Thirst and salt appetite in horses treated with furosemide

1991 ◽  
Vol 71 (6) ◽  
pp. 2380-2386 ◽  
Author(s):  
K. A. Houpt ◽  
N. Northrup ◽  
T. Wheatley ◽  
T. R. Houpt
Keyword(s):  
Sodium Chloride ◽  
Sodium Intake ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Salt Appetite ◽  
Blood Constituents ◽  
Salt Consumption ◽  
Plasma Sodium Concentration ◽  
Sodium Loss ◽  
Control Injection

When a preliminary experiment in sodium-replete ponies revealed an increase, but not a significant increase, in salt consumption after furosemide treatment, the experiment was repeated using sodium-deficient horses in which aldosterone levels might be expected to be elevated to test the hypothesis that a background of aldosterone is necessary for salt appetite. Ten Standardbred mares were injected intravenously with furosemide or an equivalent volume of 0.9% sodium chloride as a control to test the effect of furosemide on their salt appetite and blood constituents. Sodium intake and sodium loss in urine, as well as water intake and urine output, were measured and compared to determine accuracy of compensation for natriuresis and diuresis. Plasma protein and packed cell volume showed significant increases in response to furosemide treatment (F = 29.31, P less than 0.001 and F = 11.20, P less than 0.001, respectively). There were no significant changes in plasma sodium concentration or osmolality in response to the treatment (P greater than 0.05). The furosemide-treated horses consumed 126 +/- 14.8 g salt, significantly more than when they were given the control injection (94.5 +/- 9.8 g; t = 2.22, P = 0.05). In response to furosemide, horses lost 962 +/- 79.7 and consumed 2,170 +/- 5 meq sodium; however, compared with control, they lost 955 meq more sodium and ingested only 570 meq more sodium, so they were undercompensating for natriuresis. The furosemide-treated horses drank 9.6 +/- 0.8 kg of water, significantly more than when they received the control injection (6.4 +/- 0.8 kg; t = 6.9, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Elevated cerebrospinal fluid sodium in hypertensive human subjects with a family history of Alzheimer’s disease

2020 ◽  
Vol 52 (3) ◽  
pp. 133-142
Author(s):  
Lucas A. C. Souza ◽  
Fatima Trebak ◽  
Veena Kumar ◽  
Ryousuke Satou ◽  
Patrick G. Kehoe ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Sodium Intake ◽  
Human Subjects ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Chronic Hypertension ◽  
Plasma Sodium Concentration ◽  
History Of

High salt (sodium) intake leads to the development of hypertension despite the fact that plasma sodium concentration ([Na+]) is usually normal in hypertensive human patients. Increased cerebrospinal fluid (CSF) sodium contributes to elevated sympathetic activity and high blood pressure (BP) in rodent models of hypertension. However, whether there is an increased accumulation of sodium in the CSF of humans with chronic hypertension is not well defined. Here, we investigated CSF [Na+] from hypertensive and normotensive human subjects with family histories of Alzheimer’s disease in samples collected in a clinical trial, as spinal tap is not a routine clinical procedure for hypertensive patients. The [Na+] and osmolality in plasma and CSF were measured by flame photometry. Daytime ambulatory BP was monitored while individuals were awake. Participants were deidentified and data were analyzed in conjunction with a retrospective analysis of patient history and diagnosis. We found that CSF [Na+] was significantly higher in participants with high BP compared with normotensive participants; there was no difference in plasma [Na+], or plasma and CSF osmolality between groups. Subsequent multiple linear regression analyses controlling for age, sex, race, and body mass index revealed a significant positive correlation between CSF [Na+] and BP but showed no correlation between plasma [Na+] and BP. In sum, CSF [Na+] was higher in chronic hypertensive individuals and may play a key role in the pathogenesis of human hypertension. Collectively, our findings provide evidence for the clinical significance of CSF [Na+] in chronic hypertension in humans.

Severe Hyponatremia, Hyperglycemia, and Hyperlactatemia Are Associated with Intraoperative Hyperthermic Intraperitoneal Chemoperfusion with Oxaliplatin

2008 ◽  
Vol 28 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Filip De Somer ◽  
Wim Ceelen ◽  
Joris Delanghe ◽  
Dirk De Smet ◽  
Martin Vanackere ◽  
...  
Keyword(s):  
Metabolic Disorder ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Severe Hyponatremia ◽  
Plasma Sodium Concentration ◽  
Surgical Debulking ◽  
Major Loss ◽  
Sodium Loss ◽  
Total Body ◽  
Intraperitoneal Chemoperfusion

Background Since the introduction of surgical debulking in combination with intraoperative hyperthermic intra-peritoneal chemoperfusion (HIPEC) with oxaliplatin in our institution, severe hyponatremia (sodium: 126.5 ± 3.8 mmol/L), hyperglycemia (glucose: 22.37 ± 4.89 mmol/L), and hyperlactatemia (lactate: 3.17 ± 1.8 mmol/L) have been observed post HIPEC. This metabolic disorder was not observed in patients in whom cisplatin or mitomycin C was used as a chemotherapeutic drug. Methods In order to understand the pathophysiology of this finding, an analysis of our data was made. In a first analysis, plasma sodium was corrected for hyperglycemia based on the formula of Hillier. In a second analysis, the influence of total exchangeable sodium, total exchangeable potassium, and total body water on plasma sodium concentration was modeled. Results Analysis of our data revealed a double mechanism for the observed metabolic disorder: hyperglycemia caused by dextrose 5%, which is used as a carrier for the oxaliplatin, and major loss of sodium into the dialysate (256.7 ± 68.7 mmol). Conclusion Better control of hyperglycemia and intravenous compensation of sodium loss into the dialysate can attenuate the reported biochemical disturbance.

