Hypertonic Sodium Chloride Solution Research Articles

An in vitro cataract model for practice of cataract surgery.

We have developed an in vitro cataract model using enucleated animal eyes. A cataract is produced by immersing the enucleated eyes in hypertonic sodium chloride solution for one hour and re-incubating them for another hour in normal saline solution. The model is useful for practicing various techniques of cataract extraction.

Efferent renal nerve activity during intracarotid and intracerebroventricular infusions of hypertonic sodium chloride solutions and isotonic volume expansion in the rat.

The change in renal nerve activity under conditions known to increase renal sodium excretion was studied. In adult Sprague Dawley rats, anaesthetized with Inactin, normotonic and hypertonic NaCl solutions were infused into 1) a vein, 2) a carotid artery and 3) the third ventricle. The left kidney was freed and placed in a plastic cup. A renal nerve was dissected free and placed on a stainless bipolar electrode. The nerve was cut distal to the electrode. The nerve signals were amplified and recorded on a tape recorder. Simultaneously integrated nerve signals and also atrial and venous pressures were recorded. Intracarotid infusion of a 1 M NaCl solution increased sodium output and temporarily decreased renal nerve activity by some 35%. Corresponding intravenous (i.v.) infusion gave an increase in renal nerve activity and also in sodium output. The latter increase was delayed compared with that caused by the intracarotid infusion. No variations in blood pressure were noted. In control experiments with a slow i.v. infusion of physiological saline, renal nerve activity increased throughout the experiment, while sodium excretion remained constant. During infusion of a 1 M NaCl solution into the third ventricle, renal nerve activity decreased in about half of the cases. This reduction was often accompanied by an increased arterial blood pressure and an increased sodium output. Arterial blood pressure increases were especially pronounced at the highest infusion rats, i.e. 800 ml-min-1. Isotonic volume expansion of 2% of the body weight resulted in a transient decrease in renal nerve activity by about 30%. Venous blood pressure rose and sodium output increased six-fold. The decrease in nerve activity was observed both when the vagal nerves were intact and when they were cut.

Heterogeneity in regulation of glomerular function.

The aim was to study differences in filtration driving forces and glomerular filtration rates between superficial and deep nephrons when urine flow rate was altered at the macula densa region. In young rats stop-flow pressures and single nephron glomerular filtration rates (SNGFR) were measured in the superficial proximal tubules and in the loops of Henle in the papilla. SNGFR was also measured with a modified Hanssen technique. The stop-flow pressures of superficial nephrons amounted to 30.9 +/- 0.8 mmHg (mean +/- SE) and those of juxtamedullary nephrons to 52.2 +/- 1.6 mmHg. In the stop-flow condition the net driving filtration forces were calculated to be about 19 mmHg and 50 mmHg for the superficial and deep glomeruli, respectively. In free flow conditions both net driving forces were calculated to be 19 mmHg. The micropuncture technique gave a SNGFR value for superficial nephrons of 29.6 +/- 2.9 and for deep nephrons of 84.1 +/- 8.5 nl x min-1 . g-1 kidney weight (KW). With a modified Hanssen technique the corresponding values were 25.8 +/- 3.3 and 27.7 +/- 2.9 nl . min-1 . g-1 KW. The tubuloglomerular feedback mechanism is considered to have a powerful regulatory influence on the glomerular filtration rate of deep nephrons.

Active ion transport in dog tongue: a possible role in taste.

An in vitro preparation of the dorsal epithelium of the dog tongue actively transports ions, producing a transepithelial potential difference characteristic of the ions and their concentration. Hypertonic sodium chloride solutions generally cause increased potentials and short-circuit currents and reduced resistances when placed on the mucosal surface. This hypertonic flux is eliminated by ouabain and is not found in ventral lingual epithelia. When either sodium acetate or tetramethylammonium chloride is substituted for sodium chloride in the mucosal medium, the currents are diminished but their sum at a given concentration approximates that for sodium chloride at the same concentration. This result suggests a current composed of inward sodium ion movement and outward chloride ion movement. Actively regulated potentials and currents, whether generated in the taste buds or in supporting cells, may be important in both normal chemotransduction and in taste responses evoked by currents passing through the tongue.

