Effects Of Hypertonic Solutions Research Articles

Effects of Hypertonic Solutions on Two Species of Human Intestinal Parasites During Fecal Examination

Aim: Ova and parasite examination by flotation requires hypertonic solutions, which can damage the egg and cyst membranes, leading to false negatives. The authors investigated the harmful effects of ZnSO4 and C12H22O11 solutions on the ova and parasite examination. Materials & methods: The authors processed samples using the Three Fecal Test technique. Aliquots were floated in different pH levels, temperatures and solution densities. Results: Densities above 1.12g/ml ledstructures to collapse after 6-10min. pH neutralization of the ZnSO4 solution did not prevent the parasites from changing. Conclusion: All structures were altered when standard methods were performed. To delay collapse, the parasite floating under 5 °C is highly desirable.

Comparative effects of hypertonic solutions and pentoxifylline in sepsis

Comparative effects of hypertonic solutions and pentoxifylline in sepsis

Hypertonic saline inhibits airway smooth muscle contraction by inhibiting Ca2+ sensitization

The effects of hypertonic solution on airway smooth muscle (ASM) contraction and the underlying mechanisms are largely unknown. We found that hypertonic saline (HS) inhibited acetylcholine (ACh)-induced contraction of ASM from the mouse trachea and human bronchi. In single mouse ASM cells (ASMCs), ACh induced an increase in intracellular Ca2+ that was further enhanced by 5% NaCl, indicating that the HS-induced inhibition of ASM contraction was not mediated by a decrease in cytosolic Ca2+ . The Rho-associated kinase (ROCK) inhibitor Y-27632 relaxed ACh-induced precontraction of mouse tracheal rings. However, such inhibition was not observed after the relaxation induced by 5% NaCl. Moreover, the incubation of mouse tracheal rings with 5% NaCl decreased ACh-induced phosphorylation of myosin light chain 20 and myosin phosphatase target subunit 1. These data indicate that HS inhibits the contraction of ASM by inhibiting Ca2+ sensitization, not by decreasing intracellular Ca2+ .

Reversal of transtentorial herniation with hypertonic saline

Over the years, The Hopkins Neurocritical Care group has carefully studied the effect of hypertonic solutions clinically and experimentally. The recent report by Koenig et al.1 invites the following comments. Hypertonic saline or mannitol could improve neurologic examination in a patient with a new mass. We and others have observed rapid dramatic changes with osmotic agents. For example, we have observed dilated pupils and extensor responses at baseline, but soon after injection, pupils normalize and improvement to localization to noxious stimuli is seen. Koenig et al. and the editorialists suggest the immediacy of such a response is reversal of transtentorial herniation (TTH), but evidence of that is not provided; there are few clinical details except a GCS sumscore and no CT or MR studies. We are not certain that the clinical improvement is due to decompression or dislodging of tissue squeezed through the tentorium. In fact, when the effects are studied in mannitol, change in midline shift is not observed as changes are too minimal or almost too subtle to catch the eye on serial MRI.2 Many consider that osmotic diuresis cannot physiologically explain the rapid improvement (within 30 minutes or less in many patients). Alternatively, sudden hypertonicity may cause vasodilatation of the cerebral resistance vessels and with an …

EFFECT OF WATER AND SALINE LOAD ON URINARY OUTPUT IN HEALTHY UNDERGRADUATE MEDICAL STUDENTS

ABSTRACTWater and electrolyte balance is a vital homeostatic function. Their excretion depends on various factors –state of hydration, plasma osmolarity etc. There are rare reports on effect of hypertonic solution on urinaryoutput. Therefore, the study aimed at investigating the effect of water or saline (especially the hypertonic)load on urinary output (UO) in healthy undergraduate male medical students (17-20 years). They (n=20)were randomised into 4 equal groups: control, water, normal and hypertonic saline (1.8%). The study wasa part of undergraduate practical conducted under controlled conditions in the Physiology Department,BPKIHS. The day before the experiment, all of them were given same instructions. Next day, the experimentalgroups drank water/saline solution 12 ml/kg. Then the UO was measured ½-hourly. A non-parametric –Friedman test was used for intra- and inter-group differences in UO and specific gravity. The data arepresented as median (range). In water group the 60-min UO was significantly higher than the 30-min UO[178.5 (24-415) vs. 22.5 (21-81) ml, p<0.05]. This group also had significantly higher UO than the control at90-min [84 (20-250) vs. 19 (18-23) ml, p<0.05)]. The UO of normal-saline group was significantly higherthan that of control at 90-min [40 (22-250) vs. 19 (18-23) ml, p<0.05]. There was no significant difference inspecific gravity. The water and normal saline loads were adequate to elicit physiological response, thehypertonic solution was not strong enough to show significant physiological response suggesting need ofsaline load to be more than twice of the plasma osmolarity.Key Words: homeostasis, water-electrolyte balance, salt load, water load.

