- Email: [email protected]
HOW MUCH FLUORINE?
935
The possibility of insipient addisonian ansemia underlying sterility also arises from Dr. Adams’ data and is the more apparent in the observations from Dr. Watson and Df Sharp. Indeed it seems desirable to screen all patients, both male and female, with unexplained sterility for subclinical evidence of addisonian anaemia, and this seems the more important because it is not current practice to try the effect of vitamin-Bl2 for these patients. Department of Hæmatology, Stobhill General Hospital,
MARY D. SMITH.
Glasgow.
nightmare dream. In seeking to understand the mechanism of
sleep paralysis,
account should be taken of the evidence for the existence of two
kinds of sleep, brilliantly elucidated in the cat and other animals by Jouvet,2 and called by him fore-brain sleep and "hind-brain sleep" (or the "paradoxical phase "). The former is the traditional kind of sleep. In hind-brain sleep ", the E.E.G. is of low voltage, and the eyes make frequent rapid conjugate movements. The two kinds of sleep alternate during the night, but prior to waking hind-brain sleep occupies proportionately more of the time. Similar alternation between these kinds of sleep has been found in man, deliberate arousal from the hind-brain sleep " being followed by a "
"
"
"
"
"
of having just been dreaming.33 Associated with " hind-brain sleep " in cats, there is a jtamatic loss of skeletal muscle tone. In man, surface electrode " recordings show so great a loss of tone during fore-brain sleep" anyway that it is difficult to demonstrate a further fall with the onset of " hind-brain sleep ". My colleague, R. J. Berger,’ first observed such a fall in the extrinsic laryngeal muscles, however, since which time I have observed the same phenomenon in other muscle groups also, occurring particuMy in temporal relation to certain characteristic saw-toothed U.G. waves which bear a special connection5 with the rapid " " eye movements of hind-brain sleep and the dreams which s accompany them. There is, therefore, now evidence that during the progress of our dreams our skeletal musculature is paralysed. In further experiments, Bergerhas shown that awareness, albeit faulty, of external events can occur in dreams. It may be plausibly suggested that the victim of sleep paralysis is in, a state of "hind-brain sleep"in which he dreams, yet with a vague awareness of the environment, and in which he is therefore paralysed, a touch causing true awakening.
description
Department of Psychological Medicine, University of Edinburgh.
IAN I OSWALD. AN 0 SWALD.
SIR,-I read your leader with interest because I used to fairly frequent attacks. They usually occurred on waking and were accompanied by an unreasoning fear of falling asleep again. Subjectively, the condition resembled a light hypnotic trance. I found that it was possible to end an attack by breathing in sharply, though often more than one attempt was needed to produce the necessary sniff ". I pass this on in the hope that others may find this method suffer
"
1. Oswald, I. Proc. R. Soc. Med. (in the press). Jouvet, M. Arch. ital. Biol. 1962, 100, 125. Oswald, I. Sleeping and Waking: Physiology and Psychology. Amsterdam, 1962. 4. Berger, R. J. Science, 1961, 134, 840. 5. Berger, R. J., Olley, P. C., Oswald, I. Quart. J. exp. Psychol. 1962, 14,
2. 3.
183.
6. Berger, R. J., Oswald, I. Science, 1962, 137, 601. 7. Berger, R. J. University of Edinburgh, PH.D. thesis,
1962.
Noble’s
Hospital, Douglas,
Isle of Man.
J.
B. CAINE.
EARLY DIAGNOSIS OF IMPAIRED POSTOPERATIVE RENAL FUNCTION SIR,-May I congratulate Mr. Molloy (Oct. 6) on drawing attention to the usefulness of the urinary urea
concentration in
SLEEP PARALYSIS SIR,-Your leading article of Oct. 20 states that the victim " is usually fully aware of external events (unlike " the victim of nightmare)" and then quotes a typical " description in which the individual would feel that headless people or animals were climbing on the bed, or that he was being strangled. I would suggest, Sir, that the description is hardly that of someone " fully aware " and that his unpleasant experiences clearly resembled those of a
effective, because attacks of this condition are unpleasant and, as your leader states, can sometimes be extremely alarming.
assessing renal function postoperatively ? My experience1 confirms that this is the single most helpful piece of information that one can have in deciding whether a postoperative patient has an early acute renal failure, and thus needs a carefully balanced fluid intake, or whether the kidneys are ready to respond by diuresis to own
an
increased intake.
