Early fluid retention and severe acute mountain sickness

2005 ◽  
Vol 98 (2) ◽  
pp. 591-597 ◽  
Author(s):  
Jack A. Loeppky ◽  
Milton V. Icenogle ◽  
Damon Maes ◽  
Katrina Riboni ◽  
Helmut Hinghofer-Szalkay ◽  
...  
Keyword(s):  
Acute Mountain Sickness ◽  
Plasma Concentrations ◽  
Free Water ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Respiratory Alkalosis ◽  
Fluid Retention ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Mountain Sickness

Field studies of acute mountain sickness (AMS) usually include variations in exercise, diet, and environmental conditions over days and development of clinically apparent edemas. The purpose of this study was to clarify fluid status in persons developing AMS vs. those remaining without symptoms during simulated altitude with controlled fluid intake, diet, temperature, and without exercise. Ninety-nine exposures of 51 men and women to reduced barometric pressure (426 mmHg = 16,000 ft. = 4,880 m) were carried out for 8–12 h. AMS was evaluated by Lake Louise (LL) and AMS-C scores near the end of exposure. Serial measurements included fluid balance, electrolyte excretions, and plasma concentrations, regulating hormones, and free water clearance. Comparison between 16 subjects with the lowest AMS scores near the end of exposure (“non-AMS”: mean LL = 1.0, range = 0–2.5) and 16 others with the highest AMS scores (“AMS”: mean LL = 7.4, range = 5–11) demonstrated significant fluid retention in AMS beginning within the first 3 h, resulting from reduced urine flow. Plasma Na+ decreased significantly after 6 h, indicating dilution throughout the total body water. Excretion of Na+ and K+ trended downward with time in both groups, being lower in AMS after 6 h, and the urine Na+-to-K+ ratio was significantly higher for AMS after 6 h. Renal compensation for respiratory alkalosis, plasma renin activity, aldosterone, and atrial natriuretic peptide were not different between groups, with the latter tending to rise and aldosterone falling with time of exposure. Antidiuretic hormone fell in non-AMS and rose in AMS within 90 min of exposure and continued to rise in AMS, closely associated with severity of symptoms and fluid retention.

Renin, aldosterone, electrolyte, and cortisol responses to hypoxic decompression

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Cortisol ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Plasma Aldosterone Concentration ◽  
Urinary Potassium ◽  
Mountain Sickness

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.

Mechanism of Action of Indomethacin in Tubular Defects

PEDIATRICS ◽  
1985 ◽  
Vol 75 (3) ◽  
pp. 501-507
Author(s):  
Mario Usberti ◽  
Carmine Pecoraro ◽  
Stefano Federico ◽  
Bruno Cianciaruso ◽  
Bruna Guida ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Diabetes Insipidus ◽  
Mechanism Of Action ◽  
Nephrogenic Diabetes Insipidus ◽  
Fanconi Syndrome ◽  
Free Water ◽  
Synthesis Inhibitor ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Load

Indomethacin, a potent prostaglandin synthesis inhibitor, has been proven to be effective in a number of tubular defects characterized by enhanced prostaglandin (namely, prostaglandin E2 (PGE2) production, but its mechanism of action is poorly understood. To elucidate further the mechanism(s) by which indomethacin reverses the abnormal tubular functions, five children with different tubular defects (nephrogenic diabetes insipidus, three cases; Fanconi syndrome, one case; and pseudohypoaldosteronism, one case) were treated with indomethacin. Indomethacin, 1 mg/kg every eight hours, was given for 1 week to all children and then was given chronically to four of the children who responded to the drug. Its use was suspended in a 10 year-old-boy with nephrogenic diabetes insipidus because it proved ineffective. To assess the site along the nephron where indomethacin affects the solute and water excretion, an acute water load study was performed in three responsive children before and during the treatment. Indomethacin did not significantly alter the glomerular filtration rate but was effective in reducing diuresis and levels of urinary sodium and potassium excretion. In the child with Fanconi syndrome, indomethacin was also effective in controlling the urinary loss of phosphate, urate, glucose, and bicarbonate. Results of the water load studies show that indomethacin decreases the delivery of solute from the proximal tubule, reduces the fractional free water clearance, and increases the urine-plasma osmolar ratio. The rate of urinary excretion of prostaglandin E2 was high in all five children; it decreased below normal values in four of them after 1 week of treatment. In the child with nephrogenic diabetes insipidus who did not respond to indomethacin therapy, prostaglandin E2 excretion decreased but the rate remained higher than normal. These results suggest that indomethacin induces retention of solute and water mainly through an enhanced proximal tubular reabsorption.

