Decrease In Plasma Na Research Articles

Hyperglycemia-induced hyponatremia: Reevaluation of the Na+ correction factor

This study addresses the clinically important relationship between the decreases in plasma Na+ and the increases in plasma glucose concentrations seen in diabetes and other hyperglycemic syndromes. This plasma ‘Na+ correction factor’, is generally accepted as 1.6mM Na+ per 100mg% glucose (0.29mM/mM in SI units) assuming osmotic equilibrium, although much larger numbers have been measured in experiments on normal humans. To resolve this controversy, a mathematical model of whole-body fluid-electrolyte balance was used to perform the experiment wherein plasma glucose concentration was increased to diabetic levels and the plasma Na+ concentration changes assessed, without the complications seen in human experiments. The findings, based on osmotic grounds, were that the factor 1) was significantly <1.6, approaching 1 in some cases, 2) depended upon the anthropometry of the subject; it was inversely proportional to the ratio of extracellular to total body water, which increases with higher fat content and 3) was approximately linear up to glucose concentrations of about 800mg%, but decreased up to 10% for higher glucose concentrations. To explain the experimental data, a hypothesis of Na+ sequestration in cells was incorporated in the model, resulting in close prediction of measured transient Na+ changes.

Ionoregulatory Impairment in African Catfish (&lt;i&gt;Clarias gariepinus&lt;/i&gt;) Exposed to Combined Stressors of Lead and Cypermethrin

The contamination of aquatic ecosystem with heavy metals and pesticides has increased dramatically over the years, and this has generated a lot of attention by environmental experts. There are reports on impacts of different single toxicants on aquatic organisms but not much has been done to investigate the impacts of mixtures of toxicants on aquatic life. In this study we investigated the effects of multiple stressors of Pb and cypermethrin on ionoregulation in the African catfish (Clarias gariepinus). Adults C. gariepinus were exposed to either borehole water (control), 2 mg/L Pb, 0.5 μg/L cypermetrin or a mixture of 2 mg/L Pb and 0.5 μg/L cypermethrin for 96 h, after which the levels of plasma Na+, Cl- and K+ were determined as a measure of branchial ionoregulatory disturbance. The exposure of C. gariepinus to 0.5 μg/L cypermethrin resulted in a significant reduction in plasma Na+ (43% decrease) and Cl- (31% decrease) but a 2-fold increase in plasma K+ concentrations. Exposure to a mixture of cypermethrin and Pb resulted in 53% decrease in plasma Na+, 40% decrease in plasma Cl- and a 3- fold increase in plasma K+. There was no significant difference between the control and those exposed to just only 2 mg/L Pb for all the parameters measured. The results of this study indicated that exposure of aquatic organisms to combined stressors of heavy metals pollution as well as pesticide contamination could have a serious effect on the physiology especially on ionic regulation in the exposed fish.

Increased susceptibility of db/db mice to rosiglitazone-induced plasma volume expansion: role of dysregulation of renal water transporters

Thiazolidinediones (TZDs), which are synthetic peroxisome proliferator-activated receptor subtype-γ (PPARγ), agonists are highly effective for treatment of type 2 diabetes. However, the side effect of fluid retention has significantly limited their application. Most of the previous studies addressing TZD-induced fluid retention employed healthy animals. The underlying mechanism of this phenomenon is still incompletely understood, particularly in the setting of disease state. The present study was undertaken to examine rosiglitazone (RGZ)-induced fluid retention in db/db mice and to further investigate the underlying mechanism. In response to RGZ treatment, db/db mice exhibited an accelerated plasma volume expansion as assessed by hematocrit (Hct) and fluorescent nanoparticles, in parallel with a greater increase in body weight, compared with lean controls. In response to RGZ-induced fluid retention, urinary Na(+) excretion and urine volume were significantly increased in lean mice. In contrast, the natriuretic and diuretic responses were significantly blunted in db/db mice. RGZ db/db mice exhibited a parallel decrease in plasma Na(+) concentration and plasma osmolality, contrasting to unchanged levels in lean controls. Imunoblotting analysis showed downregulation of renal aquaporin (AQP) 2 expression in response to RGZ treatment in lean mice but not in db/db mice. Renal AQP3 protein expression was unaffected by RGZ treatment in lean mice but was elevated in db/db mice. In contrast, the expression of Na(+)/H(+) exchanger-3 (NHE3) and NKCC2 was unchanged in either mouse strain. Together these results suggest that compared with the lean controls, db/db mice exhibited accelerated plasma volume expansion that was in part due to the inappropriate response of renal water transporters.

Dynamics of blood electrolytes in repeated hyper- and/or hypoglycaemic events in patients with type 1 diabetes

Electrolyte disturbances are well-known consequences of the diabetic pathology. However, less is known about the cumulative effects of repeated changes in glycaemia, a characteristic of diabetes, on the electrolyte balance. We therefore investigated the ionic profiles of patients with type 1 diabetes during consecutive hyper- and/or hypoglycaemic events using the glucose clamp. In protocol 1, two successive hyperglycaemic excursions to 18 mmol/l were induced; in protocol 2, a hypoglycaemic excursion (2.5 mmol/l) was followed by a hyperglycaemic excursion (12 mmol/l) and another hypoglycaemic episode (3.0 mmol/l). Blood osmolarity increased during hyperglycaemia and was unaffected by hypoglycaemia. Hyperglycaemia induced decreases in plasma Na(+) Cl(-) and Ca(2+) concentrations and increases in K(+) concentrations. These changes were faithfully reproduced during a second hyperglycaemia. Hypoglycaemia provoked rapid and rapidly reversible increases in Na(+), Cl(-) and Ca(2+). In sharp contrast, K(+) levels displayed a rapid and substantial fall from which they did not fully recover even 2 h after the re-establishment of euglycaemia. A second hypoglycaemia caused an additional fall. Repeated hyperglycaemia events