Skeletal muscle resting membrane potential in potassium deficiency.

The resting transmembrane potential of skeletal muscle (E(m)) is thought to be a function of the ratio of intracellular to extracellular potassium concentration ([K(i)]/[K(o)]). In potassium deficiency, the fall of [K(i)] is proportionately less than the fall of [K(o)], thus theoretically predicting a rise of E(m). To examine this theory and to characterize E(m) in kaliopenic myopathy, muscle composition and E(m) were measured during moderate (n = 5) and severe (n = 11) K deficiency in the dog and compared with measurements in the severely K-deficient rat (n = 10). Mean measured E(m) rose during moderate K deficiency in four of five dogs (-85.4 to -94.6 mV) and during severe K deficiency in the rat (-89.1 to -94.9 mV). Both values closely approximated the increase in E(m) predicted by the Goldman equation. In contrast, during severe K deficiency in the dog, a significant decline (P < 0.001) of mean E(m) to -55 mV was observed.Since skeletal myopathy and paralysis do not occur in the rat as a consequence of K deficiency, the observation that E(m) falls as paralysis occurs in the unexercised dog suggests that alteration of muscle membrane function may play a role in kaliopenic myopathy. Such an event could explain the ease with which frank muscle necrosis may be induced by exercise in the K-deficient dog.

Hyperglucagonemia of renal failure.

Elevation of plasma glucagon concentration has been observed in starvation and illnesses associated with increased catabolism such as diabetes mellitus and severe infections. Thus, we examined plasma glucose, immunoreactive insulin (IRI, microunits per milliliter) and glucagon (IRG, picograms per milliliter) responses to a beef meal (1 g/kg body wt) and intravenous glucose (1.5 g/min for 45 min) in patients with chronic renal failure (CRF). After the beef meal (n = 6), plasma glucose did not change, IRI rose from 10.1+/-1.2 to 16.3+/-1.1 (P < 0.01), and IRG rose from a fasting value of 225+/-26 to 321+/-40 (P < 0.01) by 90 min (mean+/-SEM). Intravenous infusion of glucose in CRF patients resulted in significant elevations and prolonged disappearance of plasma glucose and insulin when compared to control subjects (P < 0.01). Glucose infusion failed to suppress elevated plasma glucagon concentrations to normal levels.6 wk of chronic hemodialysis in five patients resulted in normal plasma glucose and insulin responses to the same intravenous glucose load. In contrast, plasma glucagon concentration remained unchanged after hemodialysis and there was no correlation of plasma glucagon levels with carbohydrate intolerance.

Sequential changes in body composition during infection: electron probe study IV.

Alterations occur in human muscle electrolyte and water composition in response to infection. There appear to be at least two basic mechanisms; the first is an exchange of sodium for potassium without alteration in water content of muscle. The second is an increase in cellular Na and water without a loss of K on a dry weight basis. In a series of studies in monkeys, Salmonella typhimurium sepsis was induced as an experimental model. Both patterns of muscle response to infection were detected. Electron probe microanalysis revealed that the loss of K concentration was due to an accumulation of intracellular saline which dilute the K content. The mechanism of this is unclear; however, a concomitant increase in undertermined osmoles in the serum suggests that there may be an increase in organic osmoles within the cell which leads to the dilution of intracellular K concentration.

Electrolyte metabolism in rhesus monkeys with experimental salmonella sepsis.

Prior investigations in the human indicate that alterations occur in electrolyte balance and serum concentration during infectious diseases. In order to explore these alterations in greater detail, electrolyte metabolism has been investigated in rhesus monkeys with a sublethal illness induced by intravenous inoculation with Salmonella typhimurium. The response to this illness was evaluated by a variety of measurements including serum and muscle electrolyte composition and renal function studies. In the animals with ad libitum dietary intake, a loss in muscle and serum potassium concentrations was evident within 24 h after inoculation. This was reflected in increased urinary potassium losses during the febrile phase of illness. Serum and muscle K concentrations returned to normal after 5 days of illness. Sodium and water content of muscle responded to infection in a more complex pattern. During the febrile phase, muscle sodium and water increased and sodium concentrations in serum and urine were elevated. During convalescence, renal retention of sodium was marked and overlapped the period of weight loss and the increased urine volume. This asynchrony in recovery of normal renal function appeared to be the cause of relatively large swings in plasma sodium concentrations during the early convalescent period. These investigations indicate that the altered serum concentrations in infectious diseases are the sum of renal and extrarenal factors controlling electrolyte metabolism, and that some of the most remarkable alterations occur during early convalescence as renal function returns to normal.

Value of single photon absorptiometry in osteoporosis screening.

Radial bone mineral content and bone mineral density were measured in 1515 women referred for osteoporosis screening. A detailed questionnaire allowed the selection of 1069 normal white women for further analysis who had no historical evidence of bone disease or predisposing factors for bone disease. The nondominant radius was measured at two locations: the midradial bone density (MRBD) composed of predominantly cortical bone and the distal radial bone density at the 5 mm site (DRBD) composed of a mixture of cortical and trabecular bone. Women considered at risk were defined as those whose bone density values fell below fracture risk levels (0.550 g/cm2 for the MRBD and 0.325 g/cm2 for the DRBD). Between the ages of 20 and 70 years, the DRBD showed significantly greater sensitivity in defining subjects at risk (N = 223) than than MRBD (N = 80); P less than 0.001. Analysis of all ages showed that 684 women were above the fracture risk value (FRV) at both sites (64.0%), 260 were below the FRV at the DRBD 5 mm site (24.3%), 14 were below the FRV at the MRBD site (1.3%), and 111 were below the FRV at both sites (10.4%). Postmenopausal women age 50 to 70 years receiving estrogen replacement therapy (N = 221) had significantly higher values at both sites (P less than 0.001) than age-matched postmenopausal women not receiving replacement therapy (N = 239). Hereditary factors significantly correlated with both sites but neither site showed that calcium intake, activity level, or cigarette smoking were significant variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperglucagonemia in uremia: reversal by renal transplantation.

Chronic renal failure in man is associated with hyperglucagonemia that is not corrected by hemodialysis. Plasma glucagon concentrations were measured in nine patients before and after renal transplantation. Mean plasma glucagon concentration in eight patients with chronic renal failure before transplantation was 295 plus or minus 171 pg/ml (plus or minus SD). After successful transplantation, mean plasma glucagon concentration fell to 134 plus or minus 81 pg/ml (plus or minus SD) (P less than 0.001). Plasma glucagon concentration remained elevated in an additional patient who received a cadaveric graft that never functioned. Immunologic rejection of transplanted kidneys was associated with a dramatic increase of plasma glucagon concentration.