Hypothermia: alterations in cardiac and skeletal muscle electrolytes

1959 ◽  
Vol 196 (4) ◽  
pp. 706-708 ◽  
Author(s):  
W. Robert Beavers ◽  
J. T. Rogers
Keyword(s):  
Skeletal Muscle ◽  
Potassium Chloride ◽  
Cardiac Muscle ◽  
Normal Values ◽  
Intracellular Water ◽  
Sodium Potassium ◽  
Hypertonic Glucose ◽  
Plasma Electrolytes ◽  
Made In

Analyses of sodium, potassium, chloride and water of cardiac and skeletal muscle were made in normal dogs, in animals cooled to rectal temperatures of 20°C, and in cooled animals receiving 25% glucose intravenously. Using these data and determinations of plasma electrolytes, muscle intracellular water was calculated. An increase in cardiac muscle potassium and in calculated intracellular water of both cardiac and skeletal muscle was noted in the cooled animals. Administering hypertonic glucose during cooling increased cardiac muscle potassium to even higher levels and calculated intracellular water of cardiac and skeletal muscle was similar to normal values.

Effect of chlorothiazide on renal juxtaglomerular cells and tissue electrolytes

1962 ◽  
Vol 202 (5) ◽  
pp. 905-908 ◽  
Author(s):  
Louis Tobian ◽  
Jeanette Janecek ◽  
John Foker ◽  
Dorothy Ferreira
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Heart Muscle ◽  
Aortic Wall ◽  
Muscle Fibers ◽  
Extracellular Fluid ◽  
Juxtaglomerular Cells ◽  
Sodium Potassium ◽  
Tissue Weight ◽  
Cardiac Muscle Fibers

Administration of chlorothiazide to rats for 9 weeks produces an increase of intracellular sodium and a decrease of intracellular potassium in skeletal muscle. However, in cardiac muscle, in the wall of mesenteric arterioles, in aortic wall, and in kidney there is no significant alteration in the amount of sodium, potassium, or chloride per unit of dry tissue weight. The water content of heart muscle, skeletal muscle, and kidney is not altered by chlorothiazide. The intracellular concentration of Na and K in heart muscle is likewise unaltered by chlorothiazide. However, chlorothiazide produces a highly significant 44% increase in the granularity of the juxtaglomerular cells. The data in general suggest that chlorothiazide decreases the volume of extracellular fluid, but does not reduce the content of intracellular Na. Extracellular K is reduced as well as the K inside skeletal muscle fibers. However, the amount of K inside cardiac muscle fibers is unchanged by chlorothiazide.

scholarly journals Chemical composition of skeletal muscle

1969 ◽  
Vol 27 (4) ◽  
pp. 324-327 ◽  
Author(s):  
Abrão Anghihan ◽  
Francisco B. De Jorge ◽  
Julinho Aisen
Keyword(s):  
Skeletal Muscle ◽  
Chemical Composition ◽  
Tibialis Anterior ◽  
Normal Values ◽  
Sodium Potassium ◽  
Pathological Conditions ◽  
Calcium Magnesium ◽  
Anterior Deltoid ◽  
Standard Values ◽  
Neurological Conditions

The present paper aims to presents standard values for the contents of water, sodium, potassium, calcium, magnesium, phosphorus, copper and iron in muscles (tibialis anterior, deltoid and pectoralis major) in individuals without any neurological conditions. This study shall constitute the basis for the interpretation of other data, still being gathered, relating these normal values with those obtained for muscles under pathological conditions.

Sieving of electrolytes at capillary wall of cat skeletal muscle by osmotic water flow

1993 ◽  
Vol 265 (6) ◽  
pp. H1869-H1874 ◽  
Author(s):  
P. D. Watson
Keyword(s):  
Skeletal Muscle ◽  
Water Flow ◽  
Water Movement ◽  
Significant Proportion ◽  
Free Water ◽  
Mammalian Skeletal Muscle ◽  
Sodium Potassium ◽  
Osmotic Water ◽  
Significant Difference ◽  
Plasma Electrolytes

To test the hypothesis that a significant proportion of transcapillary water flow occurs through solute-restricting channels, we investigated the effects of transcapillary water movement on plasma electrolytes in isolated perfused cat skeletal muscle. The lower hindlimbs of anesthetized cats were perfused with a plasma-albumin solution and were weighed to determine transcapillary water movement. Osmolality was increased 60–70 mosmol/kgH2O with sucrose, creating water fluxes of 8–10 ml.min-1.100 g-1, and the changes in the venous concentrations of sodium, potassium, and chloride were determined. The ion concentrations were all reduced by 6–7% with no significant difference between them. The amount of reduction was quantitatively explained by the flow of ion-free water from the interstitial space into plasma and the diffusion of electrolyte in the same direction. These findings support the hypothesis that important water-only transcapillary channels exist in mammalian skeletal muscle. The observations may also explain some of the electrolyte changes seen in intense exercise.

scholarly journals THE EFFECT OF POTASSIUM ON THE ACID METABOLISM OF SURVIVING SKELETAL AND CARDIAC MUSCLES OF THE FROG

1924 ◽  
Vol 6 (6) ◽  
pp. 683-695 ◽  
Author(s):  
Fred R. Griffith
Keyword(s):  
Carbon Dioxide ◽  
Skeletal Muscle ◽  
Potassium Chloride ◽  
Cardiac Muscle ◽  
Acid Production ◽  
Chloride Solution ◽  
Acid Metabolism ◽  
Potassium Chloride Solution ◽  
Total Acid ◽  
Cardiac Muscles

The potassium contraction of skeletal muscle and relaxation of cardiac muscle have been correlated with the carbon dioxide and total acid production of these tissues. 1. The immersion of surviving sartorius muscles of the frog in isotonic potassium chloride solution causes a marked increase in the rate of acid production. 2. It is probable that carbon dioxide is the principal acid involved in the above effect. 3. The immersion of surviving cardiac muscle of the frog in isotonic potassium chloride solution causes a pronounced depression in the rate of survival acid production. 4. Reasons are given for believing that these changes in metabolism may be independent of the stimulation and inhibition of contraction which potassium simultaneously produces in these tissues.