The Therapeutic Effect of Hypertonic Solutions on the Changes in the Effective Circulating Plasma Volume in Acute Necrotizing Pancreatitis in Rats

The Therapeutic Effect of Hypertonic Solutions on the Changes in the Effective Circulating Plasma Volume in Acute Necrotizing Pancreatitis in Rats

The therapeutic effect of hypertonic solutions on the changes in the effective circulating plasma volume in acute necrotizing pancreatitis in rats.

While hypovolemia or hypovolemic shock is dominant in the early stage of severe acute pancreatitis, there have been few studies on the effects of hypertonic solutions in the management of this disease. We conducted this study to evaluate the therapeutic effects of hypertonic saline solutions (HS) on the course of severe acute pancreatitis in rats. Pancreatitis was induced in male Wistar rats by injecting a 5% solution of sodium taurocholate into the biliopancreatic duct. The effective circulating plasma volume (ECPV) was measured using radioiodinated [125I]bovine serum albumin. Samples of blood and of ascitic fluid were obtained 3, 6, and 12 h after the onset of pancreatitis. Lactated Ringer's solution (LR) and HS were administered consecutively for 3 h beginning 3 h after the induction of pancreatitis. ECPV was measured 6 h after the onset of pancreatitis. The survival rates were investigated for up to 10 days. The mean ECPV decreased significantly from 24.9 +/- 1.1 ml/kg before disease onset to 11.5 +/- 1.3 ml/kg 6 h postoperatively. LR failed to achieve a normal value for ECPV even following a 150 ml/kg infusion. HS200 and HS300 restored the ECPV to the normal level, and with smaller volumes infused. All rats in the untreated group died within 3 days. LR and HS improved the survival rates, with the infusion of HS200, 100 ml/kg, thus attaining a 45% survival at 10 days.

Endolymphatic sac morphology after instillation of hyperosmolar hyaluronan in the round window niche.

One hundred and sixty-eight mice were injected with hyaluronan (HA) of varying tonicity in the middle ear and compared with 81 control animals to study the effects of hypertonic solutions in the middle ear on inner ear fluid homeostasis and endolymphatic sac (ES) response. Six hours after 1.9% HA and 4, 6 and 8 h after 4% HA deposition there was a significant increase in the proportion of granule-containing light epithelial cells in the ES as compared with controls indicating an enhanced secretory activity from the epithelial lining. Six, 8 and 10 h after deposition of 4% HA, the ES volume was significantly reduced. The secretory activity and the ability of the ES to vary its volume could be specific responses to dehydration of the inner ear resulting from the high colloid osmotic pressure exerted by concentrated HA. The secretion of high-molecular substances into the ES may serve to keep the ES lumen patent and thus ensure a proper ES function and/or to regulate the intralabyrinthine volume and fluid pressure. Whether the findings may have clinical relevance for Ménière's patients remains to be elucidated.

Effects of Hypertonic Solutions on Conjunctival Epithelium and Mucinlike Glycoprotein Discharge

