Respiratory Acidosis 2

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Respiration Physiology (1971) l&25-35; North-Holland Publishing Company, Amsterdam

EFFECT OF ACUTE RESP IR ATOR Y ACIDOSI SON ARTER IAL P LASMA OS MO LALITY I ,

D. R. HELD AND C. A. STEINERDepartment of Physiology, University of Fribourg,

Fribourg, Switzerland

Abstract. In anesthetized and nephrectomized dogs, acute respiratory acidosis was found to raise thearterial plasma osmolality: the latter exhibited a linear dependency toward Pace, over the range of40-150 mm Hg (AOsm/APco, = 0.17 mOsm/mm Hg *kg HzO). This indicates that a Pco, rise entailsan overall increase of body fluid osmolality, the major part of which reflects apparently the filling ofwhole-body COZ stores. The possibility of minor osmotic redistributions of body water in connectionwith this phenomenon involves a disproportionately large uncertainty as to the magnitude of thetransmembrane cationic exchanges generally assumed to contribute to extracellular buffering inrespiratory acidosis. The finding of this new link between the acid-base balance and the water-and-electrolyte equilibrium in the organism may be of interest for the interpretation of some systemiceffects of acute respiratory acidosis.

Acid-base balanceCO2 storesOsmolality of body fluidsRespiratory acidosisWater and electrolyte balance

A commonly overlooked feature of buffered media is the fact that their relative pHstability in presence of Pco2 changes is achieved at the cost of a loss of osmotic stabili-ty. This property, which reflects the Pcoz-dependency of their HCO; content, is easilydemonstrable in the case of isolated blood. Thus, MARGARIA (1931) found that thewater vapor pressure of blood varies with its Pco2 ; more recently, MESCHIA andBARRON (1956) showed that the osmolality (Osm) of whole blood tonometered atvarious CO2 pressures is linearly related to its molal CO2 content by a factor of 0.9,which closely approximates the osmotic coefficient expected of a monovalent ion likeHCO; at physiological ionic strength.

As a compound CO,-buffering system, the whole body can be expected to exhibit asimilar property, and the possibility of a Pco2- dependency of body fluid Osm is notAccepted for publication 11 December 1970.

1 The main results of this paper have been published elsewhere in abstract form (HELD, 1969).2 Work supported by grant number 4846.3 from the Swiss National Fund for Scientific Research.25


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26 D. R. HELD AND C. A. STEINERwithout interest in view of the key role played by osmotic equilibrium in so manyphysiological phenomena. The present paper will show that acute respiratory acidosiscauses a significant rise of arterial plasma Osm and discuss some implications of thisphenomenon.Methods1. EXPERIMENTALMongrel dogs weighing 12-34 kg were anesthetized by an intramuscular injection ofNa-pentobarbital (40 mg/kg) supplemented as needed to reach a deep surgical nar-cosis. The kidneys were exposed by flank incisions and their pedicles were carefullydissected and tied off in several bundles. Cannulas were placed into the two femoralarteries for blood sampling and monitoring of arterial blood pressure respectively,and into a femoral vein for curarization. The latter was induced by a priming dose of0.4 ml and maintained by an infusion of 0.04 ml/min of a 5 % solution of succinyl-choline chloride in saline. The animals were ventilated by means of a Starling pumpconnected to an external tracheal cannula. The tidal volume of the pump was adjustedto maintain the end-tidal Pco2 (monitored by an infrared analyzer) in the vicinity of39 mm Hg at a respiratory frequency of 14 c/min. Every 10 min, the lungs were brieflyinflated to a pressure of 30 cm H,O in order to prevent the formation of atelectases.Clotting was inhibited by i.v. injection of 10000 units of heparin. The rectal tempera-ture was periodically noted and maintained close to 38 C by means of a heating pad.

