MOVEMENTOF POTASSIUMINTO SKELETAL MUSCLEDURINGSPONTANEOUSATTACKIN FAMILY PERIODIC PARALYSIS

BY KENNETHL. ZIERLER ANDREUBIN ANDRES

(From the Departments of Environmental Medicine and Medicine, The Johns HopkinsUniversity and Hospital, Baltimore, Md.)

(Submitted for publication July 5, 1956; accepted January 24, 1957)

It has been appreciated since the classical stud-ies of Biemond and Daniels (1) and Aitken, Allott,Castleden, and Walker (2) that the concentrationof potassium in serum falls during attacks in pa-tients with typical family periodic paralysis. Al-lott and McArdle (3), Pudenz, McIntosh, andMcEachern (4) and Ferrebee, Atchley, and Loeb(5) showed that the quantity of potassium ex-creted in urine was reduced during attacks ofparalysis. These observations implied that duringattacks potassium shifted from extracellular tosome intracellular space. Metabolic balance stud-ies by Danowski, Elkinton, Burrows, and Winkler(6) confirmed this hypothesis. The question ofwhich intracellular space accepted the potassiumthat shifted during attacks remained unanswered.

Recently it has been reported from this labora-tory that there is a diurnal variation in normalman in exchange of potassium between skeletalmuscle and extracellular water (7). During thehours between 10 P.M. and 12 noon, that is, 4 to18 hours after the last meal, with the subject at

rest, potassium moves from muscle to blood, therate declining to a minimum or even reversingslightly (potassium moves from blood to muscle)between the hours of midnight and 7 A. M., andthen rising again to a peak between 10 A.M. andnoon. It is characteristic of family periodic paraly-sis that most attacks begin during the middle of thenight (8). This suggested that in patients withthis disease there may be an exaggeration of thediurnal variation in potassium movement, and thatmovement of potassium from extracellular fluidinto skeletal muscle during the night might be re-

' This work was performed under a contract betweenthe Office of Naval Research, Department of the Navy,and The Johns Hopkins University (NR 113-241) andwas further supported by grants-in-aid from the NationalInstitutes of Health, Department of Health, Education,and Welfare (A-750) and the Muscular Dystrophy As-sociations of America, Inc.

sponsible for the attacks. It is the purpose of thisreport to present data indicating that this is thecase.

METHODS

Two subjects were studied. Both had well-documentedfamily periodic paralysis with a history of spontaneousattacks of flaccid paralysis frequently having their onsetin the middle of the night and associated with definitehypokalemia.

Subject M. H., a 14-year-old boy weighing 57 Kg.,had had episodes of weakness and paralysis since age 12.All the attacks began between 11 P.M. and 9 A.M. Theywere relieved or prevented by administration of potas-sium chloride, and serum potassium concentration duringat least one attack was found to be low. The severity ofhis attacks was much less than that of the second patient.

Subject M. H. was studied on three occasions:Study I was performed between 11:30 A.M. and 12

noon during spontaneous recovery from a mild attackwhich had begun spontaneously during the night. Hehad had no food since supper at 6 P.M. the evening priorto study.

Study II covered the hours between midnight and 7A.M. The last meal was at 6 P.M. When a spontaneousattack did not occur by 2:20 A.M., an attack was inducedby administration of glucose and of insulin.

Study III covered the hours between 1 A.M. and 7A.M. During the afternoon prior to study M. H. exer-cised heavily on a treadmill and at 6 P.M. ate a largedinner. There was no clinical evidence of an attackduring the time of this study.

Subject A. B., a 24-year-old college student weighing77 Kg., was a member of a family of whom six membershad clinical evidence of periodic paralysis. His attacksbegan at age 12. There were one to three severe attacksand more frequent mild attacks each month until age 18when he was first placed on prophylactic potassium ther-apy. Circumstances under which attacks occurred werequite predictable. Attacks followed heavy exercise andhigh carbohydrate meals, were aborted by mild exerciseand ingestion of potassium chloride. Onset of attackswas usually in the middle of the night and some of hisattacks were quite severe, involving not only the extremi-ties but also respiratory muscles.