My one query would be about the level of urinary urea (above 1-1g. per 100 ml.) which Mr. Molloy accepts as normal. My evidence led to the conclusion that with a blood-urea of 100 mg. per 100 ml. or over, a urinary urea concentration of below 2-0 g. per 100 ml. indicated renal failure. Looking again at the data2 it appears that 8 out of 15 patients who subsequently developed acute tubular necrosis-confirmed at necropsyhad urinary urea levels above 1-1g. per 100 ml. Many of our observations were made upon patients several days after operation, whereas Mr. Molloy’s data apply to the first 24 hours. There is, however, no need to limit the use of the test to this early period. Incidentally,
when the postoperative urinary urea has been above 2 g. per 100 ml., I have only once known the kidneys fail to respond with an appreciable diuresis to an increased fluid intake. The patient concerned subsequently proved to have a complete arrest of blood-flow to one kidney. The remaining kidney was apparently already functioning close to its maximum. Department of Chemical Pathology, United Liverpool Hospitals, W. H. TAYLOR. Liverpool.
HOW MUCH FLUORINE? SiR,—You call attention to the rejection by the Kilmarnock Town Council of the continued addition of fluoride to the public water-supply. Two years ago you published3 an admirable survey of the medical and biological aspects of fluoridation. Although the fluoridation of public drinking-water supplies by the addition of 1 p.p.m. fluroride may seem desirable in view of the generally poor condition of teeth among British children, there are certain considerations in this country that indicate the wisdom of Kilmarnock’s action in the present state of our ignorance. Fluorine-containing ores, fluxes, and coals are used industrially in large quantities in many parts of this country.4 Fluorine compounds are toxic when inspired or ingested, and animals are moved from contaminated pasture; but human beings remain in a polluted atmosphere. Further we do not know the level of intake at which retention of fluorine may occur in different parts of the body in different people, nor the adverse influence of such retention on any pathological process which may affect particular organs. In the recent, admittedly imperfect, data published in a report5 on mortality in areas containing natural fluoride in their water-supplies (industrial fluorosis is not mentioned), it is of interest that the results in northern fluoride towns suggest an increased mortality of nephritis and nephrosis. Bond and Murray6 described the effects in rats of chronic fluorosis on 1. Taylor, W. H. Lancet, 1957, ii, 703. 2. Taylor, W. H., Reid, J. V. O. Brit. J. Surg. 1958, 46, 136. 3. Lancet, 1960, ii, 425. 4. Murray, M. M., Wilson, D. C. ibid. 1946, ii, 821. 5. Heasman, M. A., Martin, A. F. Mon. Bull. Min. Hlth, 1962, 21, 150. 6. Bond, A. M., Murray, M. M. Brit. J. exp. Path. 1952, 33, 168.
936 structure and function before such severe intoxication had resulted as to cause obvious skeletal lesions. In man the storage of fluorine in bone is seen typically among less privileged people, but similar lesions may be determined by congenital or acquired renal disease in any population.
kidney
Until further inquiry is undertaken to determine total fluorine hazards in different neighbourhoods, together with some estimate of the increased fluorine content of animal and vegetable foods due to the use of piped water containing added fluorine, it seems most undesirable that fluorine should be added to public water-supplies in
Britain. DAGMAR WILSON. THE EFFECT OF SALICYLATE ON THE UPTAKE OF 131I TRIIODOTHYRONINE BY THE RED CELLS SiR,—The uptake of 1311 triiodothyronine by the red
cells, introduced by Hamolsky et alphas proved useful as a diagnostic test of thyroid function.2-5 The test is a measure of the concentration of binding sites on thyroxine-binding
protein (T.B.P.) not occupied by thyroxine-i.e., of free T.B.P. capacity.6 It is therefore indirectly related to the concentration of thyroxine in the plasma. Under the conditions of the test
triiodothyro-
nine is distributed between the red cells, the a2-globulins-and p-globulins, and free T.B.P. Any substance which affected the binding of triiodothyronine by the red cells, the
tX2-globulins or P-globulins or T.B.P. might be expected to interfere with the mechanism of the test.
