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Tissue and Renal Response to Chronic Respiratory Acidosis

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Tissue and Renal Response to Chronic Respiratory Acidosis TISSUE AND RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS Norman W. Carter, … , Donald W. Seldin, H. C. Teng J Clin Invest. 1959;38(6):949-960. https://doi.org/10.1172/JCI103878. Research Article Find the latest version: https://jci.me/103878/pdf TISSUE AND RENAL RESPONSE TO CHRONIC RESPIRATORY ACIDOSIS * By NORMAN W. CARTER,t DONALD W. SELDIN AND H. C. TENG (From the Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas) (Submitted for publication October 27, 1958; accepted February 26, 1959) The elevation of pCO2 which occurs during to enter during respiratory acidosis is the red cell respiratory acidosis is accompanied by a rise in (1, 3, 9). The role of renal losses in the produc- the concentration of bicarbonate and a fall in the tion of hypochloremia is less certain. In short concentration of chloride in serum (1). The term human experiments, chloruresis has not increased bicarbonate concentration results from been observed during respiratory acidosis (5, both cellular and renal responses. The cellular 10). However, in the rat, Epstein, Branscome response is characterized by the exchange of ex- and Levitin observed increased chloride excre- tracellular hydrogen ions for intracellular cations, tion during the first 24 hours of an imposed re- thereby contributing to the elevation of the ex- spiratory acidosis (11). tracellular concentration of bicarbonate (2, 3). The present study in the rat was undertaken in The renal factors responsible for the elevated an attempt to delineate the pattern of renal and bicarbonate concentration may be divided into extrarenal responses to respiratory acidosis. The two phases: 1) acid excretion, and 2) bicarbonate excretion of sodium, potassium and chloride was reabsorption. In acute human experiments, aug- studied during the early and late phases. The mented acid excretion, as evidenced by increased contribution of acid loss, as ammonia and titrata- excretion of ammonia and titratable acid, has been ble acid, to the elevation of plasma bicarbonate reported (4). Barker, Singer, Elkinton and concentration was examined. The activities of Clark observed these changes also, but noted that the renal enzymes concerned with acid excretion, if the urine was acid prior to breathing carbon glutaminase and carbonic anhydrase, were deter- dioxide, further increase in acid excretion may not mined in order to ascertain whether adaptation of occur (5). Perhaps this explains, in part at these enzymes occurs as a result of chronic re- least, the failure of Longson and Mills to find in- spiratory acidosis. Finally, possible extrarenal creased acid excretion during short term human contribution to the buffering of carbon dioxide experiments (6). was examined in both muscle and bone. In acute respiratory acidosis tubular reabsorp- tion of bicarbonate is increased (7). Moreover, PROCEDURE in chronic respiratory acidosis in dogs, there is Male Sprague-Dawley rats weighing between 300 and a further augmentation of reabsorption of bicarbo- 400 Gm. were used in all experiments. In early experi- nate that varies directly with the duration of the ments, the rats were tube-fed a liquid diet twice daily imposed acidosis (8). that provided a total of 2.0 Gm. of protein, 1.5 Gm. of fat and 2.0 Gm. of glucose per day together with essential The fall in the concentration of serum chloride minerals and vitamins. Later experiments used the same during respiratory acidosis may also result from diet; however, the diet was offered in a standard drink- both cellular and renal responses. The only cell ing fountain, a measured amount of diet being offered into which chloride has been clearly demonstrated twice daily. Particular care was taken to ascertain that each rat took the entire amount of diet offered. The * This work was supported in part by a research grant intake of equal amounts of diet by both control and ex- from the National Institutes of Health, Public Health perimental animals is essential, for, as has been previ- Service, and in part by a grant from the Dallas Heart ously pointed out, variations in dietary intake result in Association. altered excretion of acid by the kidneys (12). With t This work was done during a Traineeship granted by respect to sodium, potassium and chloride, two different the Institute of Arthritis and Metabolic Diseases, Na- diets were used. The standard diet (Std. Diet) provided tional Institutes of Health, United States Public Health 2.0 mEq. of sodium, 1.0 mEq. of potassium and 3.0 mEq. Service. of chloride per day. The electrolyte deficient diet (E.D. 949 950 NORMAN W. CARTER, DONALD W. SELDIN AND H. C. TENG Diet) contained only negligible amounts of these ions. breathing 10 per cent carbon dioxide. Groups 7 and 8 All rats were given distilled water ad libitum. were