tration as a cause of tetany. · received under mineral oil in a tube containing a little powdered...

ALKALOSIS VERSUS ABNORMAL SODIUM JON CONCEN- TRATION AS A CAUSE OF TETANY.

BY W. DENIS AND L. VON MEYSENBUG.

WITH THE ASSISTANCE OF JULIA GODDARD.

(From the Laboratory of Physiological Chemistry and the Department of Pediatrics of the School of Medicine, Tulane University, New Orleans.)

(Received for publication, June 25, 1923.)

The popularity of sodium bicarbonate therapy in pediatric practice has in recent years led to the recognition of numerous cases of tetany in children (l), presumably brought on by an excessive administration of the drug; and even a few examples of adult tetany apparently referable to an excessive administration of sodium bicarbonate have been reported in the literature (2).

Two views as to the cause of “bicarbonate tetany” have been advanced. According to Van Slyke (3) tetany is observed when the hydrogen ion concentration of the blood has attained a pH of about 7.3, whether this abnormal hydrogen ion concentration is caused by an uncompensated COa deficit or by an uncompensated alkali excess. Greenwald (4), however, maintains that the part played by alkalosis is a distinctly negligible factor, that the cause of tetany in these cases is the presence in the body of a prepon- deratingly large amount of sodium salts; in other words, that tetany following the administration of large amounts of sodium bicarbonate is a demonstration of the poisonous effect of the sodium ion. In proof of his view Greenwald has carried out many experiments on dogs in which he has shown that convulsions may be produced not only by the intravenous injection of large amounts of sodium bicarbonate but also by the administration of sodium chloride, phosphate, or sulfate.

In the summary to his last paper on the subject Greenwald makes the following statement:

“At the time convulsions appear, the concentration of sodium in the plasma is the same as was observed after the injection of other sodium

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Sodium Bicarbonate Tetany

salts (chloride, sulfate, phosphate). The convulsions are ascribed to ‘sodium poisoning,’ a disturbance, due to an excess of sodium, of the normal equilibrium between sodium and other ions.”

According to the views most commonly accepted the appearance of tetany is indicated by an increased irritability of the motor and sensory nerves to electrical or mechanical stimulation, and it is, we believe generally conceded by both clinicians and physiologists that it is practically impossible to state with absolute certainty whether convulsions observed in man or in animals are or are not due to tetany without a determination of the electrical reactions. As apparently most of the investigators who have worked on “sodium bicarbonate tetany” have not taken the precautions to make observations of electrical excitability it has seemed to us worth while to repeat some of the work involving the injection of sodium salts and in addition to observe the response of these animals to electrical stimulation.

Dogs were used throughout the investigation. These animals were brought to the laboratory at least, 1 week before operation, and only animals who appeared to be in good health were used. Our experiments were all carried out during the morning hours on animals who had had no food since noon of the previous day,

The general experimental procedures used were as follows:

After the animal had been fastened to an animal holder the inner surface of the leg and the abdomen were shaved. Ether was then administered, and as soon as anesthesia was sufficiently deep a tracheal cannula was inserted and a sample of blood (20 to 50 cc.) was removed from the carotid artery. A solution of the salt under investigation was then injected into the external jugular vein at intervals as indicated in the protocols of the individual experiments. Further samples of blood were removed from the carotid artery at appropriate times, and finally the electrical reactions of the peroneal nerve were determined before the administration of salt solutions and at approximately 15 minute intervals thereafter until the conclusion of the experiment.

At each withdrawal of blood two samples were taken; the first being received under mineral oil in a tube containing a little powdered potassium oxalate was used for the determination of the CO2 content by the method of Van Slyke and Cullen (5) and of the pH by the calorimetric procedure of Cullen (6), the second was removed with a syringe, allowed to clot in the refrigerator, and used for the determination of sodium by the method of Kramer and Tisdall (7), and of calcium by the procedure of Clark (8).

The electrical reactions were determined with a Victor galvanic wall plate to which a specially built milliammeter was attached. This milljam-


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W. Denis and L. von Meysenbug

meter has a range of from 0 to 10 milliamperes and is graduated in 0.1 milliampere. The stimulating electrode was of the globule Stinzig type, while the indifferent electrode was constructed of a wide band of copper to one margin of which a binding post had been attached, the electrode being covered with wadding so as to absorb the salt solution. This electrode was placed around the shaved abdomen of the animal and the edges were tied fairly tightly together. The peroneal nerve in the leg was sought and hav- ing been located, the Stinzig electrode was not moved until each group of reactions had been completed. Salt solution was used to keep the elec- trodes moist. Reactions which are considered characteristic of tetany or spasmophilia are those showing either anodal reversal (AOC < ACC and < 5 milliamperes) or COC < 5 milliamperes or CCTe = 5 milliamperes.

