The Renal Response to Chronic Respiratory Acidosis 1

Sullivan, W. James; Dorman, Philip J.; MacLeod, Martha B.; Parks, Mary Ellen

doi:10.1172/jci103080

Cited by 40 publications

(14 citation statements)

References 11 publications

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“…Since only the first day's urine was formed during uninterrupted hypercapnia, it is only on this day that such an artifact can be excluded. However, the finding in a number of animals that bicarbonate excretion rose appreciably on the first day, despite the fact that plasma level had risen only moderately, suggests that the maximal ability of the kidney to conserve bicarbonate had not yet been achieved, a finding consistent with earlier observations on reabsorptive capacity of such animals during acute bicarbonate loading (8).…”

Section: Resultssupporting

confidence: 83%

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. I. Adaptation*

Polak¹,

Haynie²,

Hays³

et al. 1961

J. Clin. Invest.

136

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Although chronic respiratory acidosis is one of the commonest clinical disturbances of acid-base balance, the process of adaptation which it induces has not been extensively investigated. Normal man tolerates prolonged exposure to high CO., tensions poorly and is, therefore, not a suitable subject for study. Recent observations in the rat exposed to a high CO, atmosphere (1,2) have provided much valuable information, but no balance data are available in the dog, the animal which appears more closely to resemble man in its adjustment to other disturbances of acid-base equilibrium. For this reason, and in order to provide a basis for further investigations of chronic hypercapnia in the dog, the present studies of adaptation were undertaken. METHODSEleven balance studies were carried out on 11 healthy female mongrel dogs weighing between 13 and 20 kg. Observations were made during a 4-to 7-day control period and a 6-to 15-day period of exposure to 10 to 13 per cent carbon dioxide (CO2 period).The studies were carried out with the dogs in metabolic cages maintained at a temperature of approximately 150 C inside a small, ventilated room. The cages were covered with a plastic canopy which was left open during the control period. During the CO2 period the canopy was closed, and a gas mixture of C02, 02, and compressed air was delivered into it. The ratio of the gases delivered was regulated manually. The CO2 content of the cages was monitored frequently with a Kwik-Check carbon dioxide analyzer (Burrell Corp.), * Supported in part by grants from the National Heart Institute (H-759 and HTS-5309), the American Heart Association and the Life Insurance Medical Research Fund. which was standardized with gas mixtures whose composition had been determined by the Scholander method.The oxygen content was determined by a Beckman model C oxygen analyzer.On the first day of the CO2 period, the CO2 content of the cage atmosphere was increased to approximately 10 per cent over a period of 3 to 6 hours. Over the next 1 to 2 days the level was raised slowly to the desired range of 11 to 13 per cent. The oxygen concentration was maintained at 20 + 3 per cent throughout.The dogs were removed from the cages each morning for weighing, feeding, collection of urine and feces, cage cleaning, and (on most mornings) arterial blood sampling.During the CO, period they were also removed in the evening so that the daily diet could be fed in two portions. The total time out of the high CO2 atmosphere on each of these days was about 30 minutes. In order to obtain data on the early adaptation to uninterrupted respiratory acidosis, 9 of the dogs were given their entire diet for the first day of the CO2 period 2 to 3 hours before the CO2 tension was raised, and they were then left undisturbed for 24 hours.A synthetic diet was given, consisting (in per cent) of 55 water, 14 casein, 1.5 agar, 8 hydrogenated vegetable oils, 7.5 dextrose, 14 dextrin, and supplementary vitamins. To each 100 g of diet, 9 mEq of potassium was added as neutral phosphate (4 par...

