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The Renal Response in Man to Acute Experimental Respiratory Alkalosis and Acidosis

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The Renal Response in Man to Acute Experimental Respiratory Alkalosis and Acidosis The Renal Response in Man to Acute Experimental Respiratory Alkalosis and Acidosis E. S. Barker, … , J. R. Elkinton, J. K. Clark J Clin Invest. 1957;36(4):515-529. https://doi.org/10.1172/JCI103449. Research Article Find the latest version: https://jci.me/103449/pdf THE RENAL RESPONSE IN MAN TO ACUTE EXPERIMENTAL RESPIRATORY ALKALOSIS AND ACIDOSIS 1 BY E. S. BARKER,2, 8 R. B. SINGER,4 J. R. ELKINTON,2 AND J. K. CLARK (From the Renal Section and Chemical Section of the Department of Medicine, The Department of Research Medicine, and the Department of Biochemistry, the University of Pennsylvania School of Medicine, Philadelphia, Pa.) (Submitted for publication August 7, 1956; accepted December 6, 1956) The experimental results to be presented here proximately 30 minutes in 5 of the 6 experiments, and deal with the renal component of the multiple ef- for twice that period in the last experiment; 7.5 to 7.7 fects in man of acute experimental respiratory al- per cent CO, in air or oxygen was inhaled for 21 to 30 minutes. Measurements were continued in both types kalosis (hyperventilation) and acidosis (CO2 in- of experiments during subsequent recovery periods which halation). One aim of the experiments has been ended 97 to 145 minutes after onset of the stimulus (desig- to define an integrated picture of the total body nated time zero). Standard water loading was carried response to acute respiratory acid-base disturb- out before the experiments and continued throughout ances. A previous paper (1) contained a de- with water given in amounts equivalent to urine ex- creted. In respiratory acidosis a neutral or slightly al- scription of the effects observed in the same ex- kaline control urine was considered desirable to facilitate periments on the composition of plasma and red observation of renal effects. Accordingly, in experi- cells, and a quantitative estimate of the exchanges ments 1 to 5 inclusive, the subjects were given 42 gm. of ions and water between red cells, plasma, extra- NaHCO, (50 mEq.) by mouth at -95 to - 150 minutes. cellular fluids and a phase or phases outside the As a control, in the sixth experiment NaCl was sub- stituted for the NaHCO8 and this experiment is not in- chloride space ("intracellular"). In the present cluded in statistical analyses. Four additional control report consideration is given to the changes in experiments were done in which the NaHCO. load was renal excretion and hemodynamics and an attempt given, and observations were made for the usual ex- is made to define more clearly certain mechanisms perimental time (but with no respiratory stimulus) to involved. Reference should be made to the previ- indicate the effect of the loading procedure alone. Renal clearances were determined by standard tech- ous report (1) for data on the blood or plasma niques and chemical methods (4, 5), with bladder cathe- changes; only a few of these data are included terization and appropriate anaerobic collection of urine here when they are directly important to interpre- to prevent loss of CO,. Changes in glomerular filtra- tation and renal effects. The present findings were tion rate were estimated from changes in endogenous previously reported in abstract (2, 3). creatinine clearance and effective renal plasma flow from p-aminohippurate (PAH) clearance.5 Following an equilibration period of at least 45 minutes urine was col- EXPERIMENTAL PROCEDURE AND CHEMICAL lected for 3 periods before, 1 to 4 periods during, and 3 METHODS to 4 periods after the application of the stimulus (hyper- Six normal male subjects actively hyperventilated and ventilation or CO, inhalation). six inhaled CO. as described in detail in the preceding Total CO, was determined in the anaerobically col- paper (1). Following control periods of 47 to 74 min- lected urine by the manometric method of Van Slyke and utes' duration, hyperventilation was carried out for ap- Sendroy (6), urine pH at 370 C by means of the photo- colorimetric method of Van Slyke, Weisiger, and Van 1 Laboratory facilities were aided by grants from the Slyke (7), sodium and potassium with a Barclay in- National Heart Institute of the United States Public ternal standard flame photometer (8), chloride by the Health Service (Grants H-405 and H-340), the Life In- surance Medical Research Fund, and the C. Mahlon 5Excretion of anionic PAH- in itself has some effect Kline Fund for Development in the Department of on urinary acid-base pattern. Administration was, how- Medicine. ever, at the same slow rate during both control and ex- 2Established Investigator of the American Heart As- penmental periods and there were no significant changes sociation. in PAH excretion during either type of respiratory stim- 8 In part during tenure of Post-doctorate Fellowship of ulus, when urinary acid-base changes were maximal. the National Institutes of Health, United States Public PAH could also form a buffer pair, but because it would Health Service. be a strong acid buffer (pK' = 3.83) (13), such an effect 4 Present address: 501 Boylston Street, Boston, Mass. must be very small. 