Vasopressin-independent alterations in renal water excretion in quadriplegia

1993 ◽  
Vol 265 (2) ◽  
pp. R460-R466 ◽  
Author(s):  
B. M. Wall ◽  
H. H. Williams ◽  
D. N. Presley ◽  
J. T. Crofton ◽  
L. Share ◽  
...  
Keyword(s):  
Cervical Spinal Cord ◽  
Free Water ◽  
Renal Tubules ◽  
Erect Posture ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Vasopressin Release ◽  
Control Subjects ◽  
Cord Injury ◽  
Healthy Control

Postural effects on water excretion are known to be increased in patients with cervical spinal cord injury and may result in marked impairment of the ability to excrete a water load, especially in erect posture. Both vasopressin-dependent and vasopressin-independent mechanisms have been implicated. To assess the roles of these mechanisms and further identify the factors involved in the renal response to erect posture, sustained water loading studies were performed on 11 quadriplegic subjects and 9 healthy control subjects, supine and erect (sitting). Renal blood flow was assessed by p-aminohippurate clearance (CPAH) measurements in 7 quadriplegic and 5 control subjects. During maximal water diuresis, plasma vasopressin concentrations were reduced to unquantifiable levels in all subjects. Osmolar clearance, free water clearance (CH2O), and distal delivery of filtrate (DDF) were all lower in quadriplegic than in control subjects, supine and erect. The relationship between CH2O and DDF was the same in quadriplegic as in control subjects and was not altered by change in posture in either group. Creatinine clearance and CPAH were lower in erect than in supine posture in quadriplegic subjects but not in control subjects. We conclude that impairment of water excretion in stable normonatremic quadriplegic subjects can be attributed primarily to vasopressin-independent mechanisms involving reduced filtrate delivery to diluting segments of the renal tubules rather than to resistance to normal suppression of vasopressin release.

Volume-homeostatic mechanisms in humans during a 12-h posture change

1993 ◽  
Vol 75 (1) ◽  
pp. 349-356 ◽  
Author(s):  
P. Norsk ◽  
C. Stadeager ◽  
L. B. Johansen ◽  
J. Warberg ◽  
P. Bie ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Venous Pressure ◽  
Free Water ◽  
Plasma Renin ◽  
Arterial Pulse ◽  
Free Water Clearance ◽  
Water Handling ◽  
Renal Sodium Excretion ◽  
Male Subjects ◽  
Peak Value

On one day six male subjects underwent an upright seated (SEAT) study, and on another day they were subjected to a head-down tilt of 3 degrees (HDT). Compared with SEAT, HDT induced prompt increases in central venous pressure (CVP) from -0.5 +/- 0.8 to 8.3 +/- 0.3 mmHg (P < 0.001) and in arterial pulse pressure of 8–18 mmHg (P < 0.001). CVP stabilized after 6 h at levels 2.4–2.8 mmHg below the peak value. Simultaneously, renal sodium excretion gradually increased over the initial 5 h of HDT and stabilized at a level approximately 125 mumol/min over that of SEAT (P < 0.001). Urine flow rate and solute free water clearance increased during the initial 2–6 h of HDT (P < 0.001) but returned to the level of SEAT thereafter. We concluded that CVP is slightly reduced over 12 h of HDT and that a clear temporal dissociation exists between renal sodium and water handling. We suggest that the combined effect of the sustained suppressions of plasma renin activity and plasma aldosterone and norepinephrine concentrations constitutes a mechanism of the increase in renal sodium excretion.