Reactions showing AOC < 5 milliamperes but > ACC are suggestive of approaching hyperirritability, but are not considered of the spasmophilic type by the majority of workers in this field.

Experiment I.

Adm~nnistration of Sodium Bicarbonate.

Dec. 20, 1922. Dog 1, male, weight 6 kg., a very young animal.

10.05 a.m. Ether administration started.

10.15-10.20 a.m. CCC ACC AOC cot 1.0 4.4 5.7 7.5

10.45 a.m. 40 cc. blood taken from the carotid artery (Sample 1).

10.50 a.m. CCC ACC AOC cot 1.0 4.3 >5 >5

11.20-11.30 a.m. Injected 50 cc. 10 per cent NaHCOp solution.

11.30 a.m. CCC ACC AOC cot 1.5 6.2 >lO >lO




11.45-11.55 a.m. Injected 50 cc. 10 per cent NaHCOs solution; at 11.50 a.m. respiration became much slower.

12.10 p.m. 50 cc. blood taken from the carotid artery (Sample 3).

12.20 p.m. CCC ACC AOC cot 1.5 3.5 2.7 9.0

The total amount of sodium bicarbonate injected was 15 gm. which is equivalent to 2.5 gm. per kg. (0.67 gm. Na per kg.).


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50 Sodium Bicarbonate Tetany

Analysis of Serum and Plaena.

Sample No. PH co2 NE& CS

ml. per cent mg. per 100 CC. n&7. per 1 co co.

1 7.4 42.8 361 10.3 2 7.45 78.0 449 10.4 3 7.6 94.6 478 10.4

Experiment 2.

Administration of Sodium Bicarbonate.

Dec. 29, 1922. Dog. 2, male, weight 16 kg.





11.30-11.32 a.m. Injected 50 cc. 10 per cent NaHCOa solution into external jugular vein.


12.10 p.m. 40 cc. blood taken from carotid artery (Sample 2).

12.20-12.24 p.m. Injected 100 cc. 10 per cent NaHCOa soIution into external jugular vein.

12.30 p.m. CCC ACC AOC cot 4.5 9.0 >lO >lO

12.50 p.m. Complete failure of respiration, 40 co. blood removed from the heart (Sample 3).


Sample No.

1 2 3

Anatysis of Serum and Plasma.

PH CO2 Na Ca

cd. per cent n&l. per 100 CC. mo. pe.7 100 co.

7.4 42.8 371 9.3 7.44 57.9 451 3.6 7.5 86 540 7.3


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Experiment 3.


Jan. 10, 1923. Dog 3, male, weight 9 kg.


9.40 a.m. CCC ACC AOC cot 1.0 4.0 7.3 10


10.09-10.15 a.m. Injected 50 cc. 10 per cent NaHCOs solution into the external jugular vein.


10.40 a.m. 50 cc. blood taken (Sample 2).


10.53-11.01 a.m. Injected 50 cc. 10 per cent NaHCOa solution.

11.02-11.06 a.m. Duplicated the above injections.

11.04-11.14 a.m. CCC ACC AOC cot 1.6 4.5 5.4 >lO


11.31-11.37 a.m. Injected 50 cc. 10 per cent NaHCOs solution.

12.00-12.04 p.m. CCC ACC AOC cot 1.5 3.5 4.4 >I0

12.15 p.m. 50 cc. blood taken (Sample 4).

1.00 p.m. CCC ACC AOC cot 1.0 3.3 245 9.0

3.35 p.m. Respiration failed and a final sample of blood was taken from the heart (Sample 5).


Analysis of Serum and Plasma.

Sample No. PH co, Na Ca

ml. per cent *. per 100 cc. mg. per 100 CC.

1 7.38 42.4 367 12 2 7.46 60.4 379 10.2 3 7.52 103.8 474 9.8 4 7.52 107.6 595 9.3 5 7.50 332 9.3


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Experiment 4. Administration of Sodium Bicarbonate.

Jan. 25,1923. Dog4, male, weight 12 kg.



