Effects of Chronic Hypercapnia on Electrolyte and Acid-Base Equilibrium. Ii. Recovery, With Special Reference to the Influence of Chloride Intake*

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136

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...

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

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

Polak¹,

Haynie²,

Hays³

et al. 1961

Self Cite

136

“…Such short-term observations raised the possibility that sustained changes in availability of penetrating anion might of themselves induce chronic alterations in body fluid composition. This hypothesis was supported by the subsequent observation that restriction of dietary chloride prevents correction of plasma bicarbonate elevations induced by chronic hypercapnia or administration of desoxycorticosterone acetate (DOCA) (2,3). In each of the latter circumstances, however, the elevated plasma bicarbonate presumably developed as a result of direct acceleration of sodium-cation exchange and these observations, therefore, throw no light on the possible consequences of a primary loss of chloride in a normal animal.…”

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confidence: 99%

On the Mechanism of Nitrate-Induced Alkalosis. The Possible Role of Selective Chloride Depletion in Acid-Base Regulation*

Gulyassy¹,

Strihou²,

Schwartz³

1962

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It has recently been demonstrated that the rate of both hydrogen and potassium excretion can be acutely increased when a disproportion is created between the quantity of sodium and the quantity of penetrating anion available for reabsorption (1). This experimental condition was achieved by the infusion of neutral sodium phosphate into animals which had previously been maintained on a diet poor in sodium chloride. Such short-term observations raised the possibility that sustained changes in availability of penetrating anion might of themselves induce chronic alterations in body fluid composition. This hypothesis was supported by the subsequent observation that restriction of dietary chloride prevents correction of plasma bicarbonate elevations induced by chronic hypercapnia or administration of desoxycorticosterone acetate (DOCA) (2, 3). In each of the latter circumstances, however, the elevated plasma bicarbonate presumably developed as a result of direct acceleration of sodium-cation exchange and these observations, therefore, throw no light on the possible consequences of a primary loss of chloride in a normal animal. Such a loss might be expected to produce either secondary sodium (and volume) depletion, diversion of sodium reabsorption to the cation-exchange mechanism, or some combination of the two. In order to investigate this problem, chloride deficiency has been produced in dogs by the repeated infusion of nitrate, an anion known to induce chloruresis (4).

“…Recent observations on the dog indicate that during recovery from chronic hypercapnia the chloride ion plays a critical role in permitting full restoration of plasma composition to normal (1). Plasma bicarbonate concentration remains significantly elevated, and plasma chloride concentration markedly depressed unless chloride is provided in the diet.…”

mentioning

confidence: 99%

Factors Governing Correction of the Alkalosis Associated With Potassium Deficiency; The Critical Role of Chloride in the Recovery Process*

Atkins¹,

Schwartz²

1962

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Recent observations on the dog indicate that during recovery from chronic hypercapnia the chloride ion plays a critical role in permitting full restoration of plasma composition to normal (1). Plasma bicarbonate concentration remains significantly elevated, and plasma chloride concentration markedly depressed unless chloride is provided in the diet. It was tentatively proposed that when the quantity of chloride available for reabsorption is reduced, the transtubular potential difference generated by active transport of sodium is greater than normal and that this, in turn, is responsible for a higher than normal rate of diffusion of hydrogen ions into the glomerular filtrate and for the sustained elevation of plasma bicarbonate concentration.The present study was undertaken to determine whether chloride may play a significant role in the correction of the metabolic alkalosis associated with potassium deficiency. For this purpose, studies have been performed in dogs made potassium deficient, alkalotic, and hypochloremic by the administration of deoxycorticosterone acetate (DCA)' and sodium bicarbonate.Subsequently, three consecutive maneuvers were carried out while the animals were maintained on a diet low in potassium and chloride: 1) DCA was withdrawn, 2) potassium bicarbonate was substituted for sodium bicarbonate in the daily electrolyte supplement, and 3) chloride was administered in various forms.