Skeletal and cardiac muscle protein turnover during cold acclimation in young rats

2000 ◽  
Vol 278 (3) ◽  
pp. R705-R711 ◽  
Author(s):  
T. A. McAllister ◽  
J. R. Thompson ◽  
S. E. Samuels
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Cardiac Muscle ◽  
Cold Acclimation ◽  
Protein Turnover ◽  
Muscle Protein ◽  
Muscle Protein Turnover ◽  
Protein Mass ◽  
The Absolute

The effect of long-term cold exposure on skeletal and cardiac muscle protein turnover was investigated in young growing animals. Two groups of 36 male 28-day-old rats were maintained at either 5°C (cold) or 25°C (control). Rates of protein synthesis and degradation were measured in vivo on days 5, 10, 15, and 20. Protein mass by day 20 was ∼28% lower in skeletal muscle (gastrocnemius and soleus) and ∼24% higher in heart in cold compared with control rats ( P < 0.05). In skeletal muscle, the fractional rates of protein synthesis ( k syn) and degradation ( k deg) were not significantly different between cold and control rats, although k syn was lower (approximately −26%) in cold rats on day 5; consequent to the lower protein mass, the absolute rates of protein synthesis (approximately −21%; P < 0.05) and degradation (approximately −13%; P < 0.1) were lower in cold compared with control rats. In heart, overall, k syn(approximately +12%; P < 0.1) and k deg(approximately +22%; P < 0.05) were higher in cold compared with control rats; consequently, the absolute rates of synthesis (approximately +44%) and degradation (approximately +54%) were higher in cold compared with control rats ( P < 0.05). Plasma triiodothyronine concentration was higher ( P < 0.05) in cold compared with control rats. These data indicate that long-term cold acclimation in skeletal muscle is associated with the establishment of a new homeostasis in protein turnover with decreased protein mass and normal fractional rates of protein turnover. In heart, unlike skeletal muscle, rates of protein turnover did not appear to immediately return to normal as increased rates of protein turnover were observed beyond day 5. These data also indicate that increased rates of protein turnover in skeletal muscle are unlikely to contribute to increased metabolic heat production during cold acclimation.

scholarly journals Glycogenin is Dispensable for Glycogen Synthesis in Human Muscle, and Glycogenin Deficiency Causes Polyglucosan Storage

2019 ◽  
Vol 105 (2) ◽  
pp. 557-566 ◽  
Author(s):  
Kittichate Visuttijai ◽  
Carola Hedberg-Oldfors ◽  
Christer Thomsen ◽  
Emma Glamuzina ◽  
Cornelia Kornblum ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Skeletal Muscle ◽  
Western Blot ◽  
Cardiac Muscle ◽  
Glycogen Synthesis ◽  
Muscle Fibers ◽  
Human Muscle ◽  
Missense Mutations ◽  
Skeletal Muscle Fibers ◽  
Glycogen Biosynthesis

Abstract Context Glycogenin is considered to be an essential primer for glycogen biosynthesis. Nevertheless, patients with glycogenin-1 deficiency due to biallelic GYG1 (NM_004130.3) mutations can store glycogen in muscle. Glycogenin-2 has been suggested as an alternative primer for glycogen synthesis in patients with glycogenin-1 deficiency. Objective The objective of this article is to investigate the importance of glycogenin-1 and glycogenin-2 for glycogen synthesis in skeletal and cardiac muscle. Design, Setting, and Patients Glycogenin-1 and glycogenin-2 expression was analyzed by Western blot, mass spectrometry, and immunohistochemistry in liver, heart, and skeletal muscle from controls and in skeletal and cardiac muscle from patients with glycogenin-1 deficiency. Results Glycogenin-1 and glycogenin-2 both were found to be expressed in the liver, but only glycogenin-1 was identified in heart and skeletal muscle from controls. In patients with truncating GYG1 mutations, neither glycogenin-1 nor glycogenin-2 was expressed in skeletal muscle. However, nonfunctional glycogenin-1 but not glycogenin-2 was identified in cardiac muscle from patients with cardiomyopathy due to GYG1 missense mutations. By immunohistochemistry, the mutated glycogenin-1 colocalized with the storage of glycogen and polyglucosan in cardiomyocytes. Conclusions Glycogen can be synthesized in the absence of glycogenin, and glycogenin-1 deficiency is not compensated for by upregulation of functional glycogenin-2. Absence of glycogenin-1 leads to the focal accumulation of glycogen and polyglucosan in skeletal muscle fibers. Expression of mutated glycogenin-1 in the heart is deleterious, and it leads to storage of abnormal glycogen and cardiomyopathy.

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