Effect of beta-adrenoceptor blockade on renin-aldosterone and alpha-ANF during exercise at altitude

1989 ◽  
Vol 67 (1) ◽  
pp. 141-146 ◽  
Author(s):  
P. Bouissou ◽  
J. P. Richalet ◽  
F. X. Galen ◽  
M. Lartigue ◽  
P. Larmignat ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Acute Mountain Sickness ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Suppressive Effect ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Plasma Aldosterone Concentration ◽  
Ergometer Exercise

The renin-aldosterone system may be depressed in subjects exercising at high altitude, thereby preventing excessive angiotensin I (ANG I) and aldosterone levels, which could favor the onset of acute mountain sickness. The role of beta-adrenoceptors in hormonal responses to hypoxia was investigated in 12 subjects treated with a nonselective beta-blocker, pindolol. The subjects performed a standardized maximal bicycle ergometer exercise with (P) and without (C) acute pindolol treatment (15 mg/day) at sea level, as well as during a 5-day period at high altitude (4,350 m, barometric pressure 450 mmHg). During sea-level exercise, pindolol caused a reduction in plasma renin activity (PRA, 2.83 +/- 0.35 vs. 5.13 +/- 0.7 ng ANG I.ml-1.h-1, P less than 0.01), an increase in plasma alpha-atrial natriuretic factor (alpha-ANF) level (23.1 +/- 2.9 (P) vs. 10.4 +/- 1.5 (C) pmol/1, P less than 0.01), and no change in plasma aldosterone concentration [0.50 +/- 0.04 (P) vs. 0.53 +/- 0.03 (C) nmol/1]. Compared with sea-level values, PRA (3.45 +/- 0.7 ng ANG I.ml-1.h-1) and PA (0.39 +/- 0.03 nmol/1) were significantly lower (P less than 0.05) during exercise at high altitude. alpha-ANF was not affected by hypoxia. When beta-blockade was achieved at high altitude, exercise-induced elevation in PRA was completely abolished, but no additional decline in PA occurred. Plasma norepinephrine and epinephrine concentrations tended to be lower during maximal exercise at altitude; however, these differences were not statistically significant. Our results provide further evidence that hypoxia has a suppressive effect on the renin-aldosterone system. However, beta-adrenergic mechanisms do not appear to be responsible for inhibition of renin secretion at high altitude.

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Ovine fetal renal and hormonal responses to changes in plasma epinephrine

1991 ◽  
Vol 260 (1) ◽  
pp. R82-R89
Author(s):  
M. G. Ervin ◽  
R. Castro ◽  
D. J. Sherman ◽  
M. G. Ross ◽  
J. F. Padbury ◽  
...  
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Free Water ◽  
Urine Osmolality ◽  
Plasma Epinephrine ◽  
Epinephrine Infusion ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Fourfold Increase ◽  
Fetal Plasma

Circulating epinephrine alters atrial natriuretic factor (ANF) and arginine vasopressin (AVP) secretion, and all three hormones influence renal function. To quantify the relationships among fetal plasma epinephrine levels, fetal ANF and AVP secretion, and fetal renal function, six chronically catheterized fetal lambs (132 +/- 1 days gestation) received successive 40-min epinephrine infusions (0.1, 0.4, and 1.8 micrograms.min-1.kg-1). The second epinephrine infusion dose evoked significant increases in urine flow (V; 0.7 +/- 0.2 to 1.2 +/- 0.2 ml/min), free water clearance (CH2O; 0.3 +/- 0.1 to 0.7 +/- 0.1 ml/min), glomerular filtration rate (GFR; 3.9 +/- 0.7 to 5.4 +/- 0.8 ml/min), fractional water excretion (V/CH2O; 19 +/- 3 to 25 +/- 2%), mean arterial pressure (MAP; 45 +/- 3 to 51 +/- 4 mmHg), and a 94% increase in plasma ANF levels. A fourfold increase in the infusion dose significantly increased osmolar clearance (0.3 +/- 0.1 to 0.6 +/- 0.1 ml/min), sodium excretion (28 +/- 8 to 53 +/- 13 mueq/min), and plasma AVP levels (2.4 +/- 0.5 to 6.4 +/- 2.4 pg/ml) with no additional effect on V, CH2O, GFR, V/GFR, MAP, or plasma ANF levels. Urine osmolality and fractional sodium excretion did not change in response to epinephrine infusion. Our results demonstrate that epinephrine infusion stimulates fetal ANF secretion and to a lesser extent AVP secretion and significantly influences fetal renal function.