Subject A. B. was studied on one occasion. Prophy-lactic potassium therapy was discontinued 24 hours prior

730

MUSCLEPOTASSIUM UPTAKE IN PERIODIC PARALYSIS 731

TABLE I

Net movement of potassium during sponaneous nocturnal attack-Subject A. B.*

jO OralTime A A-V P&E./min./ KCIA.M. mEq./L. mEq./L. 100mI. forearm g. Muscle strength Tendon reflexest

12:12 2.47 0.74 1.8 Normal B-1; T-2K-2, 2

1:08 2.11 0.60 1.31:25 Rapid decrease in arms; legs B-0; T-0

to fairly strong. K-1, 0; A-2, 11:552:08 2.11 0.55 0.92:55 Maximal inspiration reduced,

but no dyspnea. Neckflexion very weak.

3:08 1.91 0.44 0.84:00 1.85 0.49 1.1 Extremities almost totally

paralyzed. (Severe EKGabnormalities.)

4:10 54:40 5 Subjective improvement. No B-0; T-1

objective change. K-0, 0; A-2, 15:48 2.75 0.61 0.8 EKGless abnormal6:25 2.73 0.36 0.7 5 Extremity strength slightly B-0; T-2

improved. Inspiration K-1, 0; A-2, 1stronger. (EKG-returnto severe changes.)

7:10 57:13 3.11 -0.20 -0.4 Head can be raised off pillow.7:43 3.45 -0.50 -0.89:00 5.40 -0.61 -1.3 Nearly recovered. B-2; T-i

K-3, 2; A-2, 210:03 5.91 -0.33 -0.7 Essentially normal.

* A = c.oncentration of potassium in arterial plasma; A-V - arteriovenous difference in plasma concentration ofpotassium; Q = net uptake (or net release when value is negative) of potassium by forearm tissues.

t B = biceps, T = triceps, K = knee, A = anide. Only the right biceps and triceps reflexes could be tested;metabolic studies were made on the left arm. 0 = absent, 1 = reduced, 2 = normal, 3 = hyperactive. In the kneeand ankle jerks, the first number refers to the right side, the second to the left side.

to this study. He received 100 g. of glucose at 3:30 P.M.,ate his usual supper at 5:30 P.M. with extra dessert plus100 g. of glucose at 6:30 P.M. Measurements were madebetween midnight and 10 A.M. A severe attack occurredand it was necessary to treat him with KCI.

Measurements were made of the metabolism of forearmmuscles with the subject at rest. Uptake and release ofpotassium, O2, CO2, glucose and lactate were calculatedas described previously (7, 9) as the products of forearmblood flow and arteriovenous differences of the metabo-lites. Venous blood was obtained through a catheterplaced in a deep vein draining forearm muscles. Ar-terial blood was from the brachial artery. A pressurecuff about the wrist, inflated to greater than systolicpressure, excluded blood flow to hand and wrist duringperiods of blood collection.

Certain extrapolations of the data are made. In theseit is assumed that uptake or output per min. per 100 ml.of forearm can be converted to uptake or output per mi.per 100 g. of forearm muscle by multiplying by %, a con-version factor estimated previously (9). It is further as-sumed that extracellular fluid weighs 20 per cent of bodyweight and that total muscle mass is 40 per cent of bodyweight

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FIG. 1. ARIERAL. AND VENOUS PLASMA POTASSIUMCONCENTRATIONSDURING ATTACK AND RECOVERY INPATIENT A. B.

At each time indicated by arrows 5 g. KCI was givenorally.

KENNETHL. ZIERLER AND REUBIN ANDRES

RESULTSANDDISCUSSION

Potassium Movement During Spontaneous Attack

and Spontaneous Recovery

Subject A. B. (Table I and Figures 1 and 2)

Arterial potassium concentration was alreadyreduced greatly by the time the first sample was

drawn at midnight and continued to fall for thenext four hours, after which it was necessary to

treat the patient by administration of KCI. Insubject A. B., between midnight and 4 A.M., ex-

traction of potassium (i.e., A-V difference dividedby arterial concentration) was approximately 25per cent. In normal subjects little or no extractionof potassium occurs during these hours.