A simple, semiquantitative, histochemical method using periodic acid-Schiff (PAS) staining was developed to measure the mucinlike glycoprotein content of bathing solutions exposed to rabbit conjunctiva. Rabbit eyes were bathed in vivo in solutions of various tonicity (160, 260, 300, 330, and 363 mOsm/L). Eyes bathed in hypotonic or isotonic solutions (160, 260, and 300 mOsm/L) exhibited a steady-state glycoprotein secretion (50-100 micrograms/h). In hypertonic solutions (330 and 363 mOsm/L), glycoprotein discharge increased to 150-360 micrograms/h when the solutions were exchanged hourly for 6 h, but glycoprotein discharge increased to a much lower rate (100-167 micrograms/h) after prolonged bathing for 6 h without solution exchange. Periodic acid-Schiff--positive glycoprotein aggregates were noted more frequently on the filters of hypertonic solutions than on those of other tonicity. After eyes were bathed in hypertonic solutions, increased disruption of the surface epithelium, increased abnormal discharge of mucin granules, and decreased goblet cell density were noted in the biopsied conjunctiva. These data suggest that mucinlike glycoprotein secretion from the conjunctival goblet cells can be enhanced by the tonicity of the bathing solution, and that nonphysiological hypertonic solutions can also affect the conjunctival epithelium.

Effect of hypertonic solutions on oxygen tension in the cochlear perilymph

The effect of glycerol on oxygen tension was studied in the cochlear perilymph of guinea pigs with a polarographic technique. Following a transient fall immediately after the intravenous administration of glycerol, the oxygen tension increased to reach a peak 10 minutes later, and then decreased gradually. These changes suggest alterations of the cochlear blood flow due to the local vasodilating effect of glycerol. The increase of oxygen tension and blood flow in the cochlea is considered to be one of the possible contributory factors in the improvement of hearing in patients with Meniere's disease after glycerol administration.

Effects of hypertonic solutions on calcium transients in frog twitch muscle fibres.

1. The effects of hypertonic solutions on excitation-contraction (e.-c.) coupling in frog skeletal muscle fibres were investigated using Arsenazo III to monitor intracellular calcium transients in voltage-clamped fibres. 2. In solutions made hypertonic with sucrose or sodium chloride, the size of the Arsenazo signal evoked by a 5 ms depolarization to 0 mV was little altered by increases in tonicity up to about twice normal, but declined in higher tonicities, and was almost completely suppressed at 4 times normal tonicity. 3. The latency to onset of the Arsenazo signal was increased in hypertonic solutions (2.3 and 3.1 times normal tonicity), but the decay time constant of the signal was little changed with tonicities up to 2.3 times normal. 4. The rheobase potential for a just-detectable Arsenazo signal was shifted about 4 mV more negative by increases in tonicity up to 2.3 times normal, but further increases reversed the direction of the shift, and in 3.95 times normal tonicity the rheobase was 10 mV more positive than in normal Ringer solution. 5. With short (less than 10 ms) pulse durations the depolarization needed to elicit a threshold Arsenazo signal increased steeply with increasing tonicity. Changes in the strength-duration curve could be accounted for by an increase in the time constant for build-up of a hypothetical coupler in the e.-c. coupling process. 6. Solutions of about twice normal tonicity are commonly used to suppress muscle contraction. Since the size of the Arsenazo signal was only slightly reduced by this tonicity, the main effect is presumably on the contractile proteins.

Effects of hypertonic solutions on catecholamine release from cat adrenal glands

The effects of hypertonic solutions on the spontaneous and evoked catecholamine release from isolated, perfused cat adrenal glands were studied. Hypertonic solutions enhanced three times the spontaneous release of the amines, but markedly inhibited the release evoked by nicotine 15μM for 2 min or high K +(17.7 mM for 2 min). Using sucrose as osmoticant, the secretory response to high K + was decreased to 53 and 15% of controls at 344 and 416 mosM, respectively At 512 mosM sucrose inhibited poorly the release of catecholamines evoked by nicotine, but reduced it by 90% at 1000 mosM; sodium chloride behaved similarly to sucrose. A rise in the osmolarity of only 7.5% with choline chloride produed a complete inhibition of the K +-evoked response. These effects were not seen using isotonic choline chloride; on the contrary, isotonic choline chloride enhanced the K + response, probably by stimulating nicotinic receptors. Since atropine did not modify this effect, it seems that secretion of catecholamines evoked by choline is mediated by nicotinic receptors. While the inhibitory effects of sucrose and NaCl were completely reversed when the tonicity of the perfusion medium was restored to its normal value (320 mosM), the effects of choline seemed to be long lasting and were reversed only partially. It is worth noting that the inhibitory effects of hyperosmotic solutions developed very fast. It is concluded that an increase in the tonicity of the medium bathing the chromaffin cell depresses profoundly the exocytotic catecholamine release response to nicotine and high K + these experiments suggest that the existence of an osmotic gradient across the plasma and or vesicular membranes might be a prerequisite for fusion of both membranes and or the subsequent extracellular discharge of chromaffin granule contents to the cell exterior.