Once the end-tidal Pco2 was stabilized at the desired control value, but no less than30 min after completion of the surgical preparation, a control arterial blood samplewas taken anaerobically. Immediately thereafter, CO, breathing was started by con-necting the inlet of the Starling pump through a demand valve to a gas tank containingeither 6% CO,/20 % 0, (6 %-CO, experiments) or 20 % CO,/20 % O2 (20 %-CO2experiments); anaerobic arterial blood samples were taken 30 and 60 min after thebeginning of respiratory acidosis.2. ANALYTICALImmediately after its collection, each arterial blood sample was divided anaerobicallyinto two aliquots: one was used for pH determinations with a Radiometer capillaryelectrode thermostabilized at 37 C, and the second was centrifuged under mineral oilto provide separated plasma for additional analyses. The plasma Osm was determinedon a Fiske osmometer by a modification of the standard procedure intended to mini-mize CO, loss from the sample: 3.0-ml aliquots of separated plasma were injectedanaerobically into the bottom of osmometer test tubes containing 1.0 ml of mineraloil, which were immediately cooled for the freezing-point determination. It can beassumed that the use of oil prevented any significant drop of Osm due to CO, loss,since MESCHIA and BARRON (1956) report that the CO, loss of 2-ml samples duringfreezing-point measurements with the Fiske osmometer without oil protection neverexceeded 1.1 mM/liter. A comparison of two series of 10 Osm measurements on


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ARTERIAL SMOLALITY IN ACUTE RESPIRATORY CIDOSIS 27

physiological saline, made respectively with and without oil protection, showed thatthe addition of oil results in a somewhat larger scatter (SD: 0.46 vs. 0.32 mOsm/kgH,O) and in a slight increase (mean: +0.8 mOsm/kg HzO) of the Osm readings; nocorrection was applied for the latter effect. Duplicate Osm measurements on separateplasma aliquots were performed for each blood sample. Plasma CO, content wasdetermined with the Kopp-Natelson microgasometer within minutes after centrifu-gation of each blood sample on aliquots of plasma kept under mineral oil. Plasma(Na+) and (K+) were determined on a Model PMQ II Zeiss photometer with flameemission attachment against bracketing standards, and plasma (Cl -) was analyzed bycoulometry (Buchler-Cotlove Chloridometer).

In some experiments, plasma glucose and inorganic phosphate concentrations weredetermined by the o-toluidin and molybdate calorimetric methods respectively, andplasma water content was measured gravimetrically by drying samples of knownvolume at 110 C to constant weight.3. CALCULATIONSBlood pH readings were corrected for temperature according to ROSENTHAL (1948);arterial Pcol was calculated from blood pH and plasma CO, content, using the aand pKvalues published by SEVERINGHAUS, TUPFEL and BRADLEY (1956 , ).ResultsTable 1 summarizes the mean acid-base status and Osm values observed in arterialplasma after 30 and 60 min of respiratory acidosis in nine 6 %-CO, experiments and infifteen 20x-CO, experiments, with the corresponding control values. In fig. 1, theOsm values measured in every single experiment during the control period (triangles)and after 30 min (dots) and 60 min (circles) of respiratory acidosis are plotted againstthe corresponding Pcol values: in spite of a large overlapping of the Osm rangescorresponding to the three Pcol levels, the lines corresponding to the single experi-

TABLE 1Mean values (5 SD) of Pat+ (HCO;)a, pHa and arterial plasma Osm observed under control conditions

and after 30 and 60 min of respiratory acidosis_6 %-CO2 experiments 20 %-CO2 experiments(n =9) (n = 15)Control 30 min 60 min Control 30 min 60 min

Paw, mm Hg 38.7f4.3(HCO;)a, mM/liter 18.7k1.3

pHa 7.3017.272-7.333Osm.a, mOsm/kg Hz0 299.7

*5.3

64.7 67.9*5.1 +7.121.1 21.2*1.3 I-tl.77.131 7.1137.094-7.169 7.077-7.152303.9 304.014.5 h5.2

38.7 140.4 149.714.5 *8.6 hl3.019.6 25.8 26.0*1.4 11.5 41.27.319 6.887 6.8567.28G7.356 6.856-6.899 6.8256.889300.6 317.1 320.1I 14.0 15.9 f6.3


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28 D. R. HELD AND C. A. STEINER340

330

320

310

300

290

Osm,mOsm I kgH20

0 25 50 75 160 ii5 150 l+l 260PcR,mmHg

Fig. 1. Mass plot of arterial plasma Osm vs. Pace, values during control period (r ) and after 30 min(0) and 60 min ( 0) of respiratory acidosis.

