Effects of acute alterations in PCO2 on proximal HCO-3, Cl-, and H2O reabsorption.动脉血二氧化碳分压急性改变对近端小管碳酸氢根、氯离子和水重吸收的影响。
Am J Physiol. 1984 Jan;246(1 Pt 2):F21-6. doi: 10.1152/ajprenal.1984.246.1.F21.
8
Proximal tubular bicarbonate reabsorption and PCO2 in chronic metabolic alkalosis in the rat.大鼠慢性代谢性碱中毒时近端肾小管碳酸氢盐重吸收与二氧化碳分压
J Clin Invest. 1983 Oct;72(4):1385-95. doi: 10.1172/JCI111095.
9
Effect of respiratory acidosis on acidification by the medullary collecting duct.呼吸性酸中毒对髓质集合管酸化作用的影响。
Am J Physiol. 1983 Jan;244(1):F89-94. doi: 10.1152/ajprenal.1983.244.1.F89.
10
The effects of chronic hypoxemia on electrolyte and acid-base equilibrium: an examination of normocapneic hypoxemia and of the influence of hypoxemia on the adaptation to chronic hypercapnia.慢性低氧血症对电解质及酸碱平衡的影响:对正常碳酸血症性低氧血症以及低氧血症对慢性高碳酸血症适应性影响的研究。
J Clin Invest. 1967 Mar;46(3):369-77. doi: 10.1172/JCI105538.

大鼠呼吸性酸中毒和碱中毒时早期近端碳酸氢盐重吸收的分娩依赖性

Delivery dependence of early proximal bicarbonate reabsorption in the rat in respiratory acidosis and alkalosis.

作者信息

Santella R N, Maddox D A, Gennari F J

机构信息

University of Vermont, College of Medicine, Burlington 05405.

出版信息

J Clin Invest. 1991 Feb;87(2):631-8. doi: 10.1172/JCI115040.

DOI:10.1172/JCI115040
PMID:1991847
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC296353/
Abstract

In the intact rat kidney, bicarbonate reabsorption in the early proximal tubule (EP) is strongly dependent on delivery. Independent of delivery, metabolic acidosis stimulates EP bicarbonate reabsorption. In this study, we investigated whether systemic pH changes induced by acute or chronic respiratory acid-base disorders also affect EP HCO3- reabsorption, independent of delivery (FLHCO3, filtered load of bicarbonate). Hypercapnia was induced in rats acutely (1-3 h) and chronically (4-5 d) by increasing inspired PCO2. Hypocapnia was induced acutely (1-3 h) by mechanical hyperventilation, and chronically (4-5 d) using hypoxemia to stimulate ventilation. When compared with normocapneic rats with similar FLHCO3, no stimulation of EP or overall proximal HCO3 reabsorption was found with either acute hypercapnia (PaCO2 = 74 mmHg, pH = 7.23) or chronic hypercapnia (PaCO2 = 84 mmHg, pH = 7.31). Acute hypocapnia (PaCO2 = 29 mmHg, pH = 7.56) did not suppress EP or overall HCO3 reabsorption. Chronic hypocapnia (PaCO2 = 26 mmHg, pH = 7.54) reduced proximal HCO3 reabsorption, but this effect was reversed when FLHCO3 was increased to levels comparable to euvolemic normocapneic rats. Thus, when delivery is accounted for, we could find no additional stimulation of proximal bicarbonate reabsorption in respiratory acidosis and, except at low delivery rates, no reduction in bicarbonate reabsorption in respiratory alkalosis.

摘要

在完整的大鼠肾脏中,近端小管起始段(EP)的碳酸氢盐重吸收强烈依赖于滤过负荷。与滤过负荷无关的是,代谢性酸中毒会刺激EP的碳酸氢盐重吸收。在本研究中,我们调查了急性或慢性呼吸性酸碱紊乱引起的全身pH变化是否也会影响EP的HCO₃⁻重吸收,且与滤过负荷(FLHCO₃,碳酸氢盐的滤过负荷)无关。通过增加吸入的PCO₂,在大鼠中急性(1 - 3小时)和慢性(4 - 5天)诱导高碳酸血症。通过机械过度通气急性(1 - 3小时)诱导低碳酸血症,并使用低氧血症刺激通气慢性(4 - 5天)诱导低碳酸血症。与具有相似FLHCO₃的正常碳酸血症大鼠相比,急性高碳酸血症(PaCO₂ = 74 mmHg,pH = 7.23)或慢性高碳酸血症(PaCO₂ = 84 mmHg,pH = 7.31)均未刺激EP或近端总体HCO₃重吸收。急性低碳酸血症(PaCO₂ = 29 mmHg,pH = 7.56)并未抑制EP或总体HCO₃重吸收。慢性低碳酸血症(PaCO₂ = 26 mmHg,pH = 7.54)降低了近端HCO₃重吸收,但当FLHCO₃增加到与血容量正常的正常碳酸血症大鼠相当的水平时,这种作用被逆转。因此,当考虑滤过负荷时,我们发现在呼吸性酸中毒中近端碳酸氢盐重吸收没有额外的刺激,并且除了在低滤过负荷率时,在呼吸性碱中毒中碳酸氢盐重吸收没有减少。