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Abstract
Potassium deficiency occurs in several conditions and is reported to cause muscle
weakness and rhabdomyolysis. The mechanisms by which potassium deficiency cause muscle
disease remain unknown, but the primary purpose of the present study was to determine
whether abnormal muscle glycogen metabolism causes muscle weakness, as suggested by
previous work. We monitored the natural history of potassium deficiency in two groups
of dogs, one of which also received deoxycorticosterone acetate (DOCA), an agent commonly
used in other studies to accelerate potassium loss. Group I dogs on potassium-free
diet alone showed a 41% decrease in muscle potassium, no change in serum CO2, creatine kinase (CK), or muscle phosphorylase activity and only mild histopathologic
abnormalities before death, after 198 ± 42 days on the diet (mean ± S.D.). In contrast,
group II dogs on the same diet plus DOCA developed clinically similar severe weakness
and died more rapidly than group I, 37 ± 7 days (p < 0.03). DOCA dogs showed a more
rapid decrease in muscle potassium to the same level as group I, a 37% increase in
serum CO2, an increase in serum CK to 1060 to 2775 IU/ml, a 23% decrease in muscle phosphorylase
activity, and severe muscle histopathology, including rhabdomyolysis. Neither group
showed any change in body weight, electromyogram (EMG), muscle glycogen concentration,
glycogen synthetase activity, serum or muscle magnesium or phosphorus, or serum T3
or T4. In conclusion, dietary potassium deficiency in dogs causes severe weakness
and death without causing rhabdomyolysis or abnormal muscle glycogen metabolism. Adding
DOCA to the potassium-free diet creates a different model characterized by rapid clinical
deterioration and rhabdomyolysis.
Abbreviations:
deoxycorticosterone acetate ((DOCA)), creatine kinase ((CK)), electromyogram ((EMG)), triiodothyronine ((T3)), tetraiodothyronine ((T4)), intramuscular ((i.m.)), electrocardiogram ((EKG)), uridine diphosphoglucose ((UDP)), fat-free dry weight ((FFDW)), correlation coefficient ((r)), periodic acid-Schiff stain ((PAS)), 14C-uridine diphosphoglucose ((UDP glucose-14C))To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
June 7,
1983
Received:
January 27,
1982
Identification
Copyright
© 1983 Published by Elsevier Inc.