AOsm,m Osm / kg H20

::;

1.!//q.17mOsm I kg H20. mm Hg

0 50 100 150APc02 , mmHg

Fig. 2. Mean arterial Osm changes vs. mean Pace, changes with respect to control conditions after30 and 60 min of respiratory acidosis. The 30-min points are those shown with their SEM.


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ARTERIAL OSMOLALITY IN ACUTE RESPIRATORY ACIDOSIS 29TABLE 2

Plasma water content under control conditions and after 30 and 60 min of respiratory acidosis inthree 6 %-CO2 experiments and in five 20 %-CO2 experiments.

Plasma water content(kg HaO/liter plasma)Control 30 min 60 min0.943 0.944 0.942

6 %-COz 0.944 0.947 0.953experiments 0.953 0.952 0.951

Mean 0.947 0.948 0.9490.955 0.955 0.954

20 %-CO2 0.949 0.959 0.955experiments 0.947 0.942 0.943

0.943 0.946 0.9460.951 0.952 0.952

Mean 0.949 0.951 0.950

ments uniformly exhibit a rise of Osm with increasing Pco2. This correlation emergesmore clearly when allowance is made for individual differences in control conditions:thus, fig. 2 presents the mean Osm changes plotted against the mean Pcol changeswith respect to control values; the 30 min points are shown with their SEM. Obvious-ly, the two sets of points corresponding to 30 and 60 min respectively are compatiblewith a single dependency, the implication being that the changes responsible for theOsm increase of arterial plasma in acute respiratory acidosis are essentially completedwithin 30 min or less. This dependency is linear and its slope is 0.17 mOsm/kg HzO*mm Hg.

Tables 2 and 3 present ancillary data on the concentration changes attending therise of arterial plasma Osm in acute respiratory acidosis. Table 2 displays the resultsof serial measurements of plasma water content in three 6 %-CO, experiments and infive 20x-CO, experiments; it may be noted that respiratory acidosis was not asso-ciated with any systematic change of arterial plasma water content. Based on thesedata, a factor of 0.95 was used throughout for conversion from molar to molal plasmaconcentrations. The mean changes of relevant arterial plasma concentrations aresummarized in table 3. Section A of this table presents the molal concentration changesof Na+, Kf, Cl-, HCOJ, inorganic phosphate and glucose. Section B shows someadditional derived data. The mean change of equivalent phosphate concentration hasbeen obtained by difference of the absolute equivalent concentrations; in turn, thelatter have been calculated from the molal phosphate concentrations and from the pHvalues, using a pK, of 6.84. The changes of protein net negative charge have beenderived by means of the equation proposed by VAN SLYKE et al. (1928):

Pr-(meq)=0.104 x (g protein) x (pH-5.08),


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30 D. R. HE LD AND C. A. STEINERTABLE 3

Mean changes of plasma molal concentration observed during acute respiratory acidosis with respect to control conditionThe measured data (section A) are shown with their SEM; the figures m parentheses indicate the number of measurement

The derived data (section B) have been calculated as explained in text.6 A-CO2 experiments 20 %-CO2 experimeuls30 min 60 min 30 mitt 60 min

A. Measureddata

A(Na+),meq/kg Ha0A(K+), meqikg Hz0A(CI-), meqjkg Ha0A(HCO;), meq/kg Hz0A(POd), mM/kg HsOA(glucose), mM/kg Hz0

