The Effect of Pentobarbitone on Plasma and Intracellular Sodium, Potassium and pH in Rabbit Cardiac and Skeletal Muscle

1979 ◽  
Vol 57 (6) ◽  
pp. 549-551
Author(s):  
R. J. C. Hall ◽  
I. R. Cameron
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Sodium ◽  
Sodium Potassium ◽  
Intracellular Potassium ◽  
Intracellular Compartments

1. Pentobarbitone anaesthesia, in rabbits, produces (i) hypokalaemia, (ii) increased intracellular potassium and reduced intracellular sodium in cardiac and skeletal muscle. 2. These changes suggest that the hypokalaemia which accompanies anaesthesia results from movement of potassium between the extracellular and intracellular compartments.

scholarly journals Anti-VEGF therapy prevents Müller intracellular edema by decreasing VEGF-A in diabetic retinopathy

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Tianqin Wang ◽  
Chaoyang Zhang ◽  
Hai Xie ◽  
Mengmeng Jiang ◽  
Haibin Tian ◽  
...  
Keyword(s):  
Intracellular Sodium ◽  
Diabetic Rat ◽  
Vascular Endothelial ◽  
Sprague Dawley ◽  
Sodium Potassium ◽  
Intracellular Potassium ◽  
Sprague Dawley Rats ◽  
Endothelial Growth Factor ◽  
Inwardly Rectifying

Abstract Background Although vascular endothelial growth factor A (VEGF-A) is known to play a key role in causing retinal edema, whether and how VEGF-A induces intracellular edema in the retina still remains unclear. Methods Sprague-Dawley rats were rendered diabetic with intraperitoneal injection of streptozotocin. Intravitreal injection of ranibizumab was performed 8 weeks after diabetes onset. rMC-1 cells (rat Müller cell line) were treated with glyoxal for 24 h with or without ranibizumab. The expression levels of inwardly rectifying K+ channel 4.1 (Kir4.1), aquaporin 4 (AQP4), Dystrophin 71 (Dp71), VEGF-A, glutamine synthetase (GS) and sodium-potassium-ATPase (Na+-K+-ATPase) were examined using Western blot. VEGF-A in the supernatant of the cell culture was detected with ELISA. The intracellular potassium and sodium levels were detected with specific indicators. Results Compared with normal control, protein expressions of Kir4.1 and AQP4 were down-regulated significantly in diabetic rat retinas, which were prevented by ranibizumab. The above changes were recapitulated in vitro. Similarly, the intracellular potassium level in glyoxal-treated rMC-1 cells was increased, while the intracellular sodium level and Na+-K+-ATPase protein level remained unchanged, compared with control. However, ranibizumab treatment decreased intracellular sodium, but not potassium. Conclusion Ranibizumab protected Müller cells from diabetic intracellular edema through the up-regulation of Kir4.1 and AQP4 by directly binding VEGF-A. It also caused a reduction in intracellular osmotic pressure.

WATER AND ELECTROLYTE CONTENT OF SKELETAL MUSCLE IN ACROMEGALY

1965 ◽  
Vol 48 (3) ◽  
pp. 469-472 ◽  
Author(s):  
Genaro Palmieri ◽  
Denis Ikkos
Keyword(s):  
Skeletal Muscle ◽  
Chloride Content ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Potassium Content ◽  
Sodium Potassium ◽  
Electrolyte Content

ABSTRACT Measurements of the fat, water, sodium, potassium and chloride content of muscle were performed in biopsies obtained from nine unselected acromegalic patients. The water, sodium and chloride contents were normal, while the potassium content was significantly increased (P < 0.01) by eight per cent. These results were interpreted as showing that the intracellular sodium content of the muscle is normal in acromegaly and that there is no extracellular oedema in this disease.

