The nature of the renal adaptation to chronic hypocapnia

Gennari, F. John; Goldstein, Marc B.; Schwartz, William B.

doi:10.1172/jci106973

Cited by 131 publications

(35 citation statements)

References 20 publications

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“…29,30 Normal dogs and dogs with background metabolic acidosis have an identical secondary response to chronic hypocapnia, but this response is much larger in dogs with underlying metabolic alkalosis. 13,31,32 It is highly probable but still unknown whether humans exhibit a similar response to that demonstrated in dogs. Consequently, the direct applicability of the slopes depicted in Table 1 Figure 1.…”

Section: Impact Of Preexisting Acid-base Disordersmentioning

confidence: 97%

“…A new steady state emerges within 2 to 3 days. 13,14 Studies of normal volunteers who were exposed to hypobaric hypoxia (6 days) and unanesthetized patients who had spinal cord or head injuries and were undergoing controlled hyperventilation ( 16 -20 The secondary response appears within 30 to 120 minutes from onset of metabolic acidosis; the time interval for its completion (and its disappearance after correction of the metabolic acidosis) depends on the pace of development of the disorder. 21,22 In patients with cholera, when plasma [HCO 3 Ϫ ] falls or corrects slowly, such as by 6 mEq/L in 24 hours, the ventilatory response keeps pace with the level of plasma [HCO 3 Ϫ ].…”

Section: Respiratory Alkalosismentioning

confidence: 99%

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Secondary Responses to Altered Acid-Base Status

Adrogué¹,

Madias²

2010

Journal of the American Society of Nephrology

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Section: Impact Of Preexisting Acid-base Disordersmentioning

confidence: 97%

Section: Respiratory Alkalosismentioning

confidence: 99%

Secondary Responses to Altered Acid-Base Status

Adrogué¹,

Madias²

2010

Journal of the American Society of Nephrology

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“…As far as the acid-base equilibrium is concerned, the kidney reacts by decreasing the urinary [SID], as inferred from the urinary anion gap, when infusing a solution causing acidosis and increasing it when infusing a solution causing alkalosis. This is a normal kidney ''compensatory'' response to plasma acid-base alterations [16,17].…”

Section: Discussionmentioning

confidence: 99%

In vivo conditioning of acid–base equilibrium by crystalloid solutions: an experimental study on pigs

et al. 2012

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Purpose: Large infusion of crystalloids may induce acid-base alterations according to their strong ion difference ([SID]). We wanted to prove in vivo, at constant PCO 2 , that if the [SID] of the infused crystalloid is equal to baseline plasma bicarbonate, the arterial pH remains unchanged, if lower it decreases, and if higher it increases. Methods: In 12 pigs, anesthetized and mechanically ventilated at PCO 2 &40 mmHg, 2.2 l of crystalloids with a [SID] similar to (lactated Ringer's 28.3 mEq/l), lower than (normal saline 0 mEq/l), and greater than (rehydrating III 55 mEq/l) baseline bicarbonate (29.22 ± 2.72 mEq/l) were infused for 120 min in randomized sequence. Four hours of wash-out were allowed between the infusions. Every 30 min up to minute 120 we measured blood gases, plasma electrolytes, urinary volume, pH, and electrolytes. Albumin, hemoglobin, and phosphates were measured at time 0 and 120 min. Results: Lactated Ringer's maintained arterial pH unchanged (from 7.47 ± 0.06 to 7.47 ± 0.03) despite a plasma dilution around 12%. Normal saline caused a reduction in pH (from 7.49 ± 0.03 to 7.42 ± 0.04) and rehydrating III induced an increase in pH (from 7.46 ± 0.05 to 7.49 ± 0.04). The kidney reacted to the infusion, minimizing the acidbase alterations, by increasing/ decreasing the urinary anion gap, primarily by changing sodium and chloride concentrations. Lower urine volume after normal saline infusion was possibly due to its greater osmolarity and chloride concentration as compared to the other solutions. Conclusions: Results support the hypothesis that at constant PCO 2 , pH changes are predictable from the difference between the [SID] of the infused solution and baseline plasma bicarbonate concentration.

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“…Stanbury and Thomson (1) found an increased urine sodium and potassium excretion in respiratory alkalosis and suggested that this might reflect decreased distal nephron hydrogen ion secretion. Gennari et al (21) demonstrated that net acid excretion was decreased in dogs with chronic hyperventilation. Malnic et al (22) demonstrated in micropuncture studies that hypocapnia in rats reduced fractional and absolute bicarbonate reabsorption in both the proximal and distal tubules.…”

Section: Discussionmentioning

confidence: 99%

The effect of hyperventilation on distal nephron hydrogen ion secretion.

Giammarco¹,

Goldstein²,

Ml³

et al. 1976

J. Clin. Invest.

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A B S T R A C T This study was designed to determine the effect of acute hyperventilation on distal nephron hydrogen ion secretion. The blood Pco2 declined and stabilized rapidly when bicarbonate loaded rats were hyperventilated. In contrast, the urine Pcoa declined slowly, resulting in an early increase in the urine minus blood (U-B) Pco2 which could not be obliterated by carbonic anhydrase infusion. Within approximataely 50 min, the U-B PcO2 in the hyperventilated and carbonic anhydrase infused rats approached zero. Consequently, equilibrium between collecting duct urine and arterial blood Pco2 was then presumed to exist. This provided the basis for the subsequent studies on a series of rats. The U-B Pco2 decreased from a control of 22+1 mm Hg (mean+SEM) to 11±2 mm Hg (mean+SEM) with hypocapnia, and rose again to its control value when the blood Pco2 returned to prehyperventilation values. This decline in U-B PcO2 with acute hyperventilation could not be attributed to changes in urine flow, phosphate, or bicarbonate excretion, suggesting, therefore, a decrease in distal nephron (probably collecting duct) hydrogen ion secretion with acute hyperventilation. Possible pitfalls in the interpretation of the U-B Pco2 are illustrated. INTRODUCTIONThe effect of hyperventilation on the rate of hydrogen ion secretion in the terminal segments of the nephron has not been elucidated. Stanbury and Thomson (1) suggested that the electrolyte excretion patterns observed during hypocapnia might be due to inhibition of hydrogen ion secretion in the kidney. Micropuncture studies have shown that hyperventilation decreases hydrogen ion secretion in the proximal and distal convoluted tubules (2), but information about the response of the collecting duct to this maneuver is not available.

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The nature of the renal adaptation to chronic hypocapnia

Cited by 131 publications

References 20 publications

Secondary Responses to Altered Acid-Base Status

Secondary Responses to Altered Acid-Base Status

In vivo conditioning of acid–base equilibrium by crystalloid solutions: an experimental study on pigs

The effect of hyperventilation on distal nephron hydrogen ion secretion.

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