+1.7= 1.2(9) +1.9* 1.1 (9)f0.2 & 0.1 (9) +0.4 & 0.2 (9)-0.8 IO.2 (9) - 1.2 * 0.5 (9)+2.5 $ 0.2 (9) +2.6 & 0.4 (9)+O.S 5 0.1 (6) +0.8 i 0.1 (6)~ 0.7 L 0.3 (4) -0.7 + 0.5 (4)

-2.5 =0.7(12) $2.9 3 1.1 (12,+0.4~0.1(11) +1.0~0.2(11:-3.4 Ix 0.5 (13) -4.4 It 0.6 (13;~6.5 & 0.3 (15) $6.7 & 0.3 (15:-0.9 = 0.1 (7) + I .6* 0.2 qt4.8 & 1.7(10) +6.1 i 2.4(10:

B. Deriveddata

A(POa), meq/kg Hz0A@-), meq!kg Ha0

0.6 f1.2 +0.9 +1.9ml.3 -1.4 -3.1 -3.3

Aniondeficit, meq/kg Ha0 co.9 +1.1 +2.0 $3.0

taking a plasma protein concentration of 70 g/kg H,O; this concentration corresponds(VAN SLYKE et al., 19 50 ) to th e mean plasma specific gravity of 1.025 observed as abyproduct of our plasma water content determinations. The anion deficit! has beencalculated as the difference between the sum of cation changes (Na+ and K+) and thesum of anion changes (Cl -, HCO;, HPOT, H,PO; and plasma protein); its existencehas been noted by several authors (GIEBISCH,BERGER nd PITTS, 1955; B~~NING, 968),and it represents presumably the appearance of unidentified anions during respiratoryacidosis.

Fig. 3, constructed from the data of tables I and 3, compares the rise of arterialplasma Osm evoked by respiratory acidosis with the attending concentration changes.In each pair of columns, representing a given experimental condition, the blankcolumn indicates the Osm increase and the adjacent hatched column shows the netsum of the associated molal concentration changes with respect to control conditions.From top to bottom, the subdivisions of each hatched column indicate the contri-butions of: 1. th e rise of (HCO;), 2. the increase of physically dissolved CO, ((CO,), =EPco,), and 3. the net sum of the other concentration changes (Na+, Ke, Cl-,phosphate, glucose and anion deficit). The decrease of physically dissolved N,accompanying the rise of (CO,), has been neglected since the solubility of N, is verysmall as compared with that of CO,. No great accuracy can be claimed in the esti-mation of the third term, since it represents the net sum of several small changes, bothpositive and negative. However, fig. 3 shows a fairly good agreement between the sumof the concentration changes and the corresponding Osm changes, especially at thehigher level of respiratory acidosis. As can be seen, the rise of arterial plasma Osm is


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ARTERIAL OSMOLALITY IN ACUTE RE SPIR ATORY ACIDOSIS 31mOsm /kg

ormM/kg

so-+15-

+lO-

l 5.

O-

420

H 2O I A [HCOi]IJfl&!nm,lSm X (A[misc.])0 0 Osm.

6 I. CO230 60

20%30

1ig. 3. Concentration changes (hatched columns) accounting for the Osm increases (blank columns)observed in arterial plasma after 30 and 60 min of respiratory acidosis.accountable for as follows in round numbers : one-third to one-half by the increase of(HCO;), about one-sixth by the increase of (CO,), and one-third to one-half by otherconcentration changes.DiscussionThe conspicuous feature of our results is the finding of a definite Pc,,-dependency ofarterial blood Osm in acute respiratory acidosis (fig. 2).