During the attack potassium moved from plasmainto muscle at a rate of 1.2 puEq. per min. per 100ml. forearm. Between midnight and 4 A.M., con-

centration of potassium in arterial plasma fell 0.6mEq. per L., a loss of about 9.5 mEq. of potassiumfrom total extracellular fluid. During that timeabout 2 mEq. of potassium moved from plasmainto muscles of one forearm. If all skeletalmuscles were behaving identically, about 110nEq. of potassium might have moved from ex-

tracellular fluid into muscle in the four-hour pe-riod. Since this figure is about 12 times as largeas the estimated loss of extracellular potassium itfollows either that forearm muscles were extract-ing potassium from plasma at a rate about 12

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FIG. 2. POTASSIUM MOVEMENTBETWEENPLASMA ANDMUSCLEDURING THE NIGHT

Positive values are uptake, negative values are releasefrom muscle. B, subject A. B. during attack and re-

covery; K and C, normal subjects; H, subject M. H.who had periodic paralysis but failed to get an attack

during this study. Arrows indicate oral administration of5 g. KCI to A. B.

times greater than the average muscle or that po-tassium was added to plasma from some non-muscular source.

Although the mass of potassium lost from ex-tracellular fluid was large from the viewpoint ofextracellular potassium, if it all went into skeletalmuscle this quantity of potassium would be suffi-cient to raise the average concentration of intra-muscular potassium by only a few per cent, anamount too small to be detected by availablemethods.

When KCI was administered, although therewas some elevation of arterial potassium concen-tration, extraction of potassium remained con-stant for the next two and one-half hours and po-tassium continued to move into muscle until thedirection of movement was reversed at 7 A.M.,several hours earlier than the onset of acceleratedoutput of potassium by muscle in normal subjects.

In summary, an attack of paralysis developed inthe middle of the night about seven hours after aheavy carbohydrate meal. Potassium moved fromplasma into skeletal muscle, concentration of po-tassium in plasma was reduced and paralysis oc-curred. Efforts to terminate the attack by oraladministration of potassium failed to do so duringa two-hour period in which potassium continuedto move from plasma into muscle and there wasonly a small increase in concentration of arterialpotassium. Presumably, during these two hourspotassium movement out of extracellular spaceinto muscle almost kept pace with intestinal ab-sorption of administered potassium. Later in themorning the direction of potassium movementreversed; potassium moved out of muscle intoextracellular space at a rate greater than that seenin normal subjects during these hours. Concen-tration of potassium in arterial plasma roseabruptly and the attack ended. Although the risein concentration of potassium in arterial plasmamay have been the result of absorption of ad-ministered potassium from the gut as well as ofoutpouring of potassium from skeletal muscle, thelatter factor alone was sufficient to account forthe observed rise in plasma concentration.

Subject M. H., Study I (Table II, Figure 3)Subject M. H. failed to have a spontaneous at-

tack during the time measurements of forearm

732

MUSCLEPOTASSIUM UPTAKE IN PERIODIC PARALYSIS

TABLE IIPotassium release during spontaneous recovery from

spontaneous attack-Subject M. H.*

Time A A-V !

11:39 4.09 -1.05 -3.8511:50 4.10 -1.15 -6.2312:00 4.08 -0.87 -3.70

* Time is A.M. Symbols as in Table I.

metabolism were made. However, forearm me-

tabolism was measured on the morning followinga mild spontaneous attack from which he wasI re-

covering spontaneously. At the time of the studythere was no longer any gross weakness. Deeptendon reflexes in the arms were normal butpatellar and ankle responses were still slightly de-pressed. Release of potassium from muscle was

about six times greater than the average ratefound in normal subjects during the same time ofthe day. Presumably at some earlier hour duringthe attack there was a reduction in plasma potas-sium concentration. The rate at which potassiummoved from muscle to extracellular fluid duringrecovery, 3 to 5 mEq. per hr. per Kg. of muscle,was adequate to account for an increase in plasmapotassium concentration. Despite the large con-

tribution of potassium to venous plasma frommuscle, concentration of potassium in arterialplasma was stable at about 4 mEq. per L. duringthe period of observation. This stability of ar-

terial potassium could obtain only if potassiumleft the blood stream by some other route as fastas it entered from skeletal muscle.

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FIG. 3. POTASSIUMOUTPUTFROMMUSCLETO PLASMADURING SPONTANEOUSRECOVERYFROMA SPONTANEOUSATTACK OF PARALYSIS IN SUBJECT M. H.

*, data from normal subjects in the basal state.