Salicylate increases the rate of dialysis salicylate. of thyroxine from human plasma, probably by interfering with the binding of thyroxine by the plasma proteins.’ At pH 7-4 salicylate interferes with the binding by T.B.P. of both thyroxine and triiodothyronine.8 It was therefore of interest to find out whether the administration of salicylate interfered with the uptake of "3’I-triiodothyronine by the red cells (T3 [R.B.c.]) when this was used as a test of thyroid function. T3 [R.B.c.] values have been determined in a series of patients undergoing treatment with salicylate for rheumatoid arthritis. Values above the normal range were found in more than half the patients tested (fig. 1). None of these patients had any clinical evidence of thyroid dysfunction. A significant increase in T3 [R.B.c.] values also occurs in normal people after a single oral dose of 1 -3 g. of aspirin. Salicylate added to blood in vitro has a similar effect, T3 [R.B.c.] values increasing as the concentration of salicylate in blood is increased (fig. 2). We have found that salicylate modifies the partition of triiodoFig. 1-Values for T3 [R.B.C.] in patients under treatment with
1.
2. 3. 4.
5. 6. 7. 8.
Hamolsky, M. W., Stein, M., Freedberg, A. S. J. clin. Endocrin. 1957, 17, 33. Robins, L. R. ibid. 1959, 19, 1292. Ureles, A. L., Murray, M. J. Lab. clin. Med. 1959, 54, 178. Walfish, P. G., Britton, A., Volpé, R., Ezrin, C. Canad. med. Ass. J. 1961, 84, 637. Goolden, A. W. G., Gartside, J. M., Jackson, D. J., Osorio, C. Lancet, 1962, ii, 218. Osorio, C., Jackson, D. J., Gartside, J. M., Goolden, A. W. G. Clin. Sci. 1961, 21, 355. Christensen, L. K. Nature, Lond. 1959, 183, 1189. Osorio, C. J. Physiol. 1962, 163, 151.
Fig. 2-Effect
on
T3
[R.B.C.]
values when sodium
salicylate is added
to blood in vitro.
thyronine between the red cells and the plasma-proteins by affecting the binding power of both thyroxine-binding protein and the a2- and p-globulins. These results are discussed in further detail elsewhere.e It is clearly important to exclude the recent administra-
tion of sodium salicylate or aspirin when the T3 [R.B.C.] test is used to assess thyroid function. Butazolidine in vitro also increases the uptake of 131I-triiodothyronine by the red cells and may well have a similar effect in vivo. Department of Radiotherapy, Medical Research Council Experimental Radiopathology Research Unit, Hammersmith Hospital, London, W.12.
A. W. G. GOOLDEN C. OSORIO.
HYPOXÆMIA AFTER GENERAL ANÆSTHESIA
interested in the article by Dr. Nunn and (Sept. 29). Whereas I agree that all patients suffering from a respiratory or cardiovascular insufficiency should be given oxygen in the postoperative period, I am not satisfied that hypoventilation may be ruled out as the cause of hypoxaemia in the cases under review.
SiR—I
am
Dr. Payne
All the
cases were given respiratory depressant drugs and respiration was unassisted. In my experience, by measuring tidal exchange, and acid-base levels in such anxsthetic management, I have always found a definite degree of hypoventilation, approximately 40% below preoperative level, and a rise in pCOz by 10-20 mm. Hg above preoperative level. In the series reported no mention was made of ventilation levels, or acidbase findings, during operation. It would have been interesting to have had more detailed information about the premedication of these cases. Was there
any diminution of minute volume before the induction of anarsthesia ? As there is no mention of the duration of the
operations concerned, it would be interesting to know if there could have been a hangover of the depressant effect of premedication on the postoperative period. Was there any monitoring of ventilation postoperatively? And if there was a respiratory inadequacy were the patients given any breathing exercises by the physiotherapists ? What posture was used in the postoperative period ? In the event of even mild obesity a head-up tilt of the bed will increase tidal exchange by at least 15%. These queries are of a very simple clinical nature, because I believe the solution of the problem at issue may be on such a level; the series of cases described represents
a cross-section of the type of patient met with in routine anxsthetic practice. It is well to remember that carbon dioxide is much more soluble than oxygen in aqueous fluids, and that it diffuses twenty times as rapidly. Any reduction of the alveolarcapillary membrane, as would result from the relative hypoventilation of a large proportion of alveoli, would cause hypoxaemia before there was any gross disturbance in acid-
9.