The relevance of this observation to the body fluids in general requires a briefcomment. There can be no doubt that such large changes of arterial Osm as were ob-served in our study have a counterpart in the bulk of the body fluids. On the otherhand, considering the efficiency of circulatory mixing and the extremely high permea-bility of most biological membranes for H,O, total body water can be viewed to agood approximation as a medium of uniform Osm. Therefore, our finding does indi-cate that acute respiratory acidosis entails an overall rise of body fluid Osm. Onemight still question whether arterial blood yields an accurate measure of this whole-body Osm change: mixed venous blood, of course, would be a more immediate indi-cator of body fluid Osm, and CO,-breathing may conceivably alter the arterio-venousOsm difference. However, this a-v difference is small as compared with the changesunder discussion (- I .2 mOsm/kg H,O in the dog according to ME SCHIA and BARRON,1956-1957), so that our results give presumably a fair estimate of the whole-body Osmincrease in acute respiratory acidosis.

The part played by different molecular species in this increase of the whole-bodyosmotic mass is difficult to evaluate. If the detailed study of the arterial plasma con-centrations (Table 3 and fig. 3) indicates that HCOi and dissolved CO, account to-gether for at least one-half of the Osm rise in the extracellular fluid, we have no direct


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32 D. R. HELD AND C. A. STEINERevidence as to the concentration changes contributing to the matching Osm rise in theintracellular fluid, which makes up the larger part of total body water. However, thereis reason to believe that the CO, system is largely involved in the intracellular com-partment as well, since a systemic Pco2 increase causes necessarily an intracellular riseof both (HCOJ and (CO,),. Thus, the uptake of carbon dioxide by the various bodyfluid compartments would seem to be the major contributor of the Osm rise evokedby acute respiratory acidosis. This view finds indirect support in the values of whole-body differential CO, capacity published by others (see FARHI (1964) for review) :for respiratory acidosis lasting 30-60 min as in our case, these values range from 1.5to 2.1 ml CO,/mm Hg .kg b.w. ; assuming the COZ capacity of the organism to reflectexclusively physical dissolution and buffering in body solvent water (0.555 kg H,O/kg b.w. according to EDELMAN and LEIBMAN, 1959), this amounts to 0.12-0.17 mMCOJmm Hg.kg Hz0 to be compared with our mean Osm/P,o, dependency factorof 0.17 mOsm/mm Hg*kg HZ0 (fig. 2). On the other hand, table 3 and fig. 3 show thatsubstances unrelated to the CO, system are also involved: respiratory acidosis pro-duces an increase of plasma inorganic phosphate concentration, owing to the break-down of intracellular phosphoesters, or to the mobilization of bone mineral (SAUNIERand SCHIBI, 1967), and a rise of plasma glucose concentration, at least at high PcoZlevels, as a consequence of the associated sympatho-adrenal discharge (FENN andASANO, 1956; MITHOEFERet al., 1968; NAHAS and STEINSLAND, 1968). The changes ofextracellular Na+, K+, and Cl- concentrations (table 3) are irrelevant in this contextsince they are unlikely to result to any large extent from exchanges between theliquid phase and osmotically inactive stores.

Obviously, the appreciable Osm changes we have described evoke the possibility ofosmotic water shifts. Indeed, some amount of body water redistribution, albeit small,must be expected to occur in acute respiratory acidosis, since a given Pco2 rise is mostunlikely to produce primarily proportional increases in the osmotic pools of all thebody fluid compartments: the well-known Pco2 dependency of RBC volume in iso-lated blood (e.g. HENDERSON, 1928) is an obvious example of just such a phenomenonin the simpler case of a two-compartment system. The possibility of a P,o,-dependen-cy of body fluid distribution is of interest, as will be shown in the following. It isgenerally agreed that the buffering of the extracellular space in acute respiratory aci-dosis results for a large part from net cationic transfers between extracellular andintracellular fluids, protons being exchanged for Na+ and to a much lesser extent forK+ ions. However, the transmembrane ionic fluxes postulated by this classical theoryhave not been measured directly, but estimated by two highly indirect approaches.The first (SINGER et al., 1953; ELKINTON et al., 1955) rests on a quantitative compari-son of the actual acid-base pathway followed by the extracellular fluid in respiratoryacidosis with the theoretical pathway predicted on the basis of the available extra-cellular buffers. Yet we have shown elsewhere (STEINER and HELD, 1971) that suchcalculations would be subject to considerable error if respiratory acidosis entailed theslightest change of extracellular fluid volume: thus, the observations which wereinterpreted by Elkintons group as indicative of a major role of transmembrane ion


