Salt Wastage, Plasma Volume Contraction and Hypokalemic Paralysis in Self-Induced Water Intoxication

Nephron ◽  
1993 ◽  
Vol 64 (4) ◽  
pp. 570-575 ◽  
Author(s):  
Ronan S. Tanneau ◽  
Yvon L. Pennec ◽  
Jean-François Morin ◽  
Jean-Pierre Codet ◽  
Bernard Bourbigot ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Water Intoxication ◽  
Volume Contraction ◽  
Hypokalemic Paralysis

Importance of chloride for the correction of chronic metabolic alkalosis in the rat

1987 ◽  
Vol 253 (5) ◽  
pp. F1031-F1039 ◽  
Author(s):  
B. M. Wall ◽  
G. V. Byrum ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Plasma Volume ◽  
Metabolic Alkalosis ◽  
Choline Chloride ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Volume Contraction ◽  
Chloride Depletion ◽  
Sprague Dawley Rats ◽  
Sodium And Potassium

To determine whether chloride repletion without sodium could correct chronic chloride depletion metabolic alkalosis (CDA) in Sprague-Dawley rats without volume expansion and without increasing glomerular filtration rate (GFR), CDA was generated by peritoneal dialysis (PD) against 0.15 M NaHCO3 and maintained for 7-10 days by a chloride-restricted diet supplemented with sodium and potassium salts. Control animals were dialyzed against Ringer bicarbonate. The maintenance period of chronic CDA, compared with control, was characterized by hypokalemic metabolic alkalosis (serum TCO2 31.9 +/- 0.6 vs. 23.1 +/- 0.5 meq/l, P less than 0.05), volume contraction (plasma volume 3.76 +/- 0.08 vs. 4.19 +/- 0.22 ml/100 g body wt, P less than 0.05), decreased GFR (838 +/- 84 vs. 1045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), increased plasma renin activity (PRA) (63 +/- 13 vs. 12 +/- 3 ng.ml-1.h-1, P less than 0.05), but unchanged plasma aldosterone concentrations (PAC) (4.1 +/- 1.0 vs. 3.4 +/- 1.6 ng/dl, P = NS). Complete correction of chronic CDA was accomplished by 24 h of ingestion of choline chloride drink, and despite negative sodium balance, neutral potassium balance, continued bicarbonate ingestion, and persistent volume contraction (plasma volume 3.76 +/- 0.08 vs. 3.73 +/- 0.12 ml/100 g body wt pre- and postcorrection, P = NS), GFR remained decreased (659 +/- 87 vs. 1,045 +/- 45 microliters.min-1.100 g body wt-1, P less than 0.05), PRA decreased (63 +/- 13 vs. 33 +/- 5 ng.ml-1.h-1, P less than 0.05), but PAC did not change (4.1 +/- 1.0 vs. 6.1 +/- 1.6 ng/dl, P = NS) after correction of CDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma volume contraction in portal hypertension

1993 ◽  
Vol 17 ◽  
pp. S19-S23 ◽  
Author(s):  
Yasumi Katsuta ◽  
Takumi Aramaki ◽  
Tatsuya Sekiyama ◽  
Katsuaki Satomura ◽  
Kidemasa Okumura
Keyword(s):  
Portal Hypertension ◽  
Plasma Volume ◽  
Volume Contraction

Plasma volume contraction reduces atrial natriuretic peptide after four days of hypobaric hypoxia exposure

2021 ◽  
Author(s):  
Hannes Gatterer ◽  
Simon Rauch ◽  
Ivo B Regli ◽  
Simon Woyke ◽  
Maja Schlittler ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Hypobaric Hypoxia ◽  
Right Atrial ◽  
Hypoxic Exposure ◽  
Fluid Infusion ◽  
Volume Contraction ◽  
Atrial Area ◽  
Atrial Natriuretic

We investigated whether low arterial oxygen tension (PaO2) or hypoxia-induced plasma volume (PV) contraction, which reduces central blood volume (BV) and atrial distension, explain reduction in circulating atrial natriuretic peptide (ANP) after prolonged hypoxic exposure. Ten healthy males were exposed for four days to hypobaric hypoxia corresponding to an altitude of 3,500m. PV changes were determined by carbon monoxide rebreathing. Venous plasma concentrations of mid-regional proANP (MR-ProANP) were measured before and at the end of the exposure. At the latter time-point the measurement was repeated after i. restoration of PaO2 by breathing a hyperoxic gas mixture for 30min and ii. restoration of BV by fluid infusion. Correspondingly, left ventricular end-diastolic volume (LVEDV), left atrial area (LAA) and right atrial area (RAA) were determined by ultrasound before exposure, and both pre and post fluid infusion at the end of the exposure. Hypoxic exposure reduced MR-ProANP from 37.9±18.5 to 24.5±10.3 pmol/l (p=0.034), LVEDV from 107.4±33.5 to 91.6±26.3 ml (p=0.005), LAA from 15.8±4.9 to 13.3±4.2 cm² (p=0.007) and RAA from 16.2±3.1 to 14.3±3.5 cm² (p=0.001). Hyperoxic breathing did not affect MR-ProANP (24.8±12.3 pmol/l, p=0.890). Conversely, fluid infusion restored LVEDV, LAA and RAA to near baseline values (108.0±29.3 ml, 17.2±5.7 cm² and 17.2±3.1 cm², p>0.05 vs. baseline) and increased MR-ProANP to 29.5±13.3 pmol/l (p=0.010 vs. pre-infusion and p=0.182 vs. baseline). These findings support that ANP reduction in hypoxia is at least partially attributed to plasma volume contraction, whereas reduced PaO2 does not seem to contribute.

