Br.J. Anaesth.

(1977), 49, 331

EFFECT OF THE ACUTE ADMINISTRATION OF

SODIUM BICARBONATE ON RESPIRATION
IN THE PRESENCE OF HYPEROXIA
T. NISHINO, N. HATA, Y. SAKAKIBARA AND Y. HONDA

SUMMARY

The effects, on respiration, of the acute administration of sodium bicarbonate were studied in 10
normal subjects. Carbon dioxide response curves and tidal volume v. Pcx>2 relationships were
obtained under hyperoxic conditions using a closed-circuit breathing system. During alkalosis, a
decrease in the slope, and a displacement of the response curves to the right, were observed. These
findings indicate that metabolic alkalosis, induced acutely by the administration of sodium bi-
carbonate, alters the respiratory response to carbon dioxide and that sodium bicarbonate may have a
depressant effect on respiration.

Although sodium bicarbonate (NaHCO3) is adminis-
tered commonly to patients with metabolic acidosis
to correct the acid-base disturbance, its effect on
respiration is far from clear. Mithoefer, Karetzky and
Porter (1968) found no ventilatory depression after
the i.v. administration of sodium bicarbonate. How-
ever, hypoventilation in patients with metabolic
alkalosis has been reported recently (Tuller and
Mehdi, 1971; Steer et al., 1972; Perez-Guerra, 1974).
In order to study adequately the effects of drugs
on respiration, the respiratory response to carbon
dioxide (CO2) should be assessed. Katsaros and
others (1960) reported that the CO 2 response curve
was shifted to the right during alkalosis, whereas
Goldring and others (1968) noted that metabolic
alkalosis induced by buffers (sodium bicarbonate,
THAM) was associated with alveolar hypoventilation
and a diminished ventilatory response to CO 2
(decrease in slope and shift of the CO 2 response curve).
However, such results were obtained during chronic
alkalosis and, as there are few reports of the effect of
acutely induced metabolic alkalosis, the present study
investigated the effect on the CO2 response curve of
acutely induced metabolic alkalosis produced by the
administration of NaHCO 3 . Although the ventilatory
response to CO 2 is considered most often to be
essentially linear, the respiratory response to low
concentrations of inspired CO 2 may be curvilinear in
some subjects (Lambertsen et al., 1953). In Goldring's
report and that of Katsaros, the number of points of
ventilation for varying PACOI which were plotted
TAKASHI NISHINO, M.D., Department of Anaesthesiology;
NAMIYO HATA, PH.D.; YOSHIKAZU SAKAKIBARA; YOSHIYUKI
HONDA, M.D.; Department of Physiology School of Medi-
cine, Chiba University, 1-8-1 Inohanacho, Chiba, Japan.
to obtain the response curve seem to be insufficient to
assess the ventilatory response curve precisely. We
believe that many parameters of the curve are neces-
sary. It is necessary also to repeat the test under
hyperoxic conditions to exclude any hypoxic respira-
tory response.
METHOD
Ten normal human subjects (age range 19-49 yr)
were studied in the supine position. Their weights
ranged from 57 to 72 kg. All were in good health and
were free of pulmonary disease. All studies were
performed in the morning following overnight
starvation. Each subject rested on a chair in the
recumbent position for 30 min before the first arterial
sample of blood was withdrawn through an indwelling
catheter which had been inserted 1 h before the start
of the experiment, under local anaesthesia. During
cannulation no subject complained of pain, discomfort
or anxiety nor was there evidence of hyperventilation.
Each subject breathed from a closed-circuit system
(fig. 1) incorporating an infra-red carbon dioxide
analyser (Capnograph-Godart), a Po 2 electrode
(Radiometer) and a 9-litre spirometer (Aika). End-
tidal air was sampled by a device based on that
reported by Severinghaus and Hamilton (1970). The
Po 2 electrode, which was covered with 6.25-pim
Teflon membrane and responded rapidly (95% in
1 s), was inserted in the chamber of the end-tidal
sampler. Thus breath-by-breath end-tidal Po2 (PE'Ot)
was recorded continuously. End-tidal Pco 2 (PE'COJ)
was recorded continuously also by the infra-red CO 2
analyser to which the air in the respiratory valve was
sampled at a flow rate of 2-3 litre/min. Equal propor-
tions of oxygen and nitrogen were admitted to the
332 BRITISH JOURNAL OF ANAESTHESIA