The effect of prostaglandins on the release of arginine vasopressin from the guinea pig hypothalamo-neurohypophyseal complex in organ culture.

The effect of prostaglandins (PGs) on arginine vasopressin (AVP) release was investigated using the male guinea pig hypothalamo-neurohypophyseal complex (HNC) in organ culture. The explants of HNC were used on the second day in culture. The culture medium containing PGE2 caused an increase in AVP release from the explants during a 10-min incubation period. AVP release was significantly increased at a PGE2 concentration of 2 X 10(-8) M or more. AVP release was increased in a dose-dependent manner. PGF2 alpha at concentrations of 1.4 X 10(-7) and 1.4 X 10(-6) M also increased AVP release significantly. The explants in the group treated with 7.4 X 10(-5) M indomethacin for 60 min before the experiment and throughout the experiment responded to 6.5 X 10(-8) M angiotensin II with a 166 +/- 42% increase in AVP release over control release. The response of explants to the addition of angiotensin II in this group was significantly lower (P less than 0.05) than that in the group not treated with indomethacin, which was 439 +/- 128% of the basal value (P less than 0.05). The release of AVP in the group treated with indomethacin was 120 +/- 15% of the basal value in response to a hypertonic solution of sodium chloride at 310 mosmol/kg H2O and was significantly lower (P less than 0.05) than that in the group not treated with indomethacin (203 +/- 30% of the basal value; P less than 0.005). However, indomethacin did not alter basic release of AVP. These results suggest that PGE2 and PGF2 alpha increase AVP release from the explants of HNC in organ culture, although PGF 2 alpha has a relatively weaker effect than PGE2, and PGs may modulate the regulation of AVP release in response to angiotensin II and osmotic stimulation.

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

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.

Renin, Water drinking, salt preference and blood pressure in alcohol preferring and alcohol avoiding rats

Mechanisms controlling fluid volume were studied in alcohol preferring AA (Alko, Alcohol) and alcohol avoiding ANA (Alko, Non-Alcohol) rats. Hypertonic sodium chloride solution (5%) given orally caused a higher dipsogenic response in AA rats than in the ANA's. One hour after ethanol loading (4.8 g/kg, by stomach tube), plasma renin activity of AA rats was four times as high as in ANA rats. ANA rats had higher degree of sodium chloride (0.9%) preference and higher blood pressure. The strain differences in voluntary salt intake and salt metabolism may modulate the consumption of calories and water as well as blood pressure and different reactivity of the renin system in AA and ANA rats.

Osmotic pressure and angiotensin II stimulation of arginine vasopressin release from a guinea pig hypothalamo-neurohypophyseal complex in organ culture (author's transl)

An organ culture system of a male guinea pig hypothalamo-neurohypophyseal complex (HNC) was established. On day 5 in culture, (Na+ -K+) ATPase activity was 0.83 +/- 0.11 mM Pi/mg prot/hr (mean +/- SEM): that is 67% of that on day 1 in culture. 3H-thymidine incorporated into DNA in the explants of HNC was 1,205 +/- 185 cpm/microgram DNA. The explants responded to the elevated KCl medium and the hypertonic solution of sodium chloride with a 470 +/- 38% and 298 +/- 31% increase in arginine vasopression (AVP) release, respectively. This response was inhibited by the addition of tetrodotoxin to the culture medium. AVP release from the explants in res-onse to angiotensin II increased significantly in a dose dependent manner. [Sar1, Ile8] angiotensin II, however, attenuated the response of the explants to angiotensin II when administered simultaneously with angiotensin II. These results suggest that angiotensin II and its analogue cause the AVP release from the explants in a competitive manner. The concentrations of AVP in the culture media made hypertonic with sodium chloride, sucrose and mannitol were 298 +/- 31% (p less than 0.01), 251 +/- 36% (p less than 0.01) and 255 +/- 59% (p less than 0.05) of their control values, respectively. The hypertonic solutions of sodium chloride, sucrose and mannitol caused AVP release from the explants in vitro, while the hypertonic solutions of glucose and urea were revealed to be poor osmotic stimuli on AVP release. These results support the concept of osmoreceptors to release AVP from the hypothalamo-neurohypophyseal axis.