Dietary Sodium Intake: A Determinant of Postprandial Plasma Sodium Concentration in the Dog

1982 ◽  
Vol 62 (5) ◽  
pp. 471-477 ◽  
Author(s):  
E. G. Schneider ◽  
Sarah D. Gleason ◽  
A. Zucker
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Free Access ◽  
Potassium Excretion ◽  
Plasma Sodium Concentration

1. The effect of dietary sodium intake on pre-and post-prandial plasma sodium concentrations and on the pattern of sodium and potassium excretion was determined in conscious female dogs, who were allowed free access to water and were fed on commercial low sodium diets supplemented with 0, 50, 100 or 250 mmol of sodium chloride/day for 6 days. 2. The preprandial plasma sodium concentration was not altered by the dietary sodium intake. However, the 4 h postprandial plasma sodium concentration was linearly related to the magnitude of dietary sodium intake, whereas the 8 h postprandial plasma sodium concentration was elevated only in dogs receiving 250 mmol of sodium/day. 3. The (0–8 h/0–24 h) ratio for urinary sodium excretion was significantly correlated with both the dietary sodium intake and the postprandial increase in plasma sodium concentration. 4. The 24 h excretion of potassium was not markedly affected by the dietary sodium intake; however, the (0–8 h/0–24 h) ratio for potassium excretion was significantly correlated with both the dietary sodium intake and the (0–8 h/0–24 h) ratio for sodium excretion. 5. These data indicate that: (a) postprandial increases in plasma sodium concentration need to be considered when evaluating the mechanisms involved in the daily regulation of sodium balance; (b) the daily pattern of potassium excretion is closely linked to the dietary sodium intake.

SURVEY IN SERUM ADH CONCENTRATION IN TRAUMATIC BRAIN INJURY PATIENTS

2014 ◽  
pp. 83-89
Author(s):  
Dung Ngo ◽  
Thi Nhan Nguyen ◽  
Khanh Hoang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Osmotic Pressure ◽  
Negative Correlation ◽  
Closed Head Injury ◽  
Serum Levels ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration ◽  
Closed Head

Objective: Study on 106 patients with closed head injury, assessment of serum ADH concentration, correlation with Glasgow score, sodium and plasma osmotic pressure. Patients and methods: Patients with closed head injuries were diagnosed determined by computerized tomography, admitted to the Hue Central Hospital 72 hours ago. Results: (i) Serum concentration of ADH 42.21 ± 47.80 pg/ml. (ii) There is a negative correlation between serum levels of ADH with: (1) Glasgow point r = -0.323, p <0.01; (2) Plasma sodium concentration r = - 0.211, p > 0.05; (3) Plasma osmotic pressure r = - 0.218, p> 0.05. Conclusion: There is a negative correlation between serum levels of ADH with Glasgow scale, plasma sodium concentration and osmotic pressure in plasma. Key words: ADH traumatic brain injury.

scholarly journals Effects of Tissue Sodium Storage on Plasma Sodium Concentration in Response to Hypo- and Hypertonic Stimuli

Nephron ◽  
2021 ◽  
pp. 1-3
Author(s):  
Rosa D. Wouda ◽  
Rik H.G. Olde Engberink ◽  
Eliane F.E. Wenstedt ◽  
Jetta J. Oppelaar ◽  
Liffert Vogt
Keyword(s):  
Sodium Concentration ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration ◽  
Sodium Storage ◽  
Tissue Sodium

Effects of homologous atrial natriuretic peptide on drinking and plasma ANG II level in eels

1998 ◽  
Vol 275 (5) ◽  
pp. R1605-R1610 ◽  
Author(s):  
Takamasa Tsuchida ◽  
Yoshio Takei
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Drinking Rate ◽  
Plasma Sodium Concentration ◽  
Atrial Natriuretic