Goolden, A. W. G. Symposium
on
Salicylates,
1962. To be published.
The possibility of insipient addisonian ansemia underlying sterility also arises from Dr. Adams’ data and is the more apparent in the observations from Dr. Watson and Df Sharp. Indeed it seems desirable to screen all patients, both male and female, with unexplained sterility for subclinical evidence of addisonian anaemia, and this seems the more important because it is not current practice to try the effect of vitamin-Bl2 for these patients. Department of Hæmatology, Stobhill General Hospital,
MARY D. SMITH.
Glasgow.
nightmare dream. In seeking to understand the mechanism of
sleep paralysis,
account should be taken of the evidence for the existence of two
kinds of sleep, brilliantly elucidated in the cat and other animals by Jouvet,2 and called by him fore-brain sleep and "hind-brain sleep" (or the "paradoxical phase "). The former is the traditional kind of sleep. In hind-brain sleep ", the E.E.G. is of low voltage, and the eyes make frequent rapid conjugate movements. The two kinds of sleep alternate during the night, but prior to waking hind-brain sleep occupies proportionately more of the time. Similar alternation between these kinds of sleep has been found in man, deliberate arousal from the hind-brain sleep " being followed by a "
"
"
"
"
"
of having just been dreaming.33 Associated with " hind-brain sleep " in cats, there is a jtamatic loss of skeletal muscle tone. In man, surface electrode " recordings show so great a loss of tone during fore-brain sleep" anyway that it is difficult to demonstrate a further fall with the onset of " hind-brain sleep ". My colleague, R. J. Berger,’ first observed such a fall in the extrinsic laryngeal muscles, however, since which time I have observed the same phenomenon in other muscle groups also, occurring particuMy in temporal relation to certain characteristic saw-toothed U.G. waves which bear a special connection5 with the rapid " " eye movements of hind-brain sleep and the dreams which s accompany them. There is, therefore, now evidence that during the progress of our dreams our skeletal musculature is paralysed. In further experiments, Bergerhas shown that awareness, albeit faulty, of external events can occur in dreams. It may be plausibly suggested that the victim of sleep paralysis is in, a state of "hind-brain sleep"in which he dreams, yet with a vague awareness of the environment, and in which he is therefore paralysed, a touch causing true awakening.
description
Department of Psychological Medicine, University of Edinburgh.
IAN I OSWALD. AN 0 SWALD.
SIR,-I read your leader with interest because I used to fairly frequent attacks. They usually occurred on waking and were accompanied by an unreasoning fear of falling asleep again. Subjectively, the condition resembled a light hypnotic trance. I found that it was possible to end an attack by breathing in sharply, though often more than one attempt was needed to produce the necessary sniff ". I pass this on in the hope that others may find this method suffer
"
1. Oswald, I. Proc. R. Soc. Med. (in the press). Jouvet, M. Arch. ital. Biol. 1962, 100, 125. Oswald, I. Sleeping and Waking: Physiology and Psychology. Amsterdam, 1962. 4. Berger, R. J. Science, 1961, 134, 840. 5. Berger, R. J., Olley, P. C., Oswald, I. Quart. J. exp. Psychol. 1962, 14,
2. 3.
183.
6. Berger, R. J., Oswald, I. Science, 1962, 137, 601. 7. Berger, R. J. University of Edinburgh, PH.D. thesis,
1962.
Noble’s
Hospital, Douglas,
Isle of Man.
J.
B. CAINE.
EARLY DIAGNOSIS OF IMPAIRED POSTOPERATIVE RENAL FUNCTION SIR,-May I congratulate Mr. Molloy (Oct. 6) on drawing attention to the usefulness of the urinary urea
concentration in
SLEEP PARALYSIS SIR,-Your leading article of Oct. 20 states that the victim " is usually fully aware of external events (unlike " the victim of nightmare)" and then quotes a typical " description in which the individual would feel that headless people or animals were climbing on the bed, or that he was being strangled. I would suggest, Sir, that the description is hardly that of someone " fully aware " and that his unpleasant experiences clearly resembled those of a
effective, because attacks of this condition are unpleasant and, as your leader states, can sometimes be extremely alarming.
assessing renal function postoperatively ? My experience1 confirms that this is the single most helpful piece of information that one can have in deciding whether a postoperative patient has an early acute renal failure, and thus needs a carefully balanced fluid intake, or whether the kidneys are ready to respond by diuresis to own
an
increased intake.