Renal response of ethanol-treated dogs to increased filtered loads of sodium, bicarbonate, and chloride

Twenty, male, mongrel dogs were given either 3 g/kg (33% v v solution) of ethanol or an isovolumetric quantity of water by oral intubation. Sixteen hours later the animals were anesthetized and after a control renal clearance, infused with either a hypertonic sodium chloride or sodium bicarbonate solution for an additional three clearance periods. The rate of infusion of solutions was increased progressively prior to each of the next periods. At each new rate, 45 min was permitted for equilibration before the clearance period. The hypertonic NaCl infusion produced similar increases in GFR, the filtered loads of Na and Cl, and the excretory rates of Na and Cl in both the water and ethanol groups. Although the hypertonic NaHCO 3 infusion produced equal increases in GFR and filtered loads of Na and HCO 3, there were dissimilar increases in Na and HCO 3 excretions. Sodium excretion increased by 17.1 ± 1.1 μeq/min/kg and percentage reabsorption decreased by 3.5 ± 0.3% in the water group while in the ethanol group, U Na · V increased by 10.0 ± 1.4 μeq/min/kg ( p < 0.01) and % R Na decreased by 1.9 ± 0.2% ( p < 0.01). In the ethanol group, bicarbonate excretion increased by 8.1 ± 1.3 μeq/min/kg and in the water group by 12.3 ± 1.1 μeq/min/kg ( p < 0.05). The reduction in % R HCO 3 was significantly less in the ethanol group in comparison to the water group (8.1 ± 1.0 vs 12.1 ± 0.8%). Known effectors of sodium bicarbonate reabsorption, i.e., volume status, pCO 2, potassium stores, and filtration rate were not different between groups. It is concluded that ethanol pretreatment ameliorated the depressant effect of the NaHCO 3 infusion on tubular reabsorption.

Alteration of Rumen Fermentation in Steers by Increasing Rumen Fluid Dilution Rate with Mineral Salts

Holstein steers were fed either high concentrate or high roughage diets ad libitum, and hypertonic solutions of either sodium chloride or sodium bicarbonate were infused intraruminally to increase osmotic pressure of the rumen fluid. Dry matter intake was reduced in steers fed the high roughage diet during the intraruminal infusion of 1kg of sodium chloride. Decreased cellulose degradation as a result of increased osmotic pressure of rumen fluid may have been responsible for the reduced dry matter intake. Dilution rate of rumen fluid was increased by infusion of both sodium chloride and sodium bicarbonate. An increase in water consumption accounted for, at least in part, the increase in total outflow of fluid from the rumen. The concentration of total volatile fatty acids in rumen fluid was reduced during infusion of both sodium chloride and sodium bicarbonate. The increased dilution rate of rumen fluid when hypertonic solutions were infused intraruminally into steers fed a high concentrate diet was associated with an increased molar proportion of acetate and a decreased molar proportion of propionate. In contrast, the molar proportions of acetate and propionate in the rumen fluid of steers fed a high roughage diet were not altered although dilution rate of rumen fluid was increased by infusing the hypertonic solutions.

Effect of duodenal osmolality on gastrin and secretin release and on gastric and pancreatic secretion.

AbstractWe have measured the osmolality of duodenal contents in 9 dogs after a hypertonic meal, given either by mouth or directly into the stomach or perfused into the duodenum. A test meal of 2,475 mosm/kg, given by mouth, raised the intraduodenal osmolality to 700–1,500 mosm/kg over a 1‐hour period. Hypertonic glucose solutions (2,000 and 3,400 mosm/kg), given into the stomach, were found to be diluted to about 700 and 1,100 mosm/kg, respectively, at the level of the mid‐duodenum 30 minutes later. Hypertonic saline solutions (1,800 and 2,700 mosm/kg), perfused into the duodenum, created a stable intraluminal osmolality of 800 and 1,200 mosm/kg, respectively, (about 45% that of the perfusate) after 30 minutes.In 6 Heidenhain pouch dogs, gastric secretion and gastrin release stimulated by food were significantly diminished by administration of hypertonic sodium chloride solution (1,800 mosm/kg) into the duodenum. This hyperosmolality caused greater suppression of acid secretion (52%) than of gastrin release (28%). Stimulation of pancreatic water and bicarbonate secretion and of release of radioimmunoassayable secretin by intraduodenal HCl (pH 1.3) were significantly suppressed when the osmolality of the HCl solution was raised to 2,700 mosm/kg. Pancreatic protein secretion remained unchanged with hypertonic solutions. We have confirmed that stimulation of intraduodenal osmoreceptors inhibits gastric acid secretion in dogs, and we suggest that this is due, at least in part, to a suppression of gastrin release. We further suggest that duodenal osmolar inhibition of pancreatic secretion involves suppression of secretin but does not appear to involve cholecystokinin.