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ARTERIAL SMOLALITYN ACUTERESPIRATORYCIDOSIS 33exchanges in extracellular buffering would be explained just as adequately by a mere2 % decrease of extracellular fluid volume; conversely, of course, a small expansion ofextracellular volume in acute respiratory acidosis would make the ion exchangehypothesis all the more necessary. The second approach used to evaluate these ionictransfers is based on the study of the extracellular ionic concentrations. Thus, GIE-BISCH t al. (1955) were led to postulate a large transfer of Na+ into the extracellularspace in respiratory acidosis by their finding of a plasma (Na+) rise in CO,-breathingexperiments (this (Na+) rise, it should be noted, does not seem to be an obligatoryfeature of acute respiratory acidosis, since BINNING1968) failed to confirm it in similarexperiments). Here again, however, even minor water displacements would affectconsiderably the interpretation of such experimental data, as the following examplewill show: in our 20 %-CO, experiments, plasma (Na+) rose by 2.5-2.9 meq/kg H,O(table 3); this change, albeit significant, is so small relatively to the absolute Na+ con-centration that no Na+ transfer would be required to explain it if the extracellularvolume decreased by 1.6-l .8 /, only. The fundamental fact emerging from these con-siderations is that the possibility of small changes of extracellular volume in respira-tory acidosis has far-reaching implications for the accepted theory of tissue cell parti-cipation in extracellular buffering. True, the few sucrose and radiosulfate dilution datapresented by GIEBISCH t al. (1955) are not suggestive of major distribution volumechanges in connection with respiratory acidosis; however, the evidence presented bythese authors is certainly insufficient to either demonstrate or exclude small but stillcritical fluid shifts. In disagreement with Giebisch and coworkers, we have recentlyobtained results indicating a significant rise of the apparent distribution volume ofradiosulfate activity on CO,-breathing (STEINER nd HELD, 1970) but the interpreta-tion of this effect in terms of real volume changes is complicated by the ionic nature ofthe tracer.

The fact that body fluid Osm varies with Pco2 in acute respiratory acidosis raises theintriguing possibility that an osmotic factor might be involved in some of the physiolo-gical effects accompanying in vivo Pcor changes. Admittedly, the changes of Osmcaused by Pco2 variations are not very large: for instance, a Pco2 rise of 6 mm Hg isrequired to increase the arterial Osm by 1 mOsm/kg H20. However, even smallchanges of Osm may have physiological significance, the most striking case being theexquisite sensitivity of the osmoregulation itself: according to the data of MILLER-SCHOEN nd RIGGS (1969), for example, a 1 mOsm/kg H,O rise of plasma Osm is al-ready sufficient to trigger a highly significant increase of the fractional reabsorption ofwater by the kidney. Actually, a close scrutiny of the careful balance studies done byPOLAK t al. (1961) and SCHWARTZt al. (1961) on conscious dogs exposed for severaldays to a lo-13 % CO, atmosphere suggests that the osmoregulation may well com-plicate the renal response to acute respiratory acidosis. In these animals kept on con-trolled food, salt and water intake, CO, breathing evoked a large increase of the totalurinary solute excretion; interestingly enough, two out of the three dogs for whichdetailed data were published exhibited simultaneously a marked decrease of urineoutput. Converse changes were observed after COZ withdrawal. Although no urine