Atrial natriuretic peptide levels and plasma volume contraction in acute alveolar hypoxia

1997 ◽  
Vol 82 (1) ◽  
pp. 102-110 ◽  
Author(s):  
T. S. E. Albert ◽  
V. L. Tucker ◽  
E. M. Renkin
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Urine Output ◽  
Arterial Oxygen ◽  
Volume Contraction ◽  
Alveolar Hypoxia ◽  
Oxygen Tensions ◽  
Atrial Natriuretic

Albert, T. S. E., V. L. Tucker, and E. M. Renkin.Atrial natriuretic peptide levels and plasma volume contraction in acute alveolar hypoxia. J. Appl. Physiol. 82(1): 102–110, 1997.—Arterial oxygen tensions ([Formula: see text]), atrial natriuretic peptide (ANP) concentrations, and circulating plasma volumes (PV) were measured in anesthetized rats ventilated with room air or 15, 10, or 8% O2( n = 5–7). After 10 min of ventilation, [Formula: see text] values were 80 ± 3, 46 ± 1, 32 ± 1, and 35 ± 1 Torr and plasma immunoreactive ANP (irANP) levels were 211 ± 29, 229 ± 28, 911 ± 205, and 4,374 ± 961 pg/ml, respectively. At[Formula: see text] ≤40 Torr, irANP responses were more closely related to inspired O2( P = 0.014) than to[Formula: see text] ( P= 0.168). PV was 36.3 ± 0.5 μl/g in controls but 8.5 and 9.9% lower ( P ≤ 0.05) for 10 and 8% O2, respectively. Proportional increases in hematocrit were observed in animals with reduced PV; however, plasma protein concentrations were not different from control. Between 10 and 50 min of hypoxia, small increases (+40%) in irANP occurred in 15% O2; however, there was no further change in PV, hematocrit, plasma protein, or irANP levels in the lower O2groups. Urine output tended to fall during hypoxia but was not significantly different among groups. These findings are compatible with a role for ANP in mediating PV contraction during acute alveolar hypoxia.

Plasma-volume contraction and exercise-induced hypoxaemia modulate erythropoietin production in healthy humans

1999 ◽  
Vol 98 (1) ◽  
pp. 39-45 ◽  
Author(s):  
D. ROBERTS ◽  
D. J. SMITH ◽  
S. DONNELLY ◽  
S. SIMARD
Keyword(s):  
Plasma Volume ◽  
Significant Rise ◽  
Normobaric Hypoxia ◽  
Hypoxic Exposure ◽  
Volume Depletion ◽  
Volume Contraction ◽  
Healthy Humans ◽  
Exercise Induced ◽  
Power Outputs ◽  
Response To Exercise

This study examined exercise-induced hypoxaemia (EIH) and plasma volume contraction as modulators of serum erythropoietin (Epo) production. Five athletes cycled for 3 min at supra-maximal power outputs, at each of two different elevations (1000 m and 2100 m). Five subjects were exposed to normobaric hypoxia (FIO2 = 0.159), seven subjects underwent plasmapheresis to reduce plasma volume and eight subjects were time controls for Epo levels. Oxyhaemoglobin saturation was significantly reduced during exercise and during normobaric hypoxia. The time period of haemoglobin oxygen saturation < 91% was 24±29 s (mean±S.D., n = 5) for exercise at 1000 m, 136±77 s (mean±S.D., n = 5) for exercise at 2100 m and 178±255 s (mean±S.D., n = 5) with resting hypoxic exposure. However, significantly increased serum Epo levels were observed only following exercise (24±3%; mean±S.D., n = 5 at 1000 m and 36±5%; mean±S.D., n = 5 at 2100 m). Volume contraction also resulted in increased serum Epo (35±6%; mean±S.D., n = 7) in spite of a significant rise in haematocrit of 2.2%. Despite similar degrees of arterial desaturation, only the hypoxaemia induced by exercise was associated with an increase in serum Epo. This finding indicates that other factors, in addition to hypoxaemia, are important in modulating the production of Epo in response to exercise. Volume depletion in the absence of exercise resulted in increases in Epo levels that were comparable with those observed in response to exercise. The paradoxical responses of the increased haematocrit and the increase in Epo in subjects undergoing plasmapheresis suggests that plasma volume may also modulate the production of Epo.

Plasma Volume Contraction

1980 ◽  
Vol 35 (9) ◽  
pp. 557-558 ◽  
Author(s):  
Eileen D. M. Gallery ◽  
Stephen N. Hunyor ◽  
Akos Z. Györy
Keyword(s):  
Plasma Volume ◽  
Volume Contraction
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