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Section: Resultssupporting

confidence: 83%

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. I. Adaptation*

Polak¹,

Haynie²,

Hays³

et al. 1961

J. Clin. Invest.

136

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“…Bicarbonate excretion, however, begins at plasma levels well below those necessary to saturate reabsorptive capacity (6) and, as demonstrated in the present study, is so great that even a large oral intake of bicarbonate fails to raise the plateau 2 The term spontaneous reabsorptive capacity is used to designate the amount of bicarbonate reabsorbed per unit of glomerular filtrate in the fasting animal. For all practical purposes this value can be assumed to equal the plasma bicarbonate concentration in the fasting animal.…”

Section: Recovery-administration Of Chloridementioning

confidence: 51%

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. Iii. Characteristics of the Adaptive and Recovery Process as Evaluated by Provision of Alkali*

Strihou¹,

Gulyassy²,

Schwartz³

1962

J. Clin. Invest.

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Previous studies have characterized the changes in acid-base equilibrium in dogs exposed over a prolonged period to a 12 per cent carbon dioxide atmosphere (1). Plasma bicarbonate concentration rose in a gradual curvilinear fashion over several days and became stabilized at maximal levels of 35 to 38 mEq per L. This adaptive response was not influenced by the level of sodium chloride intake. After the return of the dogs to room air, however, plasma bicarbonate concentration remained significantly elevated in dogs ingesting a low-salt diet. The resulting alkalosis persisted until chloride was provided, and then normal acidbase equilibrium was rapidly restored (2).During hypercapnia, the urine remained almost free of bicarbonate and it was therefore not possible to define fully the effects of hypercapnia on the mechanism for bicarbonate reabsorption; the capacity to reabsorb completely as much as 38 mEq of bicarbonate per L of filtrate may have been rapidly engendered by hypercapnia, but not fully employed for several days because of slow renal generation of bicarbonate. In order to evaluate further the effect of a high carbon dioxide tension on the renal threshold for bicarbonate, observations have been carried out in dogs whose diets were supplemented with large quantities of sodium bicarbonate. Under these circumstances, the rise in plasma bicarbonate concentration ought not to be limited by renal ability to generate bicarbonate, but rather by renal reabsorptive capacity. Observations have also been carried out

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“…It is clear, however, that the hyperbicarbonatemia of the chronic phase is sustained by increased renal hydrogen secretion (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). This study and data from the rat (1) indicate that this process is mediated, in great part, by an increase in the intrinsic rate of bicarbonate reabsorption by the proximal tubule.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of adaptation to chronic respiratory acidosis in the rabbit proximal tubule

Krapf

1989

Journal of Critical Care

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The hyperbicarbonatemia of chronic respiratory acidosis is maintained by enhanced bicarbonate reabsorption in the proximal tubule. To investigate the cellular mechanisms involved in this adaptation, cell and luminal pH were measured microfluorometrically using (2M,7')-bis(carboxyethyl)-(5,6)-carboxyfluorescein in isolated, microperfused S2 proximal convoluted tubules from control and acidotic rabbits. Chronic respiratory acidosis was induced by exposure to 10% CO2 for 52-56 h. Tubules from acidotic rabbits had a significantly lower luminal pH after 1-mm perfused length (7.03±0.09 vs. 7.26±0.06 in controls, perfusion rate = 10 nl/min). Chronic respiratory acidosis increased the initial rate of cell acidification (dpH1/dt) in response to luminal sodium removal by 63% and in response to lowering luminal pH (7.4-6.8) by 69%. Chronic respiratory acidosis also increased dpH,/dt in response to peritubular sodium removal by 63% and in response to lowering peritubular pH by 73%. In conclusion, chronic respiratory acidosis induces a parallel increase in the rates of the luminal Na/H antiporter and the basolateral Na/(HCO3)3 cotransporter. Therefore, the enhanced proximal tubule reabsorption of bicarbonate in chronic respiratory acidosis may be, at least in part, mediated by a parallel adaptation of these transporters.

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The Renal Response to Chronic Respiratory Acidosis 1

Cited by 40 publications

References 11 publications

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. I. Adaptation*

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. I. Adaptation*

Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. Iii. Characteristics of the Adaptive and Recovery Process as Evaluated by Provision of Alkali*

Mechanisms of adaptation to chronic respiratory acidosis in the rabbit proximal tubule

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