Methohexital Impairs Osmoregulation

1995 ◽  
Vol 82 (6) ◽  
pp. 1396-1405. ◽  
Author(s):  
Maieli Kasner ◽  
Jochen Grosse ◽  
Martin Krebs ◽  
Gabriele Kaczmarczyk
Keyword(s):  
Body Weight ◽  
Antidiuretic Hormone ◽  
Surgical Stress ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Blood Gases ◽  
Plasma Sodium ◽  
Plasma Osmolarity ◽  
Plasma Aldosterone Concentration ◽  
Arterial Blood

Background Anesthetic agents influence central regulations. This study investigated the effects of methohexital anesthesia on renal and hormonal responses to acute sodium and water loading in dogs in the absence of surgical stress. Methods Fourteen experiments (two in each dog) were performed in seven well-trained, chronically tracheotomized beagle dogs kept in highly standardized environmental and dietary conditions (2.5 mmol sodium and 91 ml water/kg body weight daily). Experiments lasted 3 h, while the dogs were conscious (7 experiments) or, after 1 h control, while they were anesthetized (7 experiments) with methohexital (initial dose 6.6 mg/kg body weight and maintenance infusion 0.34 mg.min-1.kg-1 body weight) over a period of 2 h. In both experiments, extracellular volume expansion was performed by intravenous infusion of a balanced isoosmolar electrolyte solution (0.5 ml.min-1.kg-1 body weight). Normal arterial blood gases were maintained by controlled mechanical ventilation. In another five dogs the same protocol was used, and vasopressin (0.05 mU.min-1.kg-1 body weight) was infused intravenously during methohexital anesthesia. Results Values are given as means. During methohexital anesthesia, mean arterial pressure decreased from 108 to 101 mmHg, and heart rate increased from 95 to 146 beats/min. Renal sodium excretion decreased; urine volume increased; and urine osmolarity decreased from 233 to 155 mosm/l, whereas plasma osmolarity increased from 301 to 312 mosm/l because of an increase in plasma sodium concentration from 148 to 154 mmol/l. Plasma renin activity, plasma aldosterone concentration, plasma atrial natriuretic peptide, and plasma antidiuretic hormone concentrations (range 1.8-2.8 pg/ml) did not change in either protocol. In the presence of exogenous vasopressin (antidiuretic hormone 3.3 pg/ml), water diuresis did not occur, and neither plasma osmolarity nor the plasma concentration of sodium changed. Conclusions Methohexital may impair osmoregulation by inhibiting adequate pituitary antidiuretic hormone release in response to an osmotic challenge.

scholarly journals AT II Receptor Blockade and Renal Denervation: Different Interventions with Comparable Renal Effects?

2021 ◽  
pp. 1-11
Author(s):  
Kristina Rodionova ◽  
Martin Hindermann ◽  
Karl Hilgers ◽  
Christian Ott ◽  
Roland E. Schmieder ◽  
...  
Keyword(s):  
Body Weight ◽  
Volume Expansion ◽  
Neural Control ◽  
Renal Denervation ◽  
Urine Volume ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Water Excretion ◽  
Arterial Blood ◽  
Renal Sympathetic

<b><i>Background:</i></b> Angiotensin II (Ang II) and the renal sympathetic nervous system exert a strong influence on renal sodium and water excretion. We tested the hypothesis that already low doses of an Ang II inhibitor (candesartan) will result in similar effects on tubular sodium and water reabsorption in congestive heart failure (CHF) as seen after renal denervation (DNX). <b><i>Methods:</i></b> Measurement of arterial blood pressure, heart rate (HR), renal sympathetic nerve activity (RSNA), glomerular filtration rate (GFR), renal plasma flow (RPF), urine volume, and urinary sodium. To assess neural control of volume homeostasis, 21 days after the induction of CHF via myocardial infarction rats underwent volume expansion (0.9% NaCL; 10% body weight) to decrease RSNA. CHF rat and controls with or without DNX or pretreated with the Ang II type-1 receptor antagonist candesartan (0.5 ug i.v.) were studied. <b><i>Results:</i></b> CHF rats excreted only 68 + 10.2% of the volume load (10% body weight) in 90 min. CHF rats pretreated with candesartan or after DNX excreted from 92 to 103% like controls. Decreases of RSNA induced by volume expansion were impaired in CHF rats but unaffected by candesartan pointing to an intrarenal drug effect. GFR and RPF were not significantly different in controls or CHF. <b><i>Conclusion:</i></b> The prominent function of increased RSNA – retaining salt and water – could no longer be observed after renal Ang II receptor blockade in CHF rats.