9.35 a.m. CCC ACC AOC cot 1.3 6.5 4.5 >lO


10.00 a.m. Injected 50 cc. 10 per cent NaHCOI solution into the external jugular vein.





10.50 a.m. CCC ACC AOC cot 1.0 3.1 ,2.6 >lO



11.33-11.35 a.m. Injected 50 cc. 10 per cent NaHCG solution.

12.05 p.m. CCC ACC AOC cot 1.0 4.0 3.5 CCTe6

12.25 p.m. 45 cc. blood taken from the carotid artery (Sample 2).

3.00 p.m. CCC ACC AOC cot 1.3 3.5 4.4 CCTe 4.5

3.15 p.m. 40 cc. blood taken from carotid artery (Sample 3).



Ssmple No.

1 2 3

PH Co, Na CS

s-31. per cent m#.per1wce. mg.pw1ooco.

7.4 33.4 12.0 71.58 96 .,2 444 10.1 7.44 ,69.2 463 9.6


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W. Denis and L. von Meysenbug 53

Experiment 6.


Mar. lQ,lQ23. Dog 5, young male, weight 10.2 kg.

8.50 a.m. Administration of ether started.



9.20-9.21 a.m. Injected 50 cc. 10 per cent NaHCOs solution into the external jugular vein.




10.03-10.05 a.m. Injected50 cc. 10 percent NaHCOs solution.




11.21-11.24 a.m. Injected 50 cc. 10 per cent NaHCO( solution.

11.25 a.m. CCC ACC AOC cot 2.5 5.4 3.0 9.0

11.42 a.m. Respiration which had become very slow and shallow ceased entirely.

11.44 a.m. 50 cc. blood taken from the heart (Sample 3).



sample No.

1

2 3

PH cot NU CS

ml. per unt nag. per 100 co. mo. per loo cc.

7.4 41.4 347 10.8 7.56 98.2 528 9.0 7.52 97.0 481 7.9


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Sodium Bicarbonate T&any

Experiment 6.

Administration of Sodium Chloride.

Feb. 12, 1923. Dog 6, male, weight 14 kg.


9.30 a.m. CCC ACC AOC cot 1.0 >lO >lO >lO


10.15 a.m. CCC ACC AOC cot 1.6 3.0 >5 >5

10.20-10.26 a.m. Injected 50 cc. 10 per cent NaCl solution into the external jugular vein.


10.36-10.33 a.m. Injected 50 cc. 10 per cent NaCl solution.





11.25 a.m. 40 cc. blood withdrawn (Sample 2).



11.55 a.m. Spasmodic twitching of the muscles was noted.


12.20 p.m. CCC ACC AOC cot 5.5 7.0 >lO >lO

3.00 p.m. CCC ACC AOC cot 7.5 >lO >lO >lO


3.25 p.m. Animal killed.

The total amount of sodium chloride injected was 20 gm. which is equivalent to 1.4 gm. per kg. (0.54 gm. Na per kg.).


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55

Sample No. PH CO,

7.4 7.4 7.36 7.36

001. pm cent

55.0 30.5 20.2 14.5

Na CB Cl ~-

n&g. pm 100 cc. nag. per 100 cc. mQ. pm 100 cc.

370 12.1 388 441 12.1 465 441 11.9 472 433 10.3 469

Experiment 7.

Administration of Sodium Chloride.

Feb. 21,1923. Dog 7, female, weight 15 kg.



9.45 am. 50 cc. blood taken from the carotid artery (Sample 1).

9.55-9.59 a.m. Injected 50 cc. 10 per cent NaCl solution into the external jugular vein.







10.50 a.m. Heart stopped beating. 50 cc. blood taken from the heart (Sample 2).

The total amount of sodium chloride injected was 20 gm. which is equivalent to 1.3 gm. per kg. (0.50 gm. Na per kg.).


Sample No.

1 2

co, Na Ca Cl

vol. pLw cdnt ?n*. per 100 cc. mg. per 100 cc. mg. per 100 co.

48.8 372 11.2 382 21.1 464 10.4 475


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Experiment 8.

Administration of Sodium Sulfate.

Feb. 5, 1923. Dog 8, young male, weight 7 kg.




9.26-9.29 a.m. Injected 50 cc. 10 per cent Na$Od solution (an- hydrous) into the external jugular vein.


9.46-9.48 a.m. Injected 50 cc. 10 per cent Na&Oa solution.