--1 e.c.g.
-I Spirogram I

End tidal
PCO,

End tidal

0 electrode

Calibration

Lloyd Valve Bypass

Subject
Reg. Valve

FIG. 1. The closed circuit. The subject is connected to the closed circuit and the desired value
of Pis.'co, a n d PE'o, ' s obtained by changing the bypass flow and by controlling the gas flow of
N , and O,.

circuit. By changing the proportions, it was possible
was
to adjust PE' O 2 accurately. PE'CO,. altered by
adjusting the valve which controlled the proportion
of gas bypassing the CO 2 absorber in the expiratory
line. PE'COI was increased by 0.5-kPa* steps to the
limits of the subjects' tolerance. The Po 2 electrode
and infra-red CO 2 analyser were calibrated several
times during each experiment by introducing known
concentrations of carbon dioxide and oxygen which
had been analysed previously using a Scholander
apparatus. To obtain the CO 2 response curve, P E ' C 0 2
was controlled by changing the bypass flow in the
circuit. After each change of the bypass flow, it
usually took 6-10 min to attain a stable PE' C O S and
steady-state ventilation. The spirogram was then
recorded for 2 min; seven graphs of ventilation were
* 1 kPa = 7.5 mm Hg.
recorded for each end-tidal Pco 2 . After obtaining the
control data, sodium bicarbonate 0.3-0.5 mmol/kg
orally was administered with orange juice and 20 min
later 2 mmol/kg (in 7% solution) was given i.v. over
10 min. A second blood sample was obtained 20 min
after completion of this infusion. Immediately after
taking the second sample, the subject was connected
to the closed circuit and the ventilatory response was
measured again. The subject then breathed room air
at rest for 10 min and the third blood sample was
taken.
On another day a control experiment using a 0.9%
saline solution (5 ml/kg) instead of sodium bicarbon-
ate was performed on three of the 10 subjects. During
this experiment, four blood samples were taken from
each subject through an indwelling catheter: after
30 min rest on a chair (first sample), immediately
before the infusion of the saline solution (second
RESPIRATORY EFFECTS OF NaHCO, 333