Renal Nerves Are Not Involved in Sodium and Water Retention during Mechanical Ventilation in Awake Dogs 

1998 ◽  
Vol 89 (4) ◽  
pp. 942-953 ◽  
Author(s):  
Willehad Boemke ◽  
Martin O. Krebs ◽  
Kourosh Djalali ◽  
Harald Bunger ◽  
Gabriele Kaczmarczyk
Keyword(s):  
Mechanical Ventilation ◽  
Continuous Positive Airway Pressure ◽  
Antidiuretic Hormone ◽  
Airway Pressure ◽  
Water Retention ◽  
Positive Airway Pressure ◽  
Surgical Stress ◽  
Urine Volume ◽  
Plasma Renin ◽  
Renal Nerves

Background The role of renal nerves during positive end-expiratory pressure ventilation (PEEP) has only been investigated in surgically stressed, anesthetized, unilaterally denervated dogs. Anesthesia, sedation, and surgical stress, however, decrease urine volume and sodium excretion and increase renal sympathetic nerve activity independent of PEEP. This study investigated in awake dogs the participation of renal nerves in mediating volume and water retention during PEEP. Methods Eight tracheotomized, trained, awake dogs were used. The protocol consisted of 60 min of spontaneous breathing at a continuous positive airway pressure of 4 cm H2O, followed by 120 min of controlled mechanical ventilation with a mean PEEP of 15-17 cm H2O (PEEP), and 60 min of continuous positive airway pressure. Two protocols were performed on intact dogs, in which volume expansion had (hypervolemic; electrolyte solution, 0.5 ml x kg(-1) x min(-1)) and had not (normovolemic) been instituted. This was repeated on the same dogs 2 or 3 weeks after bilateral renal denervation. Results Hypervolemic dogs excreted more sodium and water than did normovolemic dogs. There was no difference between intact and renal-denervated dogs. Arterial pressure did not decrease when continuous positive airway pressure was switched to PEEP. Plasma renin activity, aldosterone, and antidiuretic hormone concentrations were greater in normovolemic dogs. The PEEP increased aldosterone and antidiuretic hormone concentrations only in normovolemic dogs. Conclusions In conscious dogs, renal nerves have no appreciable contribution to sodium and water retention during PEEP. Retention in normovolemic dogs seems to be primarily caused by an activation of the renin-angiotensin system and an increase in the antidiuretic hormone. Excretion rates depended on the volume status of the dogs.

Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion

1979 ◽  
Vol 236 (2) ◽  
pp. H314-H322 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton ◽  
T. G. Coleman ◽  
R. E. McCaa
Keyword(s):  
Arterial Pressure ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Experimental Hypertension ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Hypotonic Saline

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.

THE SECRETION OF ANTIDIURETIC HORMONE IN RESPONSE TO HAEMORRHAGE AND THE FATE OF VASOPRESSIN IN ADRENALECTOMIZED RATS

1954 ◽  
Vol 11 (2) ◽  
pp. 165-176 ◽  
Author(s):  
M. GINSBURG
Keyword(s):  
Body Weight ◽  
Sodium Chloride ◽  
Antidiuretic Hormone ◽  
Intravenous Injection ◽  
Posterior Pituitary ◽  
Arterial Blood ◽  
Adrenalectomized Rats ◽  
Intact Rats

SUMMARY 1. The antidiuretic potency of arterial blood from adrenalectomized rats was greater than that from intact rats, but only if 2 or more ml. of blood were taken from each rat. It is concluded that the amounts of posterior pituitary antidiuretic hormone released during haemorrhage are greater in adrenalectomized than in intact rats. 2. The effect of haemorrhage on the antidiuretic potency of blood in adrenalectomized rats treated with sodium chloride or cortisone was not different from that in intact rats. 3. The disappearance of intravenously injected vasopressin (100 mU/100 g body weight) was retarded after adrenalectomy. Up to 48 hr after adrenalectomy this was due to a reduced capacity of the kidneys to remove vasopressin from the circulation. 4. Treatment with cortisone increased the rate of disappearance of vasopressin in adrenalectomized rats, but the rate was not restored to that observed in intact animals. 5. Treatment with sodium chloride did not affect the rate at which vasopressin was removed from the circulation of adrenalectomized rats. 6. The excretion of an antidiuretic agent in the urine which followed intravenous injection of vasopressin (100 mU/100 g) 48 hr after adrenalectomy was equivalent to 2·1% of the dose. This compared with an excretion of 6·7% of the dose in intact animals.

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.