10.01-10.03 a.m. Injected 50 cc. 10 per cent Na&SOc solution.

10.10 a.m. Urine, which appeared to be extremely dilute, began to drip from the urethra, and continued to do so during the remainder of the experiment.


10.13-10.20 a.m. Injected 50 cc. 10 per cent NazSOd solution.

10.40 a.m. CCC ACC AOC cot 2.5 5.2 8.5 * >lO

10.421044 a.m. Injected 50 cc. 10 per cent NazSOc solution.

10.45 a.m. Respiration very slow, pulse good, no eye reflex, but fore- legs began to shake, and a general twitching and jerking of all the muscles of the body were noted.


10.58 a.m. No eye reflex, the muscular spasms had stopped.


11.05 a.m. Muscular twitchings and jerkings had returned, there was violent twitching of the whiskers, no eye reflex.

11.09 a.m. Another convulsive seizure had begun and lasted about half a minute. In the intervals between convulsions the respirations were very rapid.

11.13 a.m. Another convulsive seizure had begun.


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11.40 a.m. Animal quiet.

ccc ACC AOC cot 3.0 4.6 7.5 >lO

11.50 a.m. Injected 20 cc. 10 per cent CaCla solution subcutaneously into two areas in the thigh.

12.10 p.m. Injected 15 cc. 10 per cent C&la solution into the femoral vein. The convulsions continued at intervals and were apparently unaffected by the administration of the calcium salt.

12.20 p.m. 50 cc. blood taken (Sample 3). The animal which still continued to have convulsions at intervals was killed at 12.35 p.m.

The total amount of sodium sulfate injected was 25 gm. which is equivalent to 3.5 gm. per kg. (1.16 gm. Na per kg.).


Sample No. pH co2 Na ca R~lWCke.

~- ___-

ml. per cent y&r . T%z

1 7.4 42 391 12.1 2 7.32 27.7 572 8.9 3 7.28 16.4 539 30.6 After CaCln injection

intravenously. -

Experiment 9.

Administration of Sodium Sulfate.

Mar. 14, 1923. Dog 9, male, weight 8.1 kg.




9.11-9.13 a.m. Injected 50 cc. 10 per cent NaaSOd solution into the external jugular vein.


9.32-9.35 a.m. Injected 50 cc. 10 per cent Na2SOh solution.



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Sodium Bicarbonate Tetany

9.53-9.55 a.m. Injected 50 cc. 10 per cent NapSOd solution.


10.14-10.16 a.m. Injected 50 cc. 10 per cent Na2SO‘ solution.

10.15 a.m. Respirations became very slow.


10.51-10.55 a.m. Injected 50 cc. 10 per cent Na,SO, solution.

11.55 a.m. Dog died of respiratory failure.

The total amount of sodium sulfate injected was 25 gm. which is equivalent to 3.1 gm. per kg. (1.03 gm. Na per kg.).

Analyses of Serum and Plasma.

Sample No.

1 2

PH co2 N8

ool. per cent mg. per 100 cc.

7.35 30.5 321 7.32 23.3 491

Ca

m!J. per 100 cc.

10.9 9.9

Controls.

In order to study the effect of prolonged etherization on the electrical excitability of the peripheral nerves the following two experiments were carried out.

Experiment 10.

Feb. 5, 1923. Dog 10, female, weight 4 kg.

9.15 a.m. Ether administration begun.

9.45 a.m. CCC ACC AOC cot 1.0 3.0 5.0 5.5

10.05 a.m. 30 cc. blood withdrawn from carotid artery.

11.00 a.m. CCC ACC AOC cot 1.2 3.0 4.9 5.5

12.00 m. ccc ACC AOC cot 1.2 2.9 5.5 >lO

1.30 p.m. Dog died.


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Experiment 11.

Feb. 8, 1923. Dog 11, male, weight 7.8 kg.

8.50 a.m. Ether begun.



11.00 a.m. Dog died.

A summary of Experiments 1 to 11 inclusive is given in Table I. It will be noted that with the exception of Experiment 2, in

which the dosage of sodium bicarbonate was low, all the experiments in which this salt was injected resulted in the attainment of a condition of hyperirritability as shown by the spasmophilic reactions, which were invariably observed. On the other hand, in the two experiments in which sodium chloride was injected the electrical reactions showed a constant decrease in irritability, although serum sodium rose 19 and 24 per cent, respectively, and the calcium showed a slight decrease. In the two experiments in which sodium sulfate was injected it was noted that after two or three injections of the salt the reactions approached the spasmophilic type, but on the injection of more sodium sulfate they again became normal. In both the sodium chloride and the sodium sulfate experiments marked acidosis developed as shown by the fall in CO2 content of the plasma, and in all these experiments there was also a fall in the calcium concentrations, which latter finding is difficult to explain except on the theory of dilution of the blood by the large volumes of fluid injected.