Potassium Movement During an Attack Producedby Administration of Glucose and Insulin

Subject M. H., Study II (Table III)During Study II of subject M. H., when a

spontaneous attack had not occurred by 2:20 A.M.a mild attack was produced by administration ofglucose and insulin. At 6:25 A.M. he was given9 g. KCI by mouth. Within 25 minutes there wassome return of deep tendon reflexes.

WhenKCI was administered there was a rapidrise in arterial potassium concentration despitea large increase in rate of potassium uptake bymuscle. An uptake of this magnitude did notoccur following potassium administration to sub-ject A. B. at approximately the same time of day.The difference in response is probably attributableto the effect of insulin, since the behavior of bloodglucose concentrations indicated that a potent in-sulin action occurred at the time of massive uptakeof potassium.

From the rise in concentration of potassium in

TABLE III

Net movement of potassium during attack induced byglucose and insulin-Subject M. H., Study II*

jiEq./Time A A-V mtn./100A.M. mEq./L. mEq./L. ml. forearm Comments

12:20 4.41 -0.06 -0.4 Strength and reflexesnormal.

1:20 4.44 -0.11 -0.82:21 4.31 -0.16 -1.2 No symptoms or signs of

impending attack.2:25 130 g. glucose in 240 ml.

to orange juice.2:402:40 Insulin, 20 U., subcu-

taneous.3:02 4.09 -0.34 -2.63:55 4.18 -0.01 -0.1 No change in strength or

reflexes.3:55 25 g. glucose, I.V.

to4:054:07 Insulin, 6 U., I.V.4:41 3.68 0.08 0.7 Strength greatly

diminished. Tendonreflexes absent.

5:29 3.73 0.26 1.86:03 3.68 0.03 0.36:15 Further weakness. Re-

flexes remain absent.6:25 9 g. KCI orally.6:40 4.95 0.68 6.6 Reflexes and strength re-

turning.6:58 5.56 0.45 6.7 Almost complete

recovery.

* Symbols as in Table I.

733

KENNETHL. ZIERLER AND REUBIN ANDRES

arterial plasma, from the measured uptake of po-tassium by muscles of the forearm, and from rea-sonable assumptions of the size of extracellularspace and total muscle mass in M. H. it can beestimated that of the 120 mEq. of potassium ad-ministered about 20 mEq. went into extracellularspace and about 65 mEq. went into skeletalmuscle in 33 minutes, leaving about one-fourthunaccounted for. Similar calculations made forthe case of A.B. following the first 10 g. of ad-ministered KCI (Table I) indicated that of the135 mEq. of potassium administered about 14mEq. went into extracellular space and about 35mEq. went into muscle in two hours, leavingabout two-thirds of the potassium unaccounted for.This suggests that the failure of oral administra-tion of KCI to produce prompt restoration of nor-mal potassium concentration in arterial plasmaand clinical recovery may have been in part due todelayed absorption of potassium from the gut dur-ing the more severe attack suffered by A. B.

Normal Pattern of Potassium Movement Duringa Night When No Paralytic Attack Occurred

Subject M. H., Study III (Figure 2)During the early part of Study II, between mid-

night and 2:20 A.M., subject M. H. had no spon-taneous attack and potassium movement at thistime was indistinguishable from that observed innormal men. In Study III, between 1 A.M. and7 A.M., subject M. H. again had no spontaneousattack and potassium movement appeared to benormal.

Fragmentary Observations on Other Abnormali-ties of Muscle Metabolism Occurring During aSpontaneous Attack of Paralysis (Table IV)Certain observations discovered during the at-

tack in A. B. which differ from those obtained innormal subjects are reported. These differencesmay prove ultimately to be of no significance sincethe number of normal subjects studied is small.On the other hand, even if they prove to be realdepartures from the normal it is not clear whetherthese differences are fundamental to the disease,whether they represent a defect parallel to butunrelated to the anomaly of potassium movement,whether they are in some way causally related to

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potassium movement, or whethquences of the disease. Nonedifferences appeared in subjectduring the night in which hespontaneous attack.

Concentration of glucose indefinitely higher in subject A. Iduring the night (Figure 4), a

the first four measurements Aences were higher than normal.previously (10) that A-V gvaried directly with arterial gtions in normal subjects duringrelation was true also for subjithe abnormally high glucose A-glucose uptakes in this subjectfrom abnormally high deliveimuscle. Since the concentraticcose tended to decrease duringunexpected that glucose uptalcrease similarly.