Hemolysis kinetics for human erythrocyte exposure to isothermal, hypertonic sodium chloride solutions

Hemolysis kinetics for human erythrocyte exposure to isothermal, hypertonic sodium chloride solutions

Surgical treatment of echinococcal cyst of the heart: Report of two cases and review of the world literature

The case histories of two children with echinococcal cysts of the left ventricular myocardium are reported. Both patients underwent successful enucleation of the cysts, after initial local treatment with 0.5 percent silver nitrate solution. A previous review of the world literature on the surgical treatment of echinococcal cyst of the heart, published in 1971, is brought up to date by the addition of 60 new cases to the 118 cases then described. Instillation of 0.5 percent silver nitrate solution into the cyst cavity is now a routine procedure in our institution to sterilize the cyst and to kill the scolices. This substance is preferable to formalin and hypertonic sodium chloride solution, because it acts rapidly and is nontoxic and nonabsorbable. The two children in this report are the first in whom silver nitrate solution was used to sterilize the myocardial cysts.

Excretion of salt and water by patients with sickle-cell anaemia: effect of a diuretic and solute diuresis.

1. Patients with sickle-cell anaemia were unable to increase free water reabsorption (TcH2O) in response to intravenous hypertonic sodium chloride solution. 2. Ethacrynic acid caused a brisk natriuresis in patients with sickle-cell anaemia but fractional sodium excretion was lower in these patients. 3. These findings could be explained by abnormal function of the loop of Henle.

Increased proliferation of neuroglia and endothelial cells in the supraoptic nucleus and hypophysial neural lobe of young rats drinking hypertonic sodium chloride solution.

AbstractMale rats aged 30 to 35 days were provided with 1.75% sodium chloride solution as drinking fluid for two weeks, to create a chronic increase in plasma osmolality. During this time, the animals and a control group of water‐drinking rats received two injections per day of 1 μCi of 3H‐thymidine per gram body weight to label dividing cells and their progeny. At the end of this period, the animals were sacrificed by aldehyde perfusion. Sections 1 μm‐thick were saved at intervals from a series cut throughout the length of the supraoptic nucleus; these sections and others taken from the caudate nucleus and the neural lobe of the hypophysis were processed for radioautography.Neuronal nuclei and nucleoli were enlarged in the supraoptic nucleus of salttreated rats, in accord with previous work indicative of neuronal enlargement associated with increased protein synthesis and probably enhanced vasopressin production. Furthermore, most axon terminals in the neural lobe were depleted of neurosecretory granules in the salt‐treated group, a fact suggesting increased release of vasopressin.Cell counts in radioautographs of the supraoptic nucleus revealed that 20.6% of the astrocytes were labeled in salt‐treated rats, but only 5.9% in controls, indicating a marked increase in the production of new astrocytes in the treated animals. Also, endothelial cells were more frequently labeled in salt‐treated rats (52.9%) than in controls (17.4%). In the caudate nucleus, by contrast, the labeling percentages of astrocytes or of endothelial cells did not differ between control and treated rats. In the neural lobe, the labelling percentage of pituicytes was 45.8% in treated, but only 3.1% in control animals. The endothelial cell labeling was also greater in treated (46.5%) than controls (23.9%). Thus, in young rats, a period of salt ingestion elicited both an enlargement of supraoptic neurons and an increase in the production of the astrocytes, pituicytes, and endothelial cells associated with these neurons and their processes.

Effect of pharmacological inhibitors on urate transport during induced uricosuria.