An integrative, in situ approach to examining K+ flux in resting skeletal muscle

2001 ◽  
Vol 79 (12) ◽  
pp. 996-1006 ◽  
Author(s):  
Michael I Lindinger ◽  
Thomas J Hawke ◽  
Lisa Vickery ◽  
Laurie Bradford ◽  
Shonda L Lipskie
Keyword(s):  
Skeletal Muscle ◽  
Drug Effects ◽  
Potassium Transport ◽  
Mammalian Skeletal Muscle ◽  
Minimal Effect ◽  
Bovine Erythrocyte ◽  
Perfusion Medium ◽  
Sodium Potassium ◽  
Unidirectional Flux

The contributions of Na+/K+-ATPase, K+ channels, and the NaK2Cl cotransporter (NKCC) to total and unidirectional K+ flux were determined in mammalian skeletal muscle at rest. Rat hindlimbs were perfused in situ via the femoral artery with a bovine erythrocyte perfusion medium that contained either 86Rb or 42K, or both simultaneously, to determine differences in ability to trace unidirectional K+ flux in the absence and presence of K+-flux inhibitors. In most experiments, the unidirectional flux of K+ into skeletal muscle (JinK) measured using 86Rb was 8–10% lower than JinK measured using 42K. Ouabain (5 mM) was used to inhibit Na+/K+-ATPase activity, 0.06 mM bumetanide to inhibit NKCC activity, 1 mM tetracaine or 0.5 mM barium to block K+ channels, and 0.05 mM glybenclamide (GLY) to block ATP-sensitive K+ (KATP) channels. In controls, JinK remained unchanged at 0.31 ± 0.03 µmol·g–1·min–1 during 55 min of perfusion. The ouabain-sensitive Na+/K+-ATPase contributed to 50 ± 2% of basal JinK, K+ channels to 47 ± 2%, and the NKCC to 12 ± 1%. GLY had minimal effect on JinK, and both GLY and barium inhibited unidirectional efflux of K+ (JoutK) from the cell through K+ channels. Combined ouabain and tetracaine reduced JinK by 55 ± 2%, while the combination of ouabain, tetracaine, and bumetanide reduced JinK by 67 ± 2%, suggesting that other K+-flux pathways may be recruited because the combined drug effects on inhibiting JinK were not additive. The main conclusions are that the NKCC accounted for about 12% of JinK, and that KATP channels accounted for nearly all of the JoutK, in resting skeletal muscle in situ.Key words: sodium potassium chloride cotransporter, NKCC, Na+/K+-ATPase, potassium channels, potassium transport, in situ rat hindlimb.

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.

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.

Effects of abamectin on intracellular potassium ion activity and membrane potential in dipteran skeletal muscle

1993 ◽  
Vol 37 (1) ◽  
pp. 49-55
Author(s):  
Elizabeth M. Fitzgerald ◽  
Jason Curry ◽  
Mustafa B. A. Djamgoz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Potassium Ion ◽  
Intracellular Potassium ◽  
Ion Activity

THE EFFECTS OF OESTRADIOL ON THE SKELETAL MUSCLE AND LIVER OF THE RAT

1952 ◽  
Vol 8 (2) ◽  
pp. 179-186
Author(s):  
D. F. COLE
Keyword(s):  
Skeletal Muscle ◽  
Chemical Composition ◽  
Nucleic Acid ◽  
Water Content ◽  
Total Water Content ◽  
Total Nucleic Acid ◽  
Total Water ◽  
Intracellular Potassium ◽  
Soluble Phosphorus ◽  
Cell Electrolytes

The chemical composition of the liver and skeletal muscle in rats which had been treated with 1·0 μg. oestradiol has been investigated. The water and electrolyte content, creatine and creatinine phosphorus fractions and total nucleoproteins were studied. The changes in the water content are reciprocal to those already described for the uterus. The creatine and creatinine content and the total nucleic acid do not change significantly. There is an increase of the acid-soluble phosphorus in the first phase of the water increase in skeletal muscle which is related to some of the changes of intracellular potassium. In the liver there is an increase of the total water content between 28 and 36 hr. after injection, which is also associated with changes of acid-soluble phosphorus and cell electrolytes.

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