sample), 20 min after completion of the saline infus- RESULTS

ion (third sample) and 10 min after completion of the
CO 2 response test (fourth sample). The total time
required to obtain each response curve was approxi-
mately 90 min and PEQ2 was maintained in the range
24.0-26.7 kPa throughout this period. PaOa and
arterial pH were measured by a Radiometer blood-gas
analyser (BMS 2 MK2) immediately after sampling.
The total plasma CO 2 concentration was measured
by the micro Van Slyke method (Van Slyke and
Plazin, 1961). PaC02 and the bicarbonate concentra-
tion (HCOg) were calculated by using the conversion
factors of Austin from the pH and the total plasma
CO 2 concentration (Austin, 1965).
The CO 2 response curve and the Pco2 v. tidal
volume curve were obtained by linear regression
analyses of the minute volume changes in relation to
changes in P E ' C 0 2 . The minute volume and the tidal
volume are presented as litre/min. m~2, ml/m2,
respectively. Respiratory depression was denned in
terms of displacements of the CO 2 response curve and
Pco 2 v. tidal volume curve measured at a minute
ventilation of 10 litre/m2 and at the tidal volume of
500 ml/m2.
The values of P E ' C 0 2 at the resting ventilation
under hyperoxic conditions before and after adminis-
tration of sodium bicarbonate were compared. The
slope of the CO 2 response curve was calculated
also.
Blood-gas analyses
There were no significant changes in pH, •Pacc,2,
Pa02 and HCO3 before and after the infusion
of normal saline. Marked changes were noted
after administration of sodium bicarbonate (fig. 2,
table I).
In the group receiving sodium bicarbonate the
arterial pH of the first blood sample (control) was
7.390 (SD 0.014) and that of the second sample (20
min after NaHCO 3 infusion) was 7.487 (SD 0.016)
(P<0.01). pH of the third sample (10 min after
completion of the experiment) was 7.477 (SD 0.013)
and this was significantly different from the control
value (P< 0.01), but there was no significant difference
between the second and the third samples. -Pa02
decreased slightly in the second and the third samples
from the control value and there was a significant
difference between the control value and the values
during alkalosis (P<0.05), but no significant differ-
ence between the second and the third blood samples
occurred. -PaC02 increased after the administration of
NaHCO 3 from 4.90 (SD0.25) kPa (control) to 5.17
(SD0.28) kPa (the second sample), and 5.53 (SD
0.46) kPa (the third sample). There were significant
differences between the control and the second sample
(P<0.05), and between the control and the third
sample (P<0.01). No significant difference was seen
between the second and third samples.

TABLE I. Blood-gas data before and after administration of NaHCO3

Subject

Y. H T. N. I. F. H. I. S. H. T. K. A. O. T. Y. S. S. Y O Mean + SD
Sample 1
pH 7.375 7.379 7.374 7.412 7.388 7.415 7.389 7.386 7.400 7.389 7.390 + 0.014
Po2 (kPa) 13.10 13.66 12.86 12.77 13.44 13.46 * 12.82 13.24 12.06 13.04 + 0.48
Pco 2 (kPa) 5.24 4.96 5.10 4.50 4.92 4.68 5.28 4.84 4.76 4.73 4.90 + 0.25
HCO3 (mmol/litre) 22.0 21.0 21.4 21.1 21.2 21.5 23.0 20.9 21.2 20.6 21.4±0.7
Sample 2
pH 7.483 7.505 7.463 7.511 7.489 7.469 7.475 7.482 7.496 7.505 7.487 + 0.016
Po2 9.80 14.44 12.33 11.22 12.70 12.05 11.64 12.37 11.58 12.65 12.07 + 1.19
Pco 2 5.50 4.70 5.52 5.09 5.04 5.02 5.53 4.94 5.33 5.12 5.17 ±0.28
HCO3 29.9 26.8 28.5 29.6 27.4 26.4 29.4 26.8 29.9 29.3 28.4+1.4
Sample 3
pH 7.490 7.487 7.499 7.488 7.472 7.471 7.484 7.467 7.479 7.491 7.477 + 0.013
Po2 10.10 13.70 12.13 11.06 11.64 10.96 12.17 11.25 11.38 11.40 11.57 + 0.95
Pco2 6.10 5.88 5.66 4.73 5.25 5.69 5.02 6.10 5.74 5.22 5.53 + 0.46
HCO3 33.8 32.2 28.2 26.1 27.7 30.1 27.3 32.0 30.9 29.0 29.7 ±2.5
* Not measured.
Sample 1: control; sample 2: 20 min after NaHCO 3 infusion; sample 3: 10 min after the completion of the experiment.
334 BRITISH JOURNAL OF ANAESTHESIA
7.500T

(mmol/litre) 2<H-
Control 1 s t B^ood 2nd Blood Saline 3rd Blood 4th Blood
Experiment Sample Sample infusion Sample Sample
* 4
NaHCOj 1st Blood NaHCO NaHCO 2nd Blood 3rd Blood
Administration Sample ingestion infusion Sample Sample
Experiment

REST COo RESPONSE TEST REST RESPONSE TEST REST

—i—
Time 0 30 60 90 120 150 V
18 21C
(min)
FIG. 2. Changes of pH, Pco 2 , Po2 and HCOj in arterial blood. Marked changes were not seen in
the control group (broken lines), while considerable changes were seen after NaHCO 3 administra-
tion (solid lines). Vertical bars are SD.