1. The effect on urate excretion of administration of probenecid and pyrazinamide was observed in normal subjects under control conditions and after induction of uricosuria by exogenous urate loading by ribonucleic acid feeding in seven subjects, by volume loading with hypertonic sodium chloride solution infusion in 11 subjects and by partial inhibition of net urate reabsorption with uricosuric drugs in 20 subjects. 2. After ribonucleic acid feeding, the uricosuric response to probenecid was intact and ribonucleic acid feeding did not produce uricosuria after pyrazinamide. 3. After volume loading, the uricosuric response to probenecid was again intact, but infusion of sodium chloride solution still produced uricosuria after pyrazinamide administration. 4. After uricosuric drugs, the uricosuric response to probenecid was diminished. 5. These responses to probenecid and pyrazinamide may reflect different mechanisms of uricosuria. Response to pharmacological inhibitors of urate reabsorption or urate secretion may be useful for classification of induced and clinical uricosuric states.

Localization of Receptors Inhibiting Gastric Emptying in the Gut

Five dogs were prepared, each with three fistulas; one fistula was placed in the stomach, the other in the first part of the duodenum, 5 cm from the pylorus, and the third at the junction of the duodenum and the jejunum. By combinations of test meals and perfusions, either a part of or the whole duodenum or jejunum was tested with 550 to 850-milliosmolar solutions (glucose, glycine, mannitol, or sodium chloride), 100 mm HCl, 10 or 20 mm sodium oleate and 40 mm tryptophan for their effect on gastric emptying. Phenol red was used as a nonabsorbable marker. Gastric emptying was not slowed by perfusion of the whole duodenum with the hypertonic solutions of glucose, glycine, mannitol and sodium chloride, or with 10 or 20 mm sodium oleate. In contrast, significant slowing of gastric emptying occurred with jejunal perfusion of the hypertonic solutions and sodium oleate. Jejunal perfusion of 100 mm HCl slowed gastric emptying, but perfusion of the second to fourth parts of the duodenum did not. Tryptophan slowed gastric emptying when allowed to perfuse the first 5 cm of the duodenum, the second to fourth parts of the duodenum, and also the jejunum. The findings from this study indicate that the jejunum has receptors for inhibition of gastric emptying responsive to tryptophan, acid, fat, and hypertonic solutions. In contrast, the duodenum has receptors responsive to tryptophan.

The effects of vasopressin on renal sodium excretion in pigs given intravascular hypertonic salt loads.

Young pigs of about 25-30 kg liveweight were given intravenous infusions of a hypertonic sodium chloride solution (4-6 mol.1(-1)) at rates varying from 2-6 mmol.min-1. Such infusions resulted in a marked increase in the urine flow and in urinary sodium excretion, the size of these increases being proportional to infusion rate. Circulating vasopressin levels were also markedly increased, the size of these increases being the same as those seen in other pigs given exogenous vasopressin in amounts which were shown to increase urinary sodium excretion. This suggests that vasopressin was probably contributing to the increase in renal sodium excretion seen in those pigs given the intravenous salt loads.

Hemolysis of human erythrocytes in hypertonic sodium chloride solutions at subphysiological temperatures

Hemolysis of human erythrocytes in hypertonic sodium chloride solutions at subphysiological temperatures

Sodium loading of inner ear fluids.

A slow intracarotid infusion of hypertonic sodium chloride solution, 350 mEq/L, and potassium chloride, 5 mEq/L, was used to increase serum sodium chloride over a 90-minute period in 85 cats. A slow, steady rise in serum sodium occurred, which reached almost 208 mEq/L at the end of 90 minutes. A concomitant rise in sodium occurred in the cerebrospinal fluid and perilymph. In contrast, the sodium showed only a transient slight increase in the cochlear and vestibular endolymph. Endolymph potassium appeared to rise in order to balance out the increase in sodium concentration of the surrounding and extracellular fluids. The ratio of sodium to potassium ions in both the endolymph and perilymph compartment remained relatively constant before and after the infusion with hypertonic NaCl. After infusion, the total concentration of ions in endolymph was similar to that of perilymph. These experiments indicate that the endolymph compartment has a built-in mechanism for maintaining a low-sodium concentration while keeping ionic balance with the surrounding perilymph and serum.