Effects of hypertonic solutions on contraction of frog tonic muscle fibers.

The influence of solution hypertonicity on contraction was studied in small bundles of tonic muscle fibers from the iliofibularis muscle of the frog Rana pipiens. Muscles were activated with high-K+ solutions that had osmolalities which were increased with tris(hydroxymethyl)aminomethanepropionate. Peak potassium contracture force decreased monotonically with tonicity and was zero in solutions with 2.5 or 3 times the osmolality of control Ringer. Contracture force at all tonicities studied (less than or equal to 3 X Ringer) was increased by increasing Ca2+ in the media 10-fold (to 20 mM) and/or by adding caffeine (10-20 mM). Nevertheless, this potentiated force also was diminished as tonicity increased. Force of single, mechanically skinned tonic fibers taken from these bundles was activated by Ca2+ over the same concentration range as that of twitch fibers. Moreover, maximal Ca2+-activated force, normalized per cross-sectional area, was similar in skinned tonic and twitch fibers. As was shown previously in twitch fibers, maximal Ca2+-activated force was decreased when ionic strength was increased. These data suggest that, as with twitch fibers, increased tonicity depresses contraction of tonic fibers by increasing the intracellular ionic strength, which in turn inhibits the ability of the contractile apparatus to generate force. Unlike twitch fibers, however, disruption of the excitation-contraction coupling process probably plays a more significant role in the action of hypertonicity on tonic fibers.

The calcium dependence of spontaneous and evoked quantal release at the frog neuromuscular junction.

1. The quantal output from stimulated nerve terminals in the frog sciatic nerve-sartorius muscle preparation in low-Ca(2+) Ringer solution was measured by the coefficient of variation and the failures methods. Adding sucrose to the Ringer to increase the tonicity or adding ethanol increased miniature end-plate potential (m.e.p.p.) frequency and also the end-plate potential (e.p.p.) amplitude. Earlier reports suggested that increases in tonicity did not increase evoked quantal release.2. Concanavalin A has been reported to block the increase in m.e.p.p. frequency caused by increasing the tonicity of the Ringer (Gorio & Mauro, 1979). This effect was confirmed. The lectin-treated preparations also failed to show an increase in evoked quantal release when the tonicity was increased.3. A model in which both spontaneous and evoked quantal releases depend on some power of the intracellular [Ca(2+)] is presented. The model predicts that rises in m.e.p.p. frequency will be accompanied by increased quantal output from stimulated nerve terminals. The maximum slope of the relationship between log (evoked quantal output) and log ([Ca(2+)](out)) will be less than the true power. A theoretical analysis shows that, as the true power approaches infinity, the maximum slope will be slightly above 4. The value for the slope usually found experimentally at the frog neuromuscular junction is also about 4.4. The model does not fit the experimental data. The observed increases in evoked quantal release are higher than those predicted for the observed increases in spontaneous release. There are several possible explanations for the discrepancy. Treatments that increase m.e.p.p. frequency may also increase Ca(2+) influx into the stimulated terminal. However, we prefer the explanation that there is a fraction of spontaneous release that is independent of the [Ca(2+)] in the terminal; if this is true the model might account for the data.5. The model can account for a variety of puzzling experimental observations, including: (a) the effect of hypertonic solutions and of diamine in decreasing the slope in the relation between log (evoked quantal output) and log ([Ca(2+)](out)); (b) the slope of near 1 observed at the crustacean neuromuscular junction; (c) the decrease in the slope produced by treatment with botulinum toxin.