Suppressed basal antidiuretic hormone release during cyclooxygenase inhibition in conscious dogs

1983 ◽  
Vol 244 (4) ◽  
pp. R487-R491
Author(s):  
B. R. Walker
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Antidiuretic Hormone ◽  
Plasma Osmolality ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Arterial Blood ◽  
The Central Nervous System

Both in vitro and in vivo experiments suggest that prostaglandins may affect antidiuretic hormone (ADH) release centrally. In addition, other studies show that prostaglandins administered peripherally may cause ADH release. However, these latter studies have been flawed by hemodynamic alterations and the use of anesthetics, which make interpretation difficult. The present study was designed to test for involvement of prostaglandins produced outside the central nervous system in ADH release in conscious dogs. Administration of meclofenamate (2 mg/kg and 2 mg X kg-1 X h 1, iv) resulted in a consistent fall in plasma ADH levels in five dogs. This diminution of ADH release occurred with no change in systemic hemodynamics, arterial blood gases, or plasma osmolality, suggesting that prostaglandins are important mediators of basal ADH release in the conscious dog. Because meclofenamate does not cross the blood-brain barrier, prostaglandins produced outside the central nervous system appear to be involved in this process. The specific prostaglandin involved or the site of action of prostaglandins on ADH release is not clear at this time.

Aldosterone effects on water and electrolyte metabolism

1984 ◽  
Vol 100 (1) ◽  
pp. 93-100 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris
Keyword(s):  
Body Weight ◽  
Water Balance ◽  
Urine Volume ◽  
Free Water ◽  
The Body ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Transient Effects ◽  
Water Metabolism ◽  
Free Water Clearance

ABSTRACT The effects of constant infusions of small doses of adrenal steroid hormones on sodium, potassium and water metabolism were studied in male adrenalectomized rats. An infusion of 1 μg aldosterone/day was sufficient to restore normal sodium and potassium balance in a group of rats fed an unsupplemented diet. Log doses of aldosterone (0·1–10 μg/day for 4 days) administered some days after adrenalectomy caused linear increases in the body weight of rats fed a sodium-supplemented diet (0·05 m-NaCl as drinking fluid) during 4 days of treatment. Increases in body weight correlated with renal sodium and water balance. When steroid treatment was started at the time of adrenalectomy, sodium balance was not significantly affected although rats treated with 1 μg aldosterone/day ate more, drank less saline, produced a smaller volume of urine of greater osmolarity and gained more weight than controls. A dose of 100 μg 18-hydroxy-deoxycorticosterone/day had no significant effects. Fluid intake and urine volume were not significantly affected by 1 mg corticosterone/day but food intake, water balance and weight gain were greater than controls. Rats treated with both aldosterone and corticosterone showed a decrease in free water clearance. Aldosterone and corticosterone, both singly and in combination, reduced plasma potassium levels. Plasma sodium levels were only increased when aldosterone was administered on its own. Long-term steroid infusions have revealed more about the physiology of aldosterone action than could acute measurements of renal function. In particular, they have indicated that dietary intake of electrolytes as well as excretion are affected, that mineralocorticoid actions are distinct from glucocorticoid actions and that there are transient effects of aldosterone on fluid regulation which are not sustained under steady-state conditions. J. Endocr. (1984) 100,93–100

Water and electrolyte changes in tropical Merino sheep exposed to dehydration during summer

1961 ◽  
Vol 12 (5) ◽  
pp. 889 ◽  
Author(s):  
WV Macfarlane ◽  
RJH Morris ◽  
B Howard ◽  
J McDonald ◽  
OE Budtz-Olsen
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Water Conservation ◽  
Renal Plasma Flow ◽  
Extracellular Volume ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Initial Increase ◽  
Fluid Loss ◽  
Plasma Urea

During three summers field studies were made of Merino wethers deprived of water while exposed to sun and to maximum air temperatures ranging from 84°F (29°C) to 10S°F (42°C) at Julia Creek, lat. 21° S. Evaporative cooling determined the rate and extent of water and electrolyte changes and produced a different pattern each year. Control of body temperature failed when 31% of body weight was lost by the end of 10 days without water. In hotter weather 5 days without water caused a 25% loss of body weight and in some sheep irreversible circulatory failure. In the course of dehydration, after an initial increase, the plasma and extracellular volume decreased up to 45% while concentrations of haemoglobin and plasma protein increased by 60%. In the plasma, potassium and sodium concentration increased less than that of haemoglobin. When 25% or more of weight was lost, plasma urea concentration rose to 136 mg/100 ml. Plasma osmolarity in some sheep reached 490 m-osmoles/l after 10 days. Urine volume fell after 2 days without water, and in a hot season less than 100 ml/24 hr was passed on the fourth or subsequent days. Concentrations increased over the first 4 or 5 days, reaching a maximum of 3.8 osmoles/l, then declined. Between half and two-thirds of the osmolarity was accountable to sodium and potassium salts. In rapid dehydration, more sodium was excreted than potassium. There was reduced sodium excretion when water was ingested after dehydration. Renal function studies in ewes indicated that filtration, renal plasma flow, and glucose reabsorption were reduced to half after 5 days without water in the heat. The chance of survival in dehydration appears to be increased by low rates of water loss in the first 3 days, together with high sodium and low potassium excretion. A full rumen, containing water up to 13% of body weight, could provide all the extracellular fluid loss. More than half of the weight loss appears, however, to come from intracellular sources. Extracellular fluid was drawn upon to a greater extent when the rate of dehydration was rapid, than in the cooler periods of slow weight loss. Survival in the sun without water depends upon insulation, water conservation, water reserves in rumen and extracellular fluid, the ability to adjust electrolyte concentrations, and the ability to maintain circulation with lowered plasma volume.