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34 D. R. HELD AND C. A. STEINEROsm data were given, these results clearly imply massive changes of free-water clear-ance under the influence of Pcol shifts. The role of a body fluid Osm change as amediator in this and possibly other in vivo effects of CO, would certainly deservefurther investigation. From a more general point of view, it can be stated that thedemonstration of an osmotic component in acute respiratory acidosis draws attentionto a new and possibly significant aspect of the relationships between the water-and-electrolyte balance and the acid-base balance.AcknowledgementsWe are indebted to Miss M. C. BIFRARE and Miss N. BOGDAN for their collaboration.ReferencesBONING, D. (1968). Verinderungen der COz-Bindungskurve des Blutes bei akuter respiratorischer

Acidose und ihre Ursachen. I. Untersuchungen an Hunden. Pfliigers Arch. ges. Physiol. 302:133-148.

EDELMAN, . S. and J. LE~BMAN1959). Anatomy of body water and electrolytes. Am. J. Med. 27:256-277.

ELKINTON, . R., R. B. SINGER,E. S. BARKERand J. K. CLARK (1955). Effects in man of acute ex-perimental respiratory alkalosis and acidosis on ionic transfers in the total body fluids. J. Clin.Invest. 34: 1671-1690.

FARHI, L. E. (1964). Gas stores of the body. In: Handbook of Physiology. Section 3. Respiration.Vol. I, edited by W. 0. Fenn and H. Rahn. Washington DC., American Physiological Society.FENN,W. 0. and T. ASANO 1956). Effects of carbon dioxide inhalation on potassium liberation fromthe liver. Am. J. Physiol. 185: 567-576.

GIEBISCH,G., L. BERGER nd R. F. PITTS(1955). The extrarenal response to acute acid-base disturb-ances of respiratory origin. J. Clin. Invest. 34: 231-245.

HELD, D. R. (1969). Changements dosmolalitt du plasma arterie associts & lacidose respiratoireaigiie in ~610. J . Physiol. (Paris) 61 (suppl. 2): 313.

HENDERSON, . J. (1928). Blood: A Study in General Physiology. New Haven, Yale University Press.MARGARIA,R. (1931). On the state of CO2 in blood and haemoglobin solutions, with an appendix on

some osmotic properties of glycine in solution. J. Physio l. (London) 73 : 31 l-330.MESCHIA,G. and D. H. BARRON 1956). The effect of COZ and 0~ content of the blood on the freezing

point of the plasma. Quart . J. Exp. Physio l. 41: 180-194.MESCHIA,G. and D. H. BARRON 1956-1957). Freezing point depression of arterial and venous plas-

mas in vivo. Yale J. Biol. Med. 29: 54-59.MILLERSCHOEN, . R. and D. S. RIGGS (1969). Homeostatic control of plasma osmolality in the dog

and the effect of ethanol. Am. J. Physiol. 217: 431437.MITHOEFER, . C., H. KAZEMI, F. D. HOLFORDand I. FRIEDMAN 1968). Myocardial potassium ex-

change during respiratory acidosis: the interaction of carbon dioxide and sympatho-adrenaldischarge. Respir. Physiol. 5: 91-107.

NAHAS, G. G. and 0. S. STEINSLAND1968). Increased rate of catecholamine synthesis during respi-ratory acidosis. Respir. Physiol. 5 : 108-l 17.

POLAK,A., G. D. HAYNIE,R. M. HAYS and W. B. SCHWARTZ 1961). Effects of chronic hypercapniaon electrolyte and acid-base equilibrium. I. Adaptation. J. Clin. Invest. 40: 1223-1237.

ROSENTHAL, . B. (1948). The effect of temperature on the pH of blood and plasma in vitro. J. Biol.Chem. 173 : 25-30.

SAUNIER,C. and M. SCHIBI 1967). Hypercapnie aigiie exptrimentale chez le chien: variations pr&coces du phosphore inorganique dans le plasma artBrie et le liquide cCphalorachidien. C. R .Sot. Biol. 161: 410414.


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STEINER,C. A. and D. R. HELD (1970). Change of apparent distribution volume of 35SOh in acuterespiratory acidosis. Experientiu 26: 684.

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