The effects of eel atrial natriuretic peptide (ANP) on drinking were investigated in eels adapted to freshwater (FW) or seawater (SW) or in FW eels whose drinking was stimulated by a 2-ml hemorrhage. An intra-arterial infusion of ANP (0.3–3.0 pmol ⋅ kg−1 ⋅ min−1), which increased plasma ANP level 1.5- to 20-fold, inhibited drinking dose dependently in all groups of eels. The drinking rate recovered to the level before ANP infusion within 2 h after infusate was replaced by saline. The inhibition at 3.0 pmol ⋅ kg−1 ⋅ min−1was profound in FW eels and hemorrhaged FW eels, whereas significant drinking still remained after inhibition in SW eels. Plasma ANG II concentration also decreased dose dependently during ANP infusion and recovered to the initial level after saline infusion in all groups of eels. The decrease at 3.0 pmol ⋅ kg−1 ⋅ min−1was large in FW eels and hemorrhaged FW eels compared with that of SW eels. Thus the changes in drinking rate and plasma ANG II level were parallel during ANP infusion. Plasma sodium concentration and osmolality decreased during ANP infusion in SW and FW eels, and they were restored after saline infusion. In hemorrhaged FW eels, however, ANP infusion did not alter plasma sodium concentration and osmolality. Hematocrit did not change during ANP infusion in any group of eels. Collectively, ANP infusion at physiological doses decreased drinking rate and plasma ANG II concentration in parallel in both FW and SW eels. It remains undetermined whether the inhibition of drinking is caused by direct action of ANP or through inhibition of ANG II, which is known as a potent dipsogen in all vertebrate species, including eels.

scholarly journals Plasma and Electrolyte Changes in Exercising Humans After Ingestion of Multiple Boluses of Pickle Juice

2015 ◽  
Vol 50 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michael A. McKenney ◽  
Kevin C. Miller ◽  
James E. Deal ◽  
Julie A. Garden-Robinson ◽  
Yeong S. Rhee
Keyword(s):  
Body Weight ◽  
Relative Humidity ◽  
Blood Sample ◽  
Plasma Volume ◽  
Potassium Concentration ◽  
Plasma Osmolality ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Plasma Sodium Concentration

Context: Twenty-five percent of athletic trainers administer pickle juice (PJ) to treat cramping. Anecdotally, some clinicians provide multiple boluses of PJ during exercise but warn that repeated ingestion of PJ may cause hyperkalemia. To our knowledge, no researchers have examined the effect of ingesting multiple boluses of PJ on the same day or the effect of ingestion during exercise. Objective: To determine the short-term effects of ingesting a single bolus or multiple boluses of PJ on plasma variables and to characterize changes in plasma variables when individuals ingest PJ and resume exercise. Design: Crossover study. Setting: Laboratory. Patients or Other Participants: Nine euhydrated men (age = 23 ± 4 years, height = 180.9 ± 5.8 cm, mass = 80.7 ± 13.8 kg, urine specific gravity = 1.009 ± 0.005). Intervention(s): On 3 days, participants rested for 30 minutes, and then a blood sample was collected. Participants ingested 0 or 1 bolus (1 mL·kg−1 body weight) of PJ, donned sweat suits, biked vigorously for 30 minutes (approximate temperature = 37°C, relative humidity = 18%), and had a blood sample collected. They either rested for 60 seconds (0- and 1-bolus conditions) or ingested a second 1 mL·kg−1 body weight bolus of PJ (2-bolus condition). They resumed exercise for another 35 minutes. A third blood sample was collected, and they exited the environmental chamber and rested for 60 minutes (approximate temperature = 21°C, relative humidity = 18%). Blood samples were collected at 30 and 60 minutes postexercise. Main Outcome Measure(s): Plasma sodium concentration, plasma potassium concentration, plasma osmolality, and changes in plasma volume. Results: The number of PJ boluses ingested did not affect plasma sodium concentration, plasma potassium concentration, plasma osmolality, or changes in plasma volume over time. The plasma sodium concentration, plasma potassium concentration, and plasma osmolality did not exceed 144.6 mEq·L−1 (144.6 mmol·L−1), 4.98 mEq·L−1 (4.98 mmol·L−1), and 289.5 mOsm·kg−1H2O, respectively, in any condition at any time. Conclusions: Ingesting up to 2 boluses of PJ and resuming exercise caused negligible changes in blood variables. Ingesting up to 2 boluses of PJ did not increase plasma sodium concentration or cause hyperkalemia.

The response of plasma minerals, free fatty acids and glucose to adrenaline and cortisol infusion in sheep

1986 ◽  
Vol 106 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Sarah C. Bolton ◽  
T. E. C. Weekes
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Marked Decrease ◽  
Plasma Concentrations ◽  
Sodium Concentration ◽  
Plasma Calcium ◽  
Plasma Sodium ◽  
Plasma Phosphate ◽  
Plasma Sodium Concentration ◽  
Plasma Magnesium

SUMMARYAdrenaline was infused at three rates, 40, 15 or 3 μ/kg/h, in normal sheep and in sheep rendered hypercortisolaemic by infusion of cortisol at 150 μg/kg/h. In both normal and hypercortisolaemic animals, plasma concentrations of glucose and free fatty acids were increased by adrenaline treatment; plasma phosphate decreased with all treatments; plasma magnesium and potassium decreased on infusion of adrenaline at 40 or 15, but not at 3 μg/kg/h; plasma calcium decreased only on infusion of adrenaline in hypercortisolaemic animals, and plasma sodium concentration was unaffected by treatment.Induction of a degree of lipolysis likely to occur in the field was not associated with a marked decrease in plasma magnesium.

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