Resting ventilation shows the CO 2 response curve obtained from three

Control PE'COZ at rest (hyperoxia; P E ' O I 24.0
kPa; no CO 2 loading) was 4.81 (SD 0.36) kPa.
Resting P E ' C 0 2 after inducing alkalosis was 5.22 (SD
0.53) kPa and this difference was significant (P< 0.05).
The resting minute ventilation (control and after
inducing alkalosis) was 4.8 (SD 0.6) and 4.8 (SD 0.8)
litre/min. m~2, respectively and there was no
significant difference between these values. There was
a slight decrease in the resting tidal volume from the
control value of 298.7 (SD 46.4) ml/m2 to 273.6
(SD 39.9) ml/m2 during induced alkalosis but the
difference was not significant.
Carbon dioxide response test
The CO 2 response curve and the Pco 2 -tidal
volume curve were obtained by linear regression
analyses and these curves included the lowest points
of Pco 2 . The correlation coefficient values (r values)
of all these curves were greater than 0.84. Figure 3
subjects in the control experiments using 0.9% saline
solution and orange juice. No significant differences
in the position and the slope were seen before and
after the administration of the saline. The CO 2
response curve of one subject after the administration
of sodium bicarbonate is shown in figure 4. The CO 2
response curves and the tidal volume v. PE'C02
relationships of all the subjects are shown in figures 5
and 6. The values of P E ' C 0 2 for the minute ventilation
of 10 litre/m2 and the tidal volume of 500 ml/m2
both in the control situation and during alkalosis are
shown in tables II and III. There were significant
differences between the values obtained under control
conditions and during alkalosis (P<0.01).
The mean slope of the control response curve was
5.28 (SD 1.28) and the mean slope of the curve
obtained during alkalosis was 4.00 (SD 1.36) litre/
min.m~ 2 .kPa~ 1 . The percentage ratio of the slope of
the response curve obtained after administration of
RESPIRATORY EFFECTS OF NaHCO3 335

TABLE I I . The values of PE'COt at VE= 10 litrelmin.m-2 TABLE 111. The values of PE'COtat tidal volume = 500 ml/m2

Subject Control (kPa) Alkalosis (kPa) Subject Control (kPa) Alkalosis (kPa)
Y.H. 5.54 6.73 Y.H. 5.44 6.09
T.N. 5.60 6.42 T.N. 5.50 7.18
I. F. 6.86 7.14 I.F. 5.80 6.41
H.I. 5.90 6.36 H.I. 5.50 6.24
S. H. 5.89 6.29 S. H. 6.58 8.82
T.K. 5.29 7.02 T.K. 4.84 6.36
A.O. 6.78 8.18 A.O. 6.17 7.18
T. Y. 5.61 6.90 T. Y. 5.96 6.80
S.S. 6.37 6.54 S.S. 5.74 6.56
Y.O. 6.50 6.98 Y.O. 7.00 7.65
Mean + SD 6.03 ±0.55 6.85 + 0.55 Mean ± SD 5.85 ±0.61 6.92 ±0.82

TABLE IV. Changes in slope of CO2 response curve

Control Alkalosis Ratio slope:

Subject (litre/min.m- 2 .kPa- 1 ) (litre/min. m~ 2 . kPa~ alkalosis/control (%)

Y.H. 8.55 3.30 38

T.N. 6.90 6.00 86
I.F. 4.12 3.37 81
H.I. 5.62 6.00 106
S.H. 4.95 3.22 65
T.K. 4 05 2.32 57
A.O. 3.82 2.85 74
T.Y. 8.02 5.62 70
S.S. 3.90 3.97 101
Y.O. 2.92 3.37 115
Mean±SD 5.28 + 1.92 4.00 ±1.36 79 ±23

