Effect of parathyroidectomy on content and availability of skeletal sodium in the rat

1960 ◽  
Vol 198 (4) ◽  
pp. 749-753 ◽  
Author(s):  
George Nichols ◽  
Nancy Nichols
Keyword(s):  
Bone Mineral ◽  
Cell Metabolism ◽  
Extracellular Fluid ◽  
Bone Destruction ◽  
Sodium Concentration ◽  
Bone Cell ◽  
Plasma Sodium ◽  
Sodium Ions ◽  
Sodium Depletion ◽  
Sodium Metabolism

The effect of parathyroidectomy on the composition of plasma and bone has been examined in rats with and without sodium depletion. Parathyroidectomy caused a marked fall in calcium and a slight decrease in chloride in the plasma and a 7.9% increase in bone mineral sodium concentration. Sodium depletion by intraperitoneal dialysis of normal animals lowered bone mineral sodium 4% while plasma sodium and pH remained at almost normal levels. In contrast, sodium depletion following parathyroidectomy failed to lower bone sodium significantly but produced a significant acidosis and a slight decrease in plasma sodium. These findings suggest that the ability of bone to release sodium ions to protect extracellular fluid pH in acute sodium depletion is dependent on the presence of the parathyroid glands. Possible mechanisms by which parathyroid activity might influence bone sodium metabolism by changes in bone cell metabolism, changes in the Na:Ca ratio of extracellular fluid, or actual bone destruction are discussed.

Effectiveness of the aldosterone-sodium and -potassium feedback control system

1976 ◽  
Vol 231 (3) ◽  
pp. 945-953 ◽  
Author(s):  
DB Young ◽  
RE McCaa ◽  
UJ Pan ◽  
AC Guyton
Keyword(s):  
Feedback Control ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Feedback Mechanism ◽  
Fluid Volume ◽  
The Body ◽  
Plasma Sodium ◽  
Aldosterone Secretion

This study was conducted to determine the quantitative importance of the aldosterone feedback mechanism in controlling each one of three major factors that have often been associated with aldosterone, namely, extracellular fluid sodium concentration, extracellular fluid potassium concentration, and extracellular fluid volume. To do this, the ability of the body to control these three factors in the face of marked changes in daily sodium or potassium intake was studied under two conditions: 1) in the normal dog, and 2) in the dog in which the aldosterone feedback mechanism was prevented from functioning by removing the adrenal glands and then providing a continuous fixed level of supportive aldosterone and glucocorticoids during the low and high electrolyte intake periods. Under these conditions, removal of feedback control of aldosterone secretion decreased the effectiveness of plasma potassium control by nearly fivefold (39% vs. 8% change in plasma potassium concentration), fluid volume by sixfold (12% vs. 2% change in sodium space) and had no effect on control of plasma sodium concentration (2% change with and without feedback control of aldosterone secretion.)

The Antidiuretic Effect of Chronic Hydrochlorothiazide Treatment in Rats with Diabetes Insipidus: Water and Electrolyte Balance

1982 ◽  
Vol 63 (6) ◽  
pp. 525-532 ◽  
Author(s):  
S. J. Walter ◽  
J. Skinner ◽  
J. F. Laycock ◽  
D. G. Shirley
Keyword(s):  
Diabetes Insipidus ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Antidiuretic Effect

1. The antidiuretic effect of hydrochlorothiazide in diabetes insipidus was investigated in rats with the hereditary hypothalamic form of the disease (Brattleboro rats). 2. Administration of hydrochlorothiazide in the food resulted in a marked fall in urine volume and a corresponding rise in osmolality. These effects persisted throughout the period of treatment (6–7 days). 3. Body weight and extracellular volume were significantly reduced in the thiazide-treated rats. 4. Hydrochlorothiazide caused an increase in urinary sodium excretion only on the first day of treatment. The resulting small negative sodium balance (in comparison with untreated rats) remained statistically significant for 2 days only. Thiazide-treated rats gradually developed a potassium deficit which was statistically significant from the fourth day of treatment. 5. Total exchangeable sodium, measured after 7 days of thiazide treatment, was not significantly different from that of untreated rats. However, plasma sodium was reduced in thiazide-treated animals, whereas erythrocyte sodium concentration was elevated. 6. It is concluded that the antidiuresis resulting from chronic hydrochlorothiazide administration is associated with a reduction in extracellular volume, but not with a significant overall sodium deficit. Hydrochlorothiazide appears to cause a redistribution of the body's sodium such that the amount of sodium in the extracellular fluid compartment is reduced.