a control group and a group subjected to 10 per A large box was constructed for use as a metabolic cent carbon dioxide, respectively. In an attempt to mag- cage for those animals subjected to respiratory acidosis. nify changes in plasma and muscle electrolytes, as well The design was such that daily urines could be collected as in urinary excretion of electrolytes, these two groups from individual rats. The proper content of carbon received the E.D. Diet. Urines were collected and dioxide within the box was maintained by automatic elec- analyzed as in Groups 4 and 5. trical controls which intermittently released carbon diox- ide into the box. By this method, the carbon dioxide METHODS content of the box could consistently be maintained within ± 1.0 per cent of the desired value. Oxygen content of Rats subjected to carbon dioxide were killed while the atmosphere in the box was frequently checked with breathing an atmosphere having the same carbon diox an Orsat gas analysis apparatus, and was found to ide content as was used for the experiment. This was range from 19 to 21 per cent. It was not necessary to accomplished by supplying an appropriate oxygen-carbon remove rats from the box during an experiment; feed- dioxide mixture to a small box into which the anesthe- ing and cage cleaning were carried out through air- tized rat's head was placed by way of a snugly fitting tight arm ports. By means of air-conditioning, both con- neck port. Both control and experimental animals were trol and experimental animals were kept in an atmosphere anesthetized by an intraperitoneal injection of pentobarbi- maintained nearly constant at 730 F. tal. Blood was received anaerobically into a previously aorta. were collected from individual heparinized syringe from the abdominal Muscle Twenty-four hour urines removed from the hind legs. In some ani- rats under oil and preserved with phenylmercuric nitrate samples were this mals, the bones of the hind legs were taken for electrolyte and toluene. Approximately midway through study, analysis. The kidneys were perfused with chilled iso- changes in the urine collection system were made that for tonic saline in order to wash out all red blood cells, then resulted in different values urinary constituents. frozen for enzyme assays. of a silicone to removed and immediately The change was the application coating Methods for the determination of plasma electrolytes, the surface of all glassware used in the collection system. from rat urine ammonia, pH and titratable acidity, muscle elec- This gave rise to an immediate flow of urine the trolytes and kidney glutaminase activity were those into the collection vessels and made it unnecessary to previously described from this laboratory (12, 13). rinse the collection system at the end of each collection of urine Urine sodium and potassium concentrations were deter- period, since there was no significant evaporation mined by flame photometry (14). Urine chloride con- the new urine collec- on the siliconized surfaces. Using centration was determined by a modification of the Vol- tion system, it was found that apparent ammonia excre- method (15). Whole blood pH was anaero- times than that found hard-Harvey tion was approximately 1.66 greater determined at 37° C. by means of a Cambridge An con- bically using the old urine collection system. additional water-jacketed glass electrode and a Cambridge pH meter. trol study, using the new urine collection system, was Plasma carbon dioxide tension was estimated by means made in order to facilitate comparison with experimental of the Henderson-Hasselbalch equation using the blood groups. The study included eight groups of rats. Groups pH, plasma carbon dioxide content and a pK of 6.11. 1 through 3 were those in which the original urine col- Buffer anion was estimated by means of a Singer- lection method was used (Table II). The new urine col- Hastings nomogram assuming a red cell hematocrit of lection method was used in the remaining five groups 50 per cent in each case (16). (Table II). Electrolyte composition of marrow-free bone was de- All groups were observed for a period of 11 days. termined in Groups 4 and 5. The method of analysis Group 1 served as a control for Groups 2 and 3. In these was a modification of the ion-exchange column method three groups, all rats received the Std. Diet, and daily of Forbes and D'Ambruso (17). urines were collected for determination of pH, ammonia Renal carbonic anhydrase activity was determined in and titratable acidity. Group 2 was subjected to an at- water homogenates of kidney tissue. The method de- mosphere of 10 per cent carbon dioxide. Group 3 was scribed by Ashby and Chan (18) was modified in the fol- subjected to 15 per cent carbon dioxide. lowing way. A veronal-sodium veronal buffer (0.03 M) Group 4 served as a control for Groups 5 and 6. These as suggested by Roughton and Booth (19) was substituted three groups received the Std.
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