TABLE V. Changes in slope of tidal volume v. -PE'CO, relationship

Control Alkalosis Ratio slope:

Subject alkalosis/control (%)

Y.H. 412 231 56

T.N. 256 250 97
I.F. 326 226 69
H.I. 300 233 77
S.H. 155 72 46
T.K. 243 134 55
A.O. 245 201 82
T.Y. 173 221 127
S.S. 268 176 65
Y.O. 102 98 96
Mean ± SD 248 + 89 184 ±62 77 + 24

sodium bicarbonate to the slope of the control curve
is shown in tables IV and V. Significant decreases in
the slopes of both the Pco2-tidal volume curve and
the Pco2-ventilation curve were seen during alkalosis
(P<0.05).
DISCUSSION
Sodium bicarbonate is used often to correct metabolic
acidosis. Sometimes metabolic alkalosis is induced
because of over-correction. There has been disagree-
ment as to whether or not such metabolic alkalosis
causes hypoventilation. However, there are many
clinical reports of hypoventilation associated with
severe metabolic alkalosis (Alexander et al., 1955;
Roberts et al., 1956; Falchuk, Lamb and Tenney,
1966; Mithoefer et al., 1969; Van Ypersele de
Strihou and Frans, 1973). There has been disagree-
ment also as to the ventilatory effect of the i.v.
 336
(litre-rain. m"J) Subject :
BTPS
20
Continued experisent without /
aUalosiJ ' '
PE CO
F I G . 3. T h e C O 2 response curves in control experiments.
Neither change in slope nor change in position was seen
I'E Baseline J'-M-m- 5-3.83w-15.94 (r-0.98)
JTPS
During Alkalosis y-sx-m J>2.86m-13.35 (r-0.86)
Subject : A.O.
FIG. 4. The CO 2 response curve of subject A. O. A decrease
in slope, and displacement of the curve to the right, was
seen during alkalosis.
administration of sodium bicarbonate. Singer, Deer-
ing and Clark (1956) reported a decrease in ventilation
in the first hour after the infusion of NaHCO 3 while
Mithoefer, Karetzky and Porter (1968) disagreed
with this observation.
One way of assessing the ventilatory depressant
effect of a drug is to compare blood-gas data obtained
before and after administration of that drug. Another
way is to measure the ventilatory response to carbon
dioxide. In our study the control Pa COi and HCO3
were relatively small and we are unable to explain
this. It may have been a result of fasting (which causes
BRITISH JOURNAL OF ANAESTHESIA
ITPS
(kPai ^ i c 5 - T h e C 0 2 response curves of all the subjects. During
alkalosis the curves were shifted to the right and their slopes
w e r e decre
a s e d in comparison with the control curves.
T-V
(ml;nr
1000
FIG. 6. The tidal volume v. Pe'co, relationship of all the
subjects. During alkalosis a shift to the right and a decrease
in slope was seen.
metabolic acidosis) or an inherent metabolic character-
istic of the individual, or another unknown cause.
Although an increase in Pa co< and a decrease in
Pa Oi were seen after the administration of sodium
bicarbonate, severe hypoventilation, sufficient to
overcome the apparent alkalaemia, was not seen.
The CO 2 response test is one of the most reliable
tests in an evaluation of effects of drugs on respiration.
However, the details of the method are critical,
especially when data between different experiments
are to be compared. In a recent report Linton and
others (1973) concluded that the rebreathing method
RESPIRATORY EFFECTS OF NaHCO,
and the steady-state method do not assess similar
aspects of the chemical control of breathing. The
closed-circuit technique which we used in this study is
fundamentally a steady-state technique although the
subject breathes part of his own expired air. This
technique is easy to perform and permits the rapid
adjustment of the CO 2 concentration by controlling
the bypass flow. There is minimum discomfort for the
subjea and the technique permits also the control of
the oxygen concentration. In the interpretation of the
response curve some workers (Anderton and Harris,