515 516 E. S. BARKER, R. B. SINGER, J. R. ELKINTON, AND J. K. CLARK Volhard-Harvey method (9), ammonia by the method Changes in rate of urinary hydrogen ion excretion of Folin and Bell (10) using a Klett-Summerson photom- (A UVH+). For the purpose of this paper a quantitative eter, phosphate by the method of Lowry and Lopez (11), index of rate of H+ excretion is defined as the sum of and titratable acidity by titrating to pH 7.4. The bi- three components: NH4+ output plus titratable acid minus carbonate concentration was calculated from the total the HCO,- output. In the case of an alkaline urine the CO, content and pH of each urine specimen by use of rate is a negative quantity dependent chiefly on the bi- factors for CO, solubility and pK' in urine as functions carbonate output while for urine of neutral or slightly of urinary total cation concentration, derived from Send- acid pH values, all three terms are significant fractions roy, Seelig, and Van Slyke (12). of the total. Excretion of bicarbonate is equivalent in Methods of blood sampling and analyses were de- acid-base effect to the addition of hydrogen ion to the scribed in the previous paper (1). body and this method of calculating UVH+ eliminates the necessity of treating HCO; output as a separate factor. CALCULATIONS It is frequently not possible to distinguish, in the case of two separate body fluids, transfer of H+ in one direction Urinary electrolytes in microequivalents per minute from transfer of HCO, in the opposite direction. (i&Eq. per min.) are presented as excretion rates (UV) In order to assess the rate of renal acid-base compen- rather than clearances, thus permitting immediate com- sation to the respiratory disturbance it is desirable to parison of cation-anion equivalents. The cations deter- consider the difference between UVH+ observed and the mined were sodium, potassium, and ammonium; the UVH+ which would have been present at the control rate. anions were chloride, bicarbonate, and (in part) phos- The change in urinary hydrogen ion excretion is there- phate. fore determined, thus, Magnitude of acid-base disturbances (A HCO,-e). Un- der conditions termed a "steady state" the rate at which A V = A UVNH4t+ + A UVTA A UVHOC8- (2) carbon dioxide from cellular metabolism is added to the This consideration of A UVH+ rather than UVH+ in ab- extracellular fluid equals the rate at which it is lost from solute terms also avoids arbitrary decisions on what con- the body, and there is no resulting acid-base effect on the stitutes a "neutral" urine as related to an extracellular extracellular fluid. When the pulmonary component is fluid pH about 7.4 and a usual dietary intake and metabo- disturbed, as by hyperventilation or CO2 inhalation, a net lism which, uncompensated, would produce a metabolic quantity of CO, is removed from or added to the extra- acidosis. cellular fluid. An acid-base effect is exerted by shifting It should be noted that under these experimental con- the following relationship toward either the left or right: ditions, once hyperventilation or CO. inhalation ceases the CO2 + H20 = H2CO3 . W + HCOI' (1) acid-base disturbance is rapidly corrected by respiratory adjustments. Therefore the most meaningful indications This disturbance may be expressed in terms of equivalents of urinary adjustments appear to be the peak A UVH+ as a change in HCO-, and this change is proposed for achieved and the cumulative change to the time the the purposes of this paper as an indication of the magni- respiratory stimulus was discontinued. tude of the acid-base disturbance. A HCOa- is defined as the change in total amount of bicarbonate in the extra- cellular fluid (plasma plus interstitial fluid) and in the RESULTS red cells. It is desirable to include the red cells since they The results are presented in Tables I A, I B, II are intimately related by the chloride shift to the acid- and III and in Figures 1 through 4 and were base changes of respiratory disturbances. The method of statistical methods. The determination, together with observed A HCO4-er in the evaluated by standard individual experiments, was given for a different pur- average control data are included in the figures pose in the portion of the work previously published (1). and the average changes, variability (standard From Equation 1 it is evident that a change in He error) and probability of chance occurrence are equivalent to that in HCO; must initially occur. How- shown below the graphic part of each figure.
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