My one query would be about the level of urinary urea (above 1-1g. per 100 ml.) which Mr. Molloy accepts as normal. My evidence led to the conclusion that with a blood-urea of 100 mg. per 100 ml. or over, a urinary urea concentration of below 2-0 g. per 100 ml. indicated renal failure. Looking again at the data2 it appears that 8 out of 15 patients who subsequently developed acute tubular necrosis-confirmed at necropsyhad urinary urea levels above 1-1g. per 100 ml. Many of our observations were made upon patients several days after operation, whereas Mr. Molloy’s data apply to the first 24 hours. There is, however, no need to limit the use of the test to this early period. Incidentally,
when the postoperative urinary urea has been above 2 g. per 100 ml., I have only once known the kidneys fail to respond with an appreciable diuresis to an increased fluid intake. The patient concerned subsequently proved to have a complete arrest of blood-flow to one kidney. The remaining kidney was apparently already functioning close to its maximum. Department of Chemical Pathology, United Liverpool Hospitals, W. H. TAYLOR. Liverpool.
HOW MUCH FLUORINE? SiR,—You call attention to the rejection by the Kilmarnock Town Council of the continued addition of fluoride to the public water-supply. Two years ago you published3 an admirable survey of the medical and biological aspects of fluoridation. Although the fluoridation of public drinking-water supplies by the addition of 1 p.p.m. fluroride may seem desirable in view of the generally poor condition of teeth among British children, there are certain considerations in this country that indicate the wisdom of Kilmarnock’s action in the present state of our ignorance. Fluorine-containing ores, fluxes, and coals are used industrially in large quantities in many parts of this country.4 Fluorine compounds are toxic when inspired or ingested, and animals are moved from contaminated pasture; but human beings remain in a polluted atmosphere. Further we do not know the level of intake at which retention of fluorine may occur in different parts of the body in different people, nor the adverse influence of such retention on any pathological process which may affect particular organs. In the recent, admittedly imperfect, data published in a report5 on mortality in areas containing natural fluoride in their water-supplies (industrial fluorosis is not mentioned), it is of interest that the results in northern fluoride towns suggest an increased mortality of nephritis and nephrosis. Bond and Murray6 described the effects in rats of chronic fluorosis on 1. Taylor, W. H. Lancet, 1957, ii, 703. 2. Taylor, W. H., Reid, J. V. O. Brit. J. Surg. 1958, 46, 136. 3. Lancet, 1960, ii, 425. 4. Murray, M. M., Wilson, D. C. ibid. 1946, ii, 821. 5. Heasman, M. A., Martin, A. F. Mon. Bull. Min. Hlth, 1962, 21, 150. 6. Bond, A. M., Murray, M. M. Brit. J. exp. Path. 1952, 33, 168.
936 structure and function before such severe intoxication had resulted as to cause obvious skeletal lesions. In man the storage of fluorine in bone is seen typically among less privileged people, but similar lesions may be determined by congenital or acquired renal disease in any population.
kidney
Until further inquiry is undertaken to determine total fluorine hazards in different neighbourhoods, together with some estimate of the increased fluorine content of animal and vegetable foods due to the use of piped water containing added fluorine, it seems most undesirable that fluorine should be added to public water-supplies in
Britain. DAGMAR WILSON. THE EFFECT OF SALICYLATE ON THE UPTAKE OF 131I TRIIODOTHYRONINE BY THE RED CELLS SiR,—The uptake of 1311 triiodothyronine by the red
cells, introduced by Hamolsky et alphas proved useful as a diagnostic test of thyroid function.2-5 The test is a measure of the concentration of binding sites on thyroxine-binding
protein (T.B.P.) not occupied by thyroxine-i.e., of free T.B.P. capacity.6 It is therefore indirectly related to the concentration of thyroxine in the plasma. Under the conditions of the test
triiodothyro-
nine is distributed between the red cells, the a2-globulins-and p-globulins, and free T.B.P. Any substance which affected the binding of triiodothyronine by the red cells, the
tX2-globulins or P-globulins or T.B.P. might be expected to interfere with the mechanism of the test.