1963; Lloyd and Cunningham, 1963) have discussed
the change both in the slope and in the intercept.
Others prefer to consider the Pco 2 at a particular level
of ventilation as the index of the displacement of the
curve insisting that extrapolation of the response curve
in a linear fashion is potentially misleading and
dangerous (Biillow, 1963; Keats and Telford, 1964;
Bellville and Green, 1965). As we agree with the latter
workers and we feel that the response curve should be
interpreted within the measured range, we chose
2
P E ' C O I at a ventilation of 10 htre/min.m~ and at a
tidal volume of 500 ml/m2 as our index of displace-
ment of the curve. Goldring and others (1968)
examined the ventilatory adjustment to induced
chronic metabolic alkalosis and reported that meta-
bolic alkalosis induced by sodium bicarbonate was
associated with alveolar hypoventilation and that a
shift to the right (in addition to a decrease in slope) of
the response curve as obtained by the steady-state
technique, was seen. Linton and others (1973) found
that, using the steady-state technique, there was a
shift of the response curve without a change in slope
during chronic metabolic alkalosis induced by sodium
bicarbonate. Our data show that in the resting state
during hyperoxia, the resting ventilation and tidal
volume after the induction of alkalosis were not
significantly different from the control values even
though the values for end-tidal Pco2 were significant-
ly higher than those of the control values (P<0.05).
This shows that the resting ventilation shifted to the
right after the administration of NaHCO 3 . During
alkalosis the values of Pz'coi a t a rninute volume of
10 litre/m2 and a tidal volume of 500 ml/m2 were
significantly higher than the control values. These
data show that the response curve was displaced to
the right during induced metabolic alkalosis. The
decrease in slope of the response curve was seen
during alkalosis and this does not accord with the
results of Katsaros and others (1960) and Linton and
others (1973), although it is in accord with the results
of Goldring and others (1968). Our data show also a
28
337
consistent decrease in tidal volume at all values of
PE'C02 during alkalosis and this suggests that the
reduction of minute ventilation was affected greatly by
the reduced tidal volume. The decrease in slope of the
response curve cannot be explained simply on the
basis of changes in the sensitivity of the respiratory
centre, because many other factors may affect the
slope of the response curve. Lung compliance, airway
resistance, muscle activity and even peripheral nerve
activity affect the slope of the response curve (Bellville
and Seed, 1960; Guz et al., 1966), but from the clinical
observations noted in this study it seems inconceivable
that these factors could have played a considerable
role in this experiment. Therefore, we suspect that
this decrease in slope is chiefly a result of decreased
sensitivity of the respiratory centre.
Disagreement exists as to the cerebrospinal fluid
(c.s.f.) acid-base relationships occurring during
alkalosis. Some studies have shown that there was
little difference in the composition of c.s.f. during
alkalosis induced by sodium bicarbonate (Swanson
and Rosengren, 1962; Monroe and Kazemi, 1973).
Others have reported that small changes occurred in
the composition of c.s.f. during alkalosis induced by
sodium bicarbonate (Pappenheimer, 1967; Hodson
et al., 1968; Lifschitz et al.. 1972). We did not study
the changes of c.s.f. composition on this occasion,
but if it is assumed that the H+ concentration of c.s.f.
has the chief role in the regulation of respiration, it is
conceivable that some changes in c.s.f. occurred to