With the exception of Experiments 2,10, and 11 there invariably occurred, sometimes after two or three injections of salt, sometimes only after the entire amount had been given, various twitching and jerking movements, frequently associated with great rigidity of the limbs, which might well be termed “convulsions,” but which in the case of the dogs injected with sodium chloride and sodium sulfate were accompanied by electrical reactions which were abso- lutely normal.

Our results are therefore confirmatory of the findings of Green- wald, as regards the production of convulsive movements in dogs


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aslt wed.

NaHCOs

NaHCOa

NaHCOs

NaHCOs

NaHCOs

NaCl

Ntl Remarka.

um. w ko.

I.67

9.25

0.59

0.54

0.65

5.54

TABLE I.

Summary of Experiments 1 to 11.

Reactions taken after the last portion of NaHCOs solution had been injected were of spasmophilic type. Examination of serum showed no change in calcium; sodium rose from 361 to 478 mg.; pH from 7.4 to 7.6; and COn from 42.8 to 94.6 vol. per cent.

Reactions show a constant decrease in irritability. Examination of serum showed a decrease of calcium from 9.3 to 7.3 mg.; sodium rose from 371 to 540 mg.; pH from 7.4 to 7.5; and CO2 from 42.8 to 86 vol. per cent.

Observations taken after final injection of NaHCOs showed reactions of spasmophilic type. Examination of serum showed a decrease in calcium from 12 to 9.3 mg.; a rise in sodium from 367 to 595 mg.; in pH from 7.38 to 7.5; and in CO* from 42.4 to 107.6 vol. per cent.

Reactions taken after the last injection of sodium bicarbonate showed definite spasmophilia. The serum calcium fell from 12 to 9.6 mg.; the pH rose from 7.4 to 7.58; and the CO* from 33.4 to 96.2 vol. per cent.

Reactions taken after the last injection of sodium bicarbonate showed definite spasmophilia. The serum calcium was found to have fallen from 10.8 to 7.9 mg.; the sodium rose from 347 to 528 mg.; pH from 7.4 to 7.52; and COz from 41.4 to 98.2 vol. per cent.

Reactions showed a constant decrease in irritability. The serum calcium was decreased from 12.6 to 10.3 mg.; sodium increased from 370 to 441 mg.; pH decreased from 7.4 to 7.36; and CO* from 55.0 to 14.5 vol. per cent.


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E;rn7 NO.

7

8

9

10

11

Salt used.

NaCl

NaaSO,

NaGSOd

Control.

Control.

TABLE I-Conchded.

NS

urn. per ko.

0.50

1.16

1.03

-

Reactions showed a constant decrease in irritability. The serum calcium decreased from 11.2 to 10.4 mg.; sodium increased from 372 to 464 mg.; and CO* decreased from 48.8 to 21.1 vol. per cent.

Reactions taken at 10.15 a.m. after the third injection of Na&SOc approached the spasmophilic type, but never definitely reached it. Those taken after the final injection were normal. Serum calcium decreased from 12.1 to 8.9 mg.; sodium increased from 391 to 572 mg.; pH decreased from 7.4 to 7.28; and CO% from 42 to 16.4 ‘vol. per cent.

Reactions taken at 9.45 a.m. after the second injection of NatSO, approached the spasmophilic type. At 10.10 a.m. (after the third injection) they were normal. The serum calcium fell from 10.9 to 9.9 mg.; sodium increased from 321 to 491 mg.; and CO8 decreased from 30.5 to 23.3 vol. per cent.

Reactions obtained at intervals for 3 hours on an etherized dog showed no striking variations.