Although interpretation of tJtrations of glucose in arterial bi

by the fact that A. B. had a highsix and nine hours before thewas collected, even the last arteri16 hours after the last meal shnormal glucose concentration,(mean arterial glucose concent18-hour fast in 24 normal subjecL. 0.27 S.D.).

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in arterial blood implies that

failed to remove circulating glucose or that hepaticcontribution of glucose was accelerated.

Concentration of lactate in arterial blood waswithin normal limits during the early part of thestudy and rose during the later hours (Figure 5),approximately coincident with recovery from

HKH K paralysis. Lactate production by muscle was er-t CK^ ratic. There is no evidence that the rise in ar-

terial lactate concentration was owing to increasedproduction of lactate by skeletal muscle in theforearm. It is possible, however, that other

6 10

GLucosEmuscles did contribute, since muscle power and

I recovery; C, K ad deep tendon reflexes were examined from time toH. who failed to de- time during this period.sis. During the night and the following morning,

forearm blood flow in subject A. B. was withiner they are conse- the limits defined by studies of two normal sub-of these metabolic jects during the night (10) and a larger group ofM. H., Study III, normal subjects during the late morning (9).

failed to have a Nor were there any deviations from normal in02 uptake, in CO2 production or in A-V differ-

arterial blood was ences of CO2 or 02 content. However, the ar-

B. than in normals terial concentration of CO2, initially normal, fellnd at least during to levels lower than those in normal subjects-V glucose differ- (mean of 24 normal subjects, 21.9 mEq. per L. 4

It has been noted 0.98 S.D.) (Figure 6). Although pH was notlucose differences measured, this decrease in arterial CO2 presum-

Ylucose concentra- ably represented extracellular metabolic acidosis.> the night. This Mean respiratory quotients of forearm musclesect A. B., so that in three normal subjects between the hours of-V differences and 10 P.M. and 4 A.M. were 0.75, 0.84 and 0.84.may have resulted In subject M. H., during the same time intervalry of glucose to)n of arterial glu-

the night, it is notke tended to de-

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ration after 16 to:ts is 5.01 mMper

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7KENNETHL. ZIERLER AND REUBIN ANDRES

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NH Km K KK was found in normal subjects during the nightK (10). This correlation could be demonstrated for

K subject M. H., who had no attack, but could notN be demonstrated for subject A. B. during and fol-

CC t lowing the attack.The possibility has been considered that changes

N in concentration of potassium in plasma may beowing to water shifts either from extravascularspace or from erythrocytes into plasma. To testthis possibility, hematocrits were determined onpaired samples of arterial and venous bloodthroughout the night. Among seven pairs of he-matocrits, mean arterial hematocrit was 44.20,range 43.1 to 45.5, mean venous hematocrit was

M.^ 44.26. ranLre 43.4 to 45.5. and mean differene be-IvrM *C CAM 4 6 a IU Z1

FIG. 6. ARTEIUAL BLOODCO2 CONTENTSymbols as in Figure 4.

when he failed to have an attack, the R.Q. was

0.82. In subject A. B. during the spontaneousattack, R.Q. was 1.00.

The fraction of O2 uptake by muscle which isspent in oxidation of glucose is defined by thefollowing relation (9): 6(glucose A-V differenceminus % lactate A-V difference)/oxygen A-Vdifference. In contrast to data found in normalsubjects during the same hours, during the earlyhours of the attack glucose uptake was greatlyin excess of the amount needed to account for allthe 02 uptake. Later, glucose uptake decreasedand was sufficient to account for only a minor frac-tion of O2 uptake, as was true in normals. In nor-

mal subjects the fraction of 02 uptake accountedfor by glucose oxidation varied directly with ar-

terial glucose concentration (10). This was truealso in subject A. B.

These data do not explain the exaggeratedmovement of potassium between plasma andmuscle seen during paralysis and recovery. Al-though unusually rapid uptake of potassium bymuscle was associated with unusually rapid glu-cose uptake, the direction of potassium movementreversed, and potassium moved from muscle toplasma during recovery at a time when arterialglucose concentration was still excessive and glu-cose uptake by muscle was still relatively large.