explain the decreased sensitivity of respiration
observed in this study. The present study was carried
out under hyperoxic conditions so that a hypoxic
stimulus can be excluded. It is thought that the major
factor which affects the peripheral chemoreceptor is
oxygen, but it is true also that the CO 2 and hydrogen
ion concentrations influence chemoreceptor activity
(Saito, Honda and Hasamura, 1960; Mitchell and
Singer, 1965). However, it is known that in animals,
the effect of CO 2 and H+ on the peripheral chemo-
receptor nerves diminishes progressively as Po 2
increases (Fitzgerald and Parks, 1971) and that, in
man, no response of peripheral chemoreceptors to
CO 2 and H+ under hyperoxia was seen (Miller et al.,
1974). Therefore, under hyperoxic conditions the
activity of the peripheral chemoreceptor must be
neglected.
Cerebral blood flow and changes in cardiac output
may affect the sensitivity of the respiratory centre
(Bellville et al., 1959; Fencl, Vale and Broch, 1969).
In the present study we did not measure either
of these and we do not know whether metabolic
338
alkalosis, induced acutely and as studied in this
experiment, changes cerebral blood flow or cardiac
output to the point at which they may affect the
respiratory centre.
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EFFET DE L'ADMINISTRATION EN FORTES
DOSES DE BICARBONATE DE SOUDE SUR LA
RESPIRATION EN PRESENCE D'HYPEROXIE
RESUME
On a etudie sur 10 sujets normaux, les effets qu'a sur la
respiration l'administration en fortes doses de bicarbonate
de soude. On a obtenu des courbes de reaction a l'acide
carbonique et des relations du volume courant par rapport
au Pco 2 dans des conditions hyperoxiques, a l'aide d'un
systeme de respiration en circuit ferme. On a observe
pendant Falcalose, une diminution de la pente ainsi qu'un
deplacement vers la droite des courbes de reaction. Ces
decouvertes indiquent que 'lalcalose metabolique, provoquee
d'une maniere aigug par radministration de bicarbonate de
soude, modifie la reaction respiratoire a l'acide carbonique
et que le bicarbonate de soude peut avoir un effet moderateur
sur la respiration.
WIRKUNG DER AKUTEN VERABREICHUNG
VON NATRIUMBICARBONAT AUF DIE ATMUNG
BEI EINEM ZU HOHEN SAUERSTOFFGEHALT
DES KREISLAUFES
ZUSAMMENFASSUNG
Es wurden in 10 normalen Versuchspersonen die Wirkungen
der akuten Verabreichung von Natriumbicarbonet auf die
339
Atmung studiert. Um die Kohlensaurereaktionskurven und
die Verhaltnisse des Atmungsvolumens gegeniiber dem
Kohlensauredruck Pcoi zu erhalten, wurde ein geschlossenes
Beatmungskreissystem benutzt. Wahrend der Alkalose
wurde festgestellt, dass sich die Steingung verringerte und
die Reaktionskurven sich nach rechts verschoben. Dieser
Befund deutet an, dass die, durch die Verabreichung von
Natriumbicarbonat akut herbeigefuhrte Stoffwechsel-
alkalose die Atmungsreaktion auf Kohlensaure andert, und
dass Natriumbicarbonat eventuell dampfend auf die Atmung
wirkt.
EFECTO DE LA ADMINISTRACION AGUDA DE
BICARBONATO SODICO SOBRE LA RESPIRACION
EN PRESENCIA DE HIPEROXIA
SUMARIO
Los efectos sobre la respiration de la administracion aguda
de bicarbonato sodico fueron estudiados en 10 sujetos
normales. Se obtuvieron las curvas de respuesta del bioxido
de carbono y relaciones volumen respiratorio pulmonar
v. Pco 2 bajo condiciones hiperoxicas, empleando un
sistema respiratorio de circuito cerrado. Durante la alcalosis
se observaron un descenso en la vertiente, y un desplaza-
miento hacia la derecha, en las curvas de respuesta. Estos
hallazgos indican que la alcalosis metabolica, inducida
agudamente mediante administracion de bicarbonato
sodico, altera la respuesta respiratoria al bioxido de carbono,
y que el bicarbonato sodico pudiera ejercer un efecto de
depresion sobre la respiration.