Reactions obtained at intervals for a period of 2 hours on an etherized dog showed no striking variations.

by the injection of large quantities of sodium bicarbonate, sulfate, and chloride, but we are entirely unable to confirm or agree with the conclusions of this author regarding the point that these convulsions are invariably those of true tetany, brought on by the pressure of an excess of the sodium ion. We have done no work with sodium phosphate as Jeppsson (9) has recently published the


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results of an extensive series of experiments in which he tested the electrical reactions after the administration of a series of sodium and potassium salts. As a result of this work he is able to state definitely that of the sodium salts used only the disodium phosphate was active in producing a spasmophilic condition. A some- what similar result was obtained by Tisdall (10) who found that dogs which received injections of phosphoric acid showed no ill effects while those which were given disodium phosphate showed muscular twitchings which this author interprets as suggestive of incipient tetany. Unfortunately, data regarding the electrical reactions are not included in this latter work. We feel that the experimental results described in this paper give support to the theory that the spasmophilic condition which sometimes follows the excessive ingestion of sodium bicarbonate is probably due to an

H&OS abnormal NaHC03 ratio (11) and not to an abnormal ratio between

the calcium and sodium ions. The suggestion has frequently been made that a decrease in the

hydrogen ion concentration of the serum might result in a decreased ionization of serum calcium, a fact which must be considered in connection with the interpretation of the results pre- sented in this paper.

Brinkman (12) and Brinkman and Van Dam (13) have recently published observations on the calcium ion concentration in serum and emphasize strongly the importance of its exact maintenance. According to these authors this maintenance of calcium ion concentration depends on the ratio between the concentration of hydrogen and bicarbonate ions.

More recently one of us together with Pappenheimer, Zucker, and Murray (14) published results obtained in dialysis of serum calcium where the serum and dialyzing fluid were saturated with COz mixtures, the saturation of the serum varying between 17 and 62 mm. of mercury tension. Such a wide range of COe saturation, while, of course, altering the pH of the fluid (from 7.6 to 7.2,) did not result in an increased ionization of the serum calcium as shown by the percentage of diffusible calcium.


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STJMMARY.

In a series of experiments which was planned to throw light on the cause of the tetany following excessive sodium bicarbonate administration it was found that when sodium bicarbonate was introduced into dogs by intravenous injection there followed, when the dosage was sufficiently large, various twitching and jerking movements, together with an increased irritability to electrical stimuli. Examination of the blood serum indicated a slight lower- ing of the calcium content, and an increase in the sodium, C02, and pH.

When sodium chloride or sodium sulfate was injected in place of the bicarbonate, “convulsions” similar to those noted above invariably appeared, but a determination of the electrical reactions showed that in these animals a normal or a decreased irritability prevailed. Examination of the blood serum showed an increased sodium content and a decrease in calcium, COz, and pH.

Our results therefore make it seem improbable that the spasmophilic condition following excessive sodium bicarbonate injection is due to “sodium poisoning,” but rather to an abnormal

H&03 NaHCOs ratio.

BIBLIOGRAPHY.

1. Howland, J., and Marriott, W. McK., Quart. J. Med., 1917-18, xi, 289. 2. Harrop, G. A., Jr., Bull. Johns Hop&&s Hosp., 1919, xxx, 62. 3. Van Slyke, D. D., J. BioZ. Chem., 1921, xlviii, 153. 4. Greenwald, I., J. Biol. Chem., 1922, liv, 285. 5. Van Slyke, D. D., and Cullen, G. E., J. Biol. Chem., 1917, xxx, 289. 6. Cullen, G. E., J. Biol. Chem., 1922,1, p. xvii. 7. Kramer, B., andTisdal1, F. F., J. BioE. Chem., 1921, xlvi, 339. 8. Clark, G. W., J. Biol. Chem., 1921, xlix, 487. 9. Jeppsson, K., Z. Kinderheilk., 1921, xxviii, 71.

10. Tisdall, F. F., J. Biot. Chem., 1922, liv, 35. 11. Collip, J. B., andBackus, P. L., Am. J. Physiol., 1920, Ii, 568. 12. Brinkman, R., Biochem. Z., 1919, xcv, 101. 13. Brinkman, R., and Van.Dam, E., Proc. Koninklijke Akad. Wetensch.

Amst., 1919, p. xxii. 14. von Meysenbug, L., Pappenheimer, A. M., Zucker, T. F., and Murray,

M. F., J. Biol. Chem., 1921, xlvii, 529.


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assistance of Julia GoddardW. Denis, L. von Meysenbug and With the

CAUSE OF TETANYSODIUM ION CONCENTRATION AS A

ALKALOSIS VERSUS ABNORMAL

1923, 57:47-63.J. Biol. Chem.

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tration as a cause of tetany. · received under mineral oil in a tube containing a little powdered...

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