Role of dehydration in changing the permeability of erythrocyte plasma membranes by freeze-thawing

The effects of hypertonic solutions and slow freezing to different temperatures in the range of 0 to −80°C on the permeability of plasma membranes of reconstituted erythrocytes were investigated. It has been found that even increased concentrations of NaCl or KCl (1.2 to 4.2 M) do not change appreciably release of K +, [ 14C]sucrose and haemoglobin (by 8 to 20%), while leakage of markers into the supernatant fluid is essentially completed on freezing to −25°C. If the content of mobile water in the sample of reconstituted erythrocytes is lower than 1 to 2%, the permeability of plasma membranes for [ 14C]sucrose and haemoglobin changes after freezing to −19 to −22°C. These findings suggest that the existence of water-dependent structural changes in the membranes can be responsible for a primary mechanism of altering the permeability at low temperatures.

Effects of hypertonic solution on action potential and input resistance in the guinea-pig ventricular muscle.

The effects of hypertonic solution on action potential and input resistance were studied using the guinea-pig ventricular muscle. Hypertonic solutions containing excess (150 and 300 mOsm/liter) sucrose, glucose, NaCl, Na2SO4, or LiCl produced a prolongation of action potential duration (APD) followed by a gradual shortening. These solutions increased the input resistance of the preparation. The prolongation of APD began immediately after the onset of perfusion with hypertonic solution and peaked within about 10 min, while the late shortening of APD developed progressively. On introducing the isotonic solution after the osmotic challenge, APD initially shortened and then gradually prolonged toward the control level. Slightly hypertonic solutions containing excess 30 or 75 mM sucrose prolonged APD, to some extent. It is concluded that the hypertonic solution exerts early and late effects on APD in guinea-pig ventricular muscle. The early effect, which is responsible for the APD prolongation, seems to be directly related to the development of cell dehydration. The hypertonic solutions produced a slight increase in the resting potential, and sucrose- and glucose-hypertonicity depressed the rising phase of the action potential. These effects can be explained by the cell dehydration and associated changes in the intracellular ion concentrations. The increase in input resistance produced by hypertonic solutions was accompanied by an enhanced spatial decay of electrotonic potentials along the muscle bundle, as determined by the two microelectrode method, suggesting that the electrical resistance of the internal current pathway increases under hypertonic conditions.

Effects of stimulus rate, temperature, and external ion compositions on hypertonicity-induced changes in the action potential in guinea-pig ventricular muscle.

When the guinea-pig ventricular muscle was exposed to hypertonic solution, duration of the action potential (APD) initially increased and then progressively decreased. To investigate the mechanism underlying this phenomenon, the preparations were perfused with the hypertonic solution under various experimental conditions. At low stimulus rates (0.1-1/min), the initial prolongation of APD was prominent while the later shortening of APD developed slowly, thereby suggesting that the effect of hypertonic solution on APD is dependent on the muscle activity. A pronounced shortening of APD occurred when the osmotic challenge was made at reduced [K]o (2 mM-K), at reduced [Na]o (50%-Na), and at elevated [Ca]o (5.4 mM-Ca). Lowering the temperature from 36 to 26-27 degrees C nearly abolished the development of APD shortening. The resting potential and the maximum rate of rise (Vmax) of the action potential changed little even when APD was rapidly shortened during the osmotic challenge. Thus, the mechanism of APD shortening is though to be independent of the factors determining the resting potential and Vmax. Mn ions (1-2 mM), verapamil (5-10 microM), and Ba ions (0.05-0.2 mM) had no effect on the hypertonicity-induced changes in APD. In partially depolarized preparations, hypertonic solution increased the duration of Ca-dependent slow action potentials without producing any parallel increase in their upstroke velocity. It is postulated that the initial prolongation of APD in response to hypertonicity is a direct result of cell dehydration. The later shortening of APD is probably derived from certain changes in the cell condition which developed secondarily to the cell dehydration. In these changes in APD, the slow Ca current seems to play a small role.

Effects of hypertonic solutions on quantal transmitter release at the crayfish neuromuscular junction.