Release of antidiuretic hormone during mass-induced elevation of intracranial pressure

1977 ◽  
Vol 46 (5) ◽  
pp. 627-637 ◽  
Author(s):  
Lynn Gaufin ◽  
W. Ronald Skowsky ◽  
Stanley J. Goodman
Keyword(s):  
Intracranial Pressure ◽  
Antidiuretic Hormone ◽  
Rhesus Monkeys ◽  
Infusion Pump ◽  
Blood Gases ◽  
Content Type ◽  
Temporal Lobes ◽  
Balloon Catheters ◽  
Arterial Blood ◽  
Mass Expansion

✓ There are complex osmotic and non-osmotic factors regulating release of antidiuretic hormone (ADH). A wide variety of intracranial pathological processes may trigger ADH release sufficient to produce clinically recognizable hyponatremia, or the “inappropriate ADH syndrome.” We systematically studied one non-osmotic trigger, namely mass-induced elevated intracranial pressure (ICP). Initial experiments established baseline data in normal rhesus monkeys: anesthetized animals displayed appropriate rises and falls in immunoreactive urinary ADH in response to intravenously administered hypertonic and hypotonic infusions. Next, balloon catheters were implanted subdurally over temporal lobes and the animals were allowed to recover. The final experiment consisted of anesthetizing the animals, monitoring arterial blood pressure and blood gases, and retrieving timed urinary specimens while continuously recording ICP during infusion-pump expansion of the subdural balloon. A nonlethal and a lethal series of balloon-expansion experiments were done. Control values of urinary ADH were 783 ± 125 µU/15 min, and ICP was less than 10 mm Hg. During nonlethal mass expansion ADH output rose to 3433 ± 269 µU/15 min while ICP averaged 65 mm Hg (measured at completion of mass expansion). While the mass was maintained, hypotonic infusion produced unchanged urinary ADH output of 3452 ± 277 µU/15 min. During lethal experiments, urinary ADH rose still higher to 4339 ± 1887 µU/15 min associated with ICP averaging 100 mm Hg. We concluded that there is a direct relationship between the magnitude of ICP and the amount of ADH release, and that during elevated ICP the ADH release is not suppressed by hypotonic infusion.

Arginine vasopressin and prolactin after hemorrhage in the fetal lamb

1980 ◽  
Vol 238 (3) ◽  
pp. E214-E219 ◽  
Author(s):  
W. H. Drummond ◽  
A. M. Rudolph ◽  
L. C. Keil ◽  
P. D. Gluckman ◽  
A. A. MacDonald ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Surgical Stress ◽  
Blood Gases ◽  
Fold Increase ◽  
Plasma Prolactin ◽  
Third Trimester ◽  
Arterial Blood ◽  
Basal Plasma ◽  
Change Temperature ◽  
Plasma Arginine

Chronically prepared fetal lambs had basal plasma arginine vasopressin (AVP) levels of 1.6 +/- 0.23 pg/ml throughout the final third of gestation. Fetal AVP levels measured by radioimmunoassay were increased significantly to 5.8 +/- 0.92, 9.95 +/- 0.95, and 10.0 +/- 5 pg/ml in association with surgical stress, acute exteriorization, and acidosis or hypoxia, respectively. At 59-65 days gestation three lamb fetuses had a 50-fold increase in plasma AVP levels after acute exteriorization and hemorrhage indicating that the 0.4 gestation lamb fetus is capable of secreting pituitary AVP stores after intravascular volume change, temperature stress, and tactile stimulation. In six chronically catheterized third trimester fetuses, a 10-min, 20% hemorrhage caused a significant fall in fetal blood pressure, heart rate, and hematocrit. Plasma AVP increased significantly to 24.3 +/- 5.8 ng/ml without change in arterial blood gases or pH. Basal plasma prolactin concentration of 9.0 +/- 2.0 ng/ml was unchanged after hemorrhage in five fetuses.

Sign in / Sign up

Export Citation Format

Share Document