Intrarenal Distribution of Plasma Flow in Cirrhosis as Measured by Transit Renography: Relationship with Plasma Renin Activity, and Sodium and Water Excretion

1977 ◽  
Vol 52 (5) ◽  
pp. 469-475 ◽  
Author(s):  
S. P. Wilkinson ◽  
I. K. Smith ◽  
M. Clarke ◽  
V. Arroyo ◽  
J. Richardson ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Free Water ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Water Excretion ◽  
Transit Times ◽  
Abnormal Pattern ◽  
Intrarenal Distribution

1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]-iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.

Intermittent altitude exposures reduce acute mountain sickness at 4300 m

2004 ◽  
Vol 106 (3) ◽  
pp. 321-328 ◽  
Author(s):  
Beth A. BEIDLEMAN ◽  
Stephen R. MUZA ◽  
Charles S. FULCO ◽  
Allen CYMERMAN ◽  
Dan DITZLER ◽  
...  
Keyword(s):  
Acute Mountain Sickness ◽  
Urine Volume ◽  
Barometric Pressure ◽  
Self Report ◽  
Altitude Exposure ◽  
Cerebral Symptom ◽  
Cycle Training ◽  
Mountain Sickness ◽  
End Tidal ◽  
Rest And Exercise

Acute mountain sickness (AMS) commonly occurs at altitudes exceeding 2000–2500 m and usually resolves after acclimatization induced by a few days of chronic residence at the same altitude. Increased ventilation and diuresis may contribute to the reduction in AMS with altitude acclimatization. The aim of the present study was to examine the effects of intermittent altitude exposures (IAE), in combination with rest and exercise training, on the incidence and severity of AMS, resting ventilation and 24-h urine volume at 4300 m. Six lowlanders (age, 23±2 years; body weight, 77±6 kg; values are means±S.E.M.) completed an Environmental Symptoms Questionnaire (ESQ) and Lake Louise AMS Scoring System (LLS), a resting end-tidal partial pressure of CO2 (PETCO2) test and a 24-h urine volume collection at sea level (SL) and during a 30 h exposure to 4300 m altitude-equivalent (barometric pressure=446 mmHg) once before (PreIAE) and once after (PostIAE) a 3-week period of IAE (4 h·day-1, 5 days·week-1, 4300 m). The previously validated factor score, AMS cerebral score, was calculated from the ESQ and the self-report score was calculated from the LLS at 24 h of altitude exposure to assess the incidence and severity of AMS. During each IAE, three subjects cycled for 45–60 min·day-1 at 60–70% of maximal O2 uptake (VO2 max) and three subjects rested. Cycle training during each IAE did not affect any of the measured variables, so data from all six subjects were combined. The results showed that the incidence of AMS (%), determined from both the ESQ and LLS, increased (P<0.05) from SL (0±0) to PreIAE (50±22) at 24 h of altitude exposure and decreased (P<0.05) from PreIAE to PostIAE (0±0). The severity of AMS (i.e. AMS cerebral symptom and LLS self-report scores) increased (P<0.05) from SL (0.02±0.02 and 0.17±0.17 respectively) to PreIAE (0.49±0.18 and 4.17±0.94 respectively) at 24 h of altitude exposure, and decreased (P<0.05) from PreIAE to PostIAE (0.03±0.02 and 0.83±0.31 respectively). Resting PETCO2 (mmHg) decreased (i.e. increase in ventilation; P<0.05) from SL (38±1) to PreIAE (32±1) at 24 h of altitude exposure and decreased further (P<0.05) from PreIAE to PostIAE (28±1). In addition, 24-h urine volumes were similar at SL, PreIAE and PostIAE. In conclusion, our findings suggest that 3 weeks of IAE provide an effective alternative to chronic altitude residence for increasing resting ventilation and reducing the incidence and severity of AMS.

Centrally administered atrial natriuretic factor increases renal water excretion

1987 ◽  
Vol 252 (6) ◽  
pp. F1011-F1015 ◽  
Author(s):  
J. Lee ◽  
J. Q. Feng ◽  
R. L. Malvin ◽  
B. S. Huang ◽  
R. J. Grekin
Keyword(s):  
Intravenous Infusion ◽  
Atrial Natriuretic Factor ◽  
Renal Plasma Flow ◽  
Plasma Concentrations ◽  
Urine Volume ◽  
Free Water ◽  
Water Excretion ◽  
Arterial Blood ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.

Sign in / Sign up

Export Citation Format

Share Document