Salicylate increases the rate of dialysis salicylate. of thyroxine from human plasma, probably by interfering with the binding of thyroxine by the plasma proteins.’ At pH 7-4 salicylate interferes with the binding by T.B.P. of both thyroxine and triiodothyronine.8 It was therefore of interest to find out whether the administration of salicylate interfered with the uptake of "3’I-triiodothyronine by the red cells (T3 [R.B.c.]) when this was used as a test of thyroid function. T3 [R.B.c.] values have been determined in a series of patients undergoing treatment with salicylate for rheumatoid arthritis. Values above the normal range were found in more than half the patients tested (fig. 1). None of these patients had any clinical evidence of thyroid dysfunction. A significant increase in T3 [R.B.c.] values also occurs in normal people after a single oral dose of 1 -3 g. of aspirin. Salicylate added to blood in vitro has a similar effect, T3 [R.B.c.] values increasing as the concentration of salicylate in blood is increased (fig. 2). We have found that salicylate modifies the partition of triiodoFig. 1-Values for T3 [R.B.C.] in patients under treatment with
1.
2. 3. 4.
5. 6. 7. 8.
Hamolsky, M. W., Stein, M., Freedberg, A. S. J. clin. Endocrin. 1957, 17, 33. Robins, L. R. ibid. 1959, 19, 1292. Ureles, A. L., Murray, M. J. Lab. clin. Med. 1959, 54, 178. Walfish, P. G., Britton, A., Volpé, R., Ezrin, C. Canad. med. Ass. J. 1961, 84, 637. Goolden, A. W. G., Gartside, J. M., Jackson, D. J., Osorio, C. Lancet, 1962, ii, 218. Osorio, C., Jackson, D. J., Gartside, J. M., Goolden, A. W. G. Clin. Sci. 1961, 21, 355. Christensen, L. K. Nature, Lond. 1959, 183, 1189. Osorio, C. J. Physiol. 1962, 163, 151.
Fig. 2-Effect
on
T3
[R.B.C.]
values when sodium
salicylate is added
to blood in vitro.
thyronine between the red cells and the plasma-proteins by affecting the binding power of both thyroxine-binding protein and the a2- and p-globulins. These results are discussed in further detail elsewhere.e It is clearly important to exclude the recent administra-
tion of sodium salicylate or aspirin when the T3 [R.B.C.] test is used to assess thyroid function. Butazolidine in vitro also increases the uptake of 131I-triiodothyronine by the red cells and may well have a similar effect in vivo. Department of Radiotherapy, Medical Research Council Experimental Radiopathology Research Unit, Hammersmith Hospital, London, W.12.
A. W. G. GOOLDEN C. OSORIO.
HYPOXÆMIA AFTER GENERAL ANÆSTHESIA
interested in the article by Dr. Nunn and (Sept. 29). Whereas I agree that all patients suffering from a respiratory or cardiovascular insufficiency should be given oxygen in the postoperative period, I am not satisfied that hypoventilation may be ruled out as the cause of hypoxaemia in the cases under review.
SiR—I
am
Dr. Payne
All the
cases were given respiratory depressant drugs and respiration was unassisted. In my experience, by measuring tidal exchange, and acid-base levels in such anxsthetic management, I have always found a definite degree of hypoventilation, approximately 40% below preoperative level, and a rise in pCOz by 10-20 mm. Hg above preoperative level. In the series reported no mention was made of ventilation levels, or acidbase findings, during operation. It would have been interesting to have had more detailed information about the premedication of these cases. Was there
any diminution of minute volume before the induction of anarsthesia ? As there is no mention of the duration of the
operations concerned, it would be interesting to know if there could have been a hangover of the depressant effect of premedication on the postoperative period. Was there any monitoring of ventilation postoperatively? And if there was a respiratory inadequacy were the patients given any breathing exercises by the physiotherapists ? What posture was used in the postoperative period ? In the event of even mild obesity a head-up tilt of the bed will increase tidal exchange by at least 15%. These queries are of a very simple clinical nature, because I believe the solution of the problem at issue may be on such a level; the series of cases described represents
a cross-section of the type of patient met with in routine anxsthetic practice. It is well to remember that carbon dioxide is much more soluble than oxygen in aqueous fluids, and that it diffuses twenty times as rapidly. Any reduction of the alveolarcapillary membrane, as would result from the relative hypoventilation of a large proportion of alveoli, would cause hypoxaemia before there was any gross disturbance in acid-
9.
Goolden, A. W. G. Symposium
on
Salicylates,
1962. To be published.