1. The effects of a hypertonic bathing medium, containing either NaCl or melezitose, on the average number (m) and the time course of quantal release following an action potential were studied using focal extracellular recording methods at synaptic sites on the opener muscle of the crayfish leg.2. After the application of hypertonic saline, the rate of spontaneous quantal release increased but m decreased to a new level within 1 min; the extent of depression depended on the magnitude of the increase in tonicity until the osmolarity was 50% greater than the normal value of 0.43 osmol/l (Osm), but greater increases in tonicity exerted little further effect.3. The synaptic delays were increased and distributed over a longer range of time in hypertonic solutions; also, the latency between the first and second quantal releases in a multiple response to a single nerve impulse was also increased.4. Hypertonicity had no significant effect on the conduction velocity of the action potential, the independence of successive quantal releases in the same response, or the uniformity of the rise and fall of the probability of quanta release following an action potential, alpha(t).5. The time course of alpha(t) is prolonged in hypertonic solutions; this was manifested as an increase in the time constant of the exponential decline in alpha(t) from its peak value following the nerve impulse.5. When the potentiating agent 5-hydroxytryptamine (5-HT) was added to the hypertonic saline, m was increased, and the time course of alpha(t) was prolonged further than in the hypertonic solution alone; 5-HT produced no change in the time course of alpha(t) when it was added to normal saline, although m was increased.6. It is concluded that in this preparation hypertonicity decreases the rate of release of each quantum from the nerve terminal following a nerve impulse.

A freeze-fracture study of intercellular junctions between various kinds of epithelial cells surrounding common endolymphatic space in the hearing organ of the chick.

Intercellular junctions between various epithelial cells in the hearing organ (basilar papilla) of the chick were studied with the freeze-fracture technique. The effects of hypertonic solutions on the intercellular junctions were also examined. The basilar papilla of the chick is primarily composed of hair cells and supporting cells in the neuroepithelium, specialized columnar cells (TMC) which attach to the tectorial membrane, and light cells (LC) and dark cells (DC) in the tegmentum vasculosum. All of these epithelial cells surround a common endolymphatic space. The tight junctions between hair and supporting cells, and those between adjacent supporting cells in the neuroepithelium are 0.1--0.3 micrometer in depth and display the usual network of branching and anastomosing strands of shared intramembrane proteins. The tight junctions in the tegmentum vasculosum have the same structure as in the neuroepithelium. In contrast, the tight junctions between the TMCs are extremely well developed. They are 1--2 micrometer in depth. In freeze-fracture replicas, they appear as a fingerprint pattern of unbranched parallel particulate strands, running both parallel and perpendicular to the cell surface. After exposure to hypertonic solutions, all the epithelial cells are shrunken and intercellular spaces are expanded; all tight junctions, however, are intact. Thus, tight junctions in the basilar papillae are resistant to dissociation by hypertonic solutions. The usual zonulae occuludentes in the neuroepithelium and tegmentum vasculosum are thought to prevent diffusion of endolymph through the intercellular spaces of epithelial cells. However, the tight junctions on the TMCs may function not only as a diffusion barrier, but also provide structural support to the cells anchoring the tectorial membrane which receives mechanical forces induced by the vibration of the basilar membrane. Extensive gap junctions are found between all the supporting cells (supporting cells in the neuroepithelium, TMCs, and LCs in the tegmentum vasculosum) surrounding the endolymphatic space.

Antiulcer activity of hypertonic solutions in the rat: Possible role of prostaglandins

The effects of hypertonic solutions on gastric acidity and on experimental gastric and duodenal ulcers as well as on gastric prostaglandins (PGs) were studied in the rat. The oral administration of a 10% NaCl solution resulted in complete absence of free acidity and very significant reductions in total acidity 24 h after pyloric ligation. The antiulcer effect of hypertonic saline was studied in three experimental models. n pyloric-ligated rats, both the incidence and the severity of gastric ulcers were remarkably reduced by hypertonic saline treatment. Indomethacin-induced gastric erosions were significantly reduced by hypertonic NaCl or sorbitol and completely prevented by hypertonic xylitol. Cysteamine-induced duodenal ulcers were also significantly reduced by hypertonic solutions of NaCl, xylitol or sorbitol. In the latter model, indomethacin potentiated the ulcerogenic effect of cysteamine and also reduced the efficacy of the hypertonic NaCl gavage. The possible contribution of PGs to these effects was further investigated by analysing PGE in the gastric mucosa and juice. Rats treated orally with hypertonic NaCl solutions had several-fold higher PGE contents in their gastric mucosa as well as higher PGE levels in the gastric juice. It is concluded that hypertonic solutions stimulate endogenous PGE biosynthesis and also exert profound antiulcer effects in the rat. A causal relationship between the two phenomena is suggested.