Net efflux of potassium from cells under the in-fluence of acidosis has been described (11) and a

suggestive correlation between potassium move-

ment from muscle and CO2 production by muscle

tween pairs of arterial and venous blood was- 0.06, range - 0.5 to + 1.0. Thus there wasno evidence of net water shift into plasma.

SUMMARY

1. A large net uptake of potassium from ar-

terial plasma by skeletal muscle (the forearm)has been demonstrated a) during the developmentof a spontaneous nocturnal attack of periodic pa-

ralysis and b) during the development of a noc-

turnal attack induced by the administration ofglucose and insulin.

2. Movement of potassium out of skeletalmuscle has been demonstrated a) during the spon-

taneous recovery from a nocturnal attack whichdeveloped spontaneously and b) during recovery

from an attack after oral KC1 administration.3. The characteristic onset of attacks during the

night with spontaneous cure later in the morningseen in many of these patients may be due to ex-

aggerations of the normal diurnal variation in netpotassium movement between muscle and plasma.

ACKNOWLEDGMENTS

Weare indebted to the patients for their cooperation,to Dr. David Grob for the opportunity of studying bothpatients, and to Dr. Saul Farber who had previouslystudied patient A. B. and sent him to Baltimore for elec-tromyographic studies by Drs. Grob, Ake Liljestrand andRichard J. Johns. Studies of A. B. by Drs. Farber andHugh J. Carroll were reported in abstract in the J. Clin.Invest., 1956, 35, 702, simultaneously with reports byGrob, Johns, and Liljestrand, J. Clin. Invest., 1956, 35,708, and our own report, J. Clin. Invest., 1956, 35, 747.Farber and Carroll reported that during an attack ofparalysis in A. B. the concentration of potassium in

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736

MUSCLEPOTASSIUM UPTAKE IN PERIODIC PARALYSIS

plasma from antecubital venous blood was less than theconcentration of potassium in arterial plasma. Theirobservations were made prior to our own studies of A. B.and were unfortunately unknown to us at the time we

performed them. We are indebted also to Miss EllenRogus and Mrs. Gerda von Ahlefeldt for their assistance.

REFERENCES

1. Biemond, A., and Daniels, A. P., Familial periodicparalysis and its transition into spinal muscularatrophy. Brain, 1934, 57, 91.

2. Aitken, R. S., Allott, E. N., Castleden, L. I. M., andWalker, M., Observations on a case of familial pe-riodic paralysis. Clin. Sc., 1937, 3, 47.

3. Allott, E. N., and McArdle, B., Further observationson familial periodic paralysis. Clin. Sc., 1938, 3,229.

4. Pudenz, R. H., McIntosh, J. F., and McEachemn, D.,The role of potassium in familial periodic paralysis.J. A. M. A., 1938, 111, 2253.

5. Ferrebee, J. W., Atchley, D. W., and Loeb, R. F., Astudy of the electrolyte physiology in a case offamilial periodic paralysis. J. Clin. Invest, 1938,17, 504.

6. Danowski, T. S., Elkinton, J. R., Burrows, B. A., andWinkler, A. W., Exchanges of sodium and potas-sium in familial periodic paralysis. J. Clin. Invest.,1948, 27, 65.

7. Andres, R., Cader, G., Goldman, P., and Zierler, K. L.,Net potassium movement between resting muscleand plasma in man in the basal state and duringthe night. J. Clin. Invest, 1957, 36, 723.

8. Talbott, J. H., Periodic paralysis; a clinical syn-drome. Medicine, 1941, 20, 85.

9. Andres, R., Cader, G., and Zierler, K. L., The quan-titatively minor role of carbohydrate in oxidativemetabolism by skeletal muscle in intact man in thebasal state. Measurements of oxygen and glu-cose uptake and carbon dioxide and lactate pro-duction in the forearm. J. Clin. Invest., 1956, 35,671.

10. Zierler, K L., and Andres, R., Carbohydrate metabo-lism in intact skeletal muscle in man during thenight. J. Clin. Invest., 1956, 35, 991.

11. Scribner, B. H., Fremont-Smith, K, and Bumnell, J.M., The effect of acute respiratory acidosis on theinternal equilibrium of potassium. J. Clin. In-vest., 1955, 34, 1276.

737