Development of indices for determining extracellular fluid sodium and water status in acute diabetic ketoacidosis: possible tools for clinical audit

1994 ◽  
Vol 40 (5) ◽  
pp. 758-762
Author(s):  
D F Davidson ◽  
J Williamson ◽  
D E Boag ◽  
T Millar
Keyword(s):  
Diabetic Ketoacidosis ◽  
Water Status ◽  
Plasma Concentrations ◽  
Extracellular Fluid ◽  
Sodium Concentration ◽  
Hydration Status ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration ◽  
Acute Diabetes ◽  
Extracellular Environment

Abstract The limitation of plasma sodium concentration as an indicator of extracellular hydration status in cases of acute diabetes is well recognized and could lead to individually inappropriate fluid therapy. However, in view of the small analytical and biological variations exhibited by plasma concentrations of protein, water, and sodium in health, we have developed simple laboratory indices that may better describe the extracellular environment. Preliminary data presented here for 20 patients with acute diabetic ketoacidosis admitted as emergencies to Crosshouse Hospital suggest that the type of approach we describe has the potential to supply meaningful therapeutic data to the managing physician and, therefore, merits further study in a clinical setting.

Forebrain control of fluid and electrolyte homeostasis and angiotensin sensitivity in rabbit

1980 ◽  
Vol 239 (5) ◽  
pp. R372-R376 ◽  
Author(s):  
G. D. Fink ◽  
W. J. Bryan
Keyword(s):  
Angiotensin Ii ◽  
Third Ventricle ◽  
Extracellular Fluid ◽  
Cardiovascular Effects ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Electrolyte Balance ◽  
Pressor Responses ◽  
Discrete Area

A small discrete area near the optic recess of the anterior ventral third ventricle (AV3V) in the rat brain has been shown to be an important mediator of cardiovascular and dipsogenic response to angiotensin II and osmotic stimuli and to be involved in normal day-to-day regulation of water and electrolyte balance. However, no attempt has been made until now to explore the function of the AV3V in species other than the rat. In the present study, rabbits subjected to electrolytic lesion of the AV3V exhibited expanded plasma volume and plasma sodium concentration, and significantly attenuated pressor responses to angiotensin II and hypertonic sodium chloride solutions injected via the lateral ventricles. Resting arterial pressure, plasma potassium concentration, extracellular fluid volume, and pressor responses to intravenous angiotensin II were not changed by lesioning. Thus, the effects of AV3V lesions in rabbits are similar, but not identical, to those previously observed in rats. Rabbits should be a suitable species in which to carry out studies aimed at distinguishing central and peripheral cardiovascular effects of angiotensin II.

Hyponatremia in Patients Undergoing CAPD: Role of Water Gain and/or Malnutrition

2001 ◽  
Vol 21 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Gonzalo Zevallos ◽  
Dimitrios G. Oreopoulos ◽  
Mitchell L. Halperin
Keyword(s):  
Extracellular Fluid ◽  
Free Water ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Fluid Composition ◽  
Major Mechanism ◽  
Plasma Sodium Concentration ◽  
Catabolic State ◽  
Water Gain

Background Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). Objective To determine the pathophysiology of hyponatremia in patients on CAPD. Methods A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2 – 4 consecutive periods when the plasma sodium concentration was ≤130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. Results An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. Conclusion When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition ( i.e., to correct malnutrition).

HYPERALDOSTERONISM IN THE SODIUM-DEPLETED RAT: MECHANISM OF ALDOSTERONE STIMULATION BY PERITONEAL DIALYSIS WITH GLUCOSE SOLUTION

1979 ◽  
Vol 82 (1) ◽  
pp. 17-25 ◽  
Author(s):  
A. SPÄT ◽  
K. NAGY ◽  
TARJÁN ÉVA
Keyword(s):  
Peritoneal Dialysis ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Glucose Solution ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Sodium Depletion ◽  
Total Body

SUMMARY Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.

Chronic effects of hyperproteinemia on blood volume and lymph protein concentration

1992 ◽  
Vol 262 (4) ◽  
pp. H937-H941 ◽  
Author(s):  
R. D. Manning
Keyword(s):  
Osmotic Pressure ◽  
Blood Volume ◽  
Protein Concentration ◽  
Extracellular Fluid ◽  
Sodium Concentration ◽  
Colloid Osmotic Pressure ◽  
Plasma Sodium ◽  
Long Term Effects ◽  
Plasma Protein Concentration ◽  
Autologous Plasma

The long-term effects of hyperproteinemia on blood volume and lymph protein concentration were studied in six conscious dogs over a 17-day period. Plasma protein concentration (PPC) was increased by daily intravenous infusion of approximately 300 ml of previously collected autologous plasma. By day 17 PPC had increased 2.4 g/dl, and plasma colloid osmotic pressure had increased 51%; however, blood volume was not changed. Also, at this time sulfate space, an index of extracellular fluid volume, had increased 12%, prenodal lymph protein concentration had increased from 1.6 to 5.1 g/dl, mean arterial pressure was unchanged, circulating protein mass was increased, and plasma sodium concentration was decreased slightly. In conclusion, the increase in lymph protein concentration during hyperproteinemia may indicate that interstitial fluid protein concentration also increased. This, in turn, would help to prevent any increase in the transcapillary colloid osmotic pressure gradient and thus attenuate any changes in blood volume.

The Role of Sodium Depletion in Hydrochlorothiazide-Induced Antidiuresis in Brattleboro Rats with Diabetes Insipidus

1978 ◽  
Vol 54 (3) ◽  
pp. 209-215
Author(s):  
D. G. Shirley ◽  
S. J. Walter ◽  
J. F. Laycock
Keyword(s):  
Glomerular Filtration Rate ◽  
Diabetes Insipidus ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Sodium Concentration ◽  
Effective Renal Plasma Flow ◽  
Plasma Sodium ◽  
Sodium Depletion

1. The mechanism of the antidiuretic effect of hydrochlorothiazide in diabetes insipidus was studied in anaesthetized Brattleboro rats with the hereditary hypothalamic form of the disease. 2. The antidiuresis caused by acute administration of hydrochlorothiazide followed an increase in sodium excretion and was associated with a significant fall in the plasma sodium concentration. There were concomitant falls in effective renal plasma flow and glomerular filtration rate. 3. When sodium depletion was prevented by adjusting the infusion of sodium chloride, the falls in plasma sodium concentration, effective renal plasma flow and glomerular filtration rate were abolished. Under these circumstances there was an increase in urine volume, which suggests that hydrochlorothiazide may inhibit fractional fluid reabsorption in the proximal convoluted tubule. 4. The results indicate that the antidiuresis caused by hydrochlorothiazide in diabetes insipidus results, at least in part, from falls in effective renal plasma flow and glomerular filtration rate. These in turn seem to be entirely secondary to the drug-induced sodium depletion.

scholarly journals Acute Hyponatremia following Hypotonic Intravenous Fluid in a 4-year-old Child

2016 ◽  
Vol 1 (2) ◽  
pp. 63-64
Author(s):  
Naina P Dalvi ◽  
Preeti Rustagi ◽  
Bharti A Tendolkar ◽  
Suhas Kotak
Keyword(s):  
Extracellular Fluid ◽  
Sodium Concentration ◽  
Brain Cell ◽  
Intravenous Fluid ◽  
Cell Swelling ◽  
Plasma Sodium ◽  
Electrolyte Disorder ◽  
Plasma Sodium Concentration ◽  
Ct Brain ◽  
Acute Hyponatremia

ABSTRACT Hyponatremia is the most frequently encountered electrolyte disorder in hospitalized patients. It develops due to either surplus water or decreased sodium in the extracellular fluid. In children, the source of excess water is frequently the administration of hypotonic intravenous fluids. The current recommendations of hypotonic maintenance fluids may be appropriate for a healthy child, but may not apply to hospitalized children who are more likely to have a nonosmotic stimulus for antidiuretic hormone (ADH) production, such as anxiety, stress, pain, etc. Fall in plasma sodium concentration acutely to < 130 mmol/L leads to brain cell swelling and devastating neurological outcome. Previous studies have reported the potential harm with these solutions and the need to reconsider their routine use in children. We present a case report of 4-year-old child, admitted with head injury and normal CT brain, who developed hyponatremic convulsions following administration of Isolyte-P as maintenance fluid as per standard guidelines. How to cite this article Rustagi P, Dalvi NP, Tendolkar BA, Kotak S. Acute Hyponatremia following Hypotonic Intravenous Fluid in a 4-year-old. Res Inno in Anesth 2016;1(2):63-64.

scholarly journals The Use of Electrical Conductivity Measurement in the Calculation of Ion-Free Water Loss in Urine

1987 ◽  
Vol 15 (4) ◽  
pp. 379-383 ◽  
Author(s):  
W. G. Parkin ◽  
R. W. Dickinson
Keyword(s):  
Electrical Conductivity ◽  
Extracellular Fluid ◽  
Free Water ◽  
Conductivity Measurement ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Electrical Conductivity Measurement ◽  
Plasma Sodium Concentration ◽  
Total Body ◽  
Water Ratio

The urine electrical conductivity is a practical guide to the ion-to-water ratio of urine. It may be used to assess the influence of urinary loss upon the total body ion-to-water ratio. It is suggested that the total body ion-to-water ratio is the object of control in water therapy, commonly administered as 5% dextrose. The total body ion-to-water ratio closely accords with the ratio in the extracellular fluid. Since sodium is the predominant extracellular cation, the plasma sodium concentration closely reflects the extracellular and total body ion-to-water ratio. As a consequence the urine electrical conductivity may be used as a continuous signal in the open or closed loop control of water balance as reflected by the plasma sodium concentration.

Sign in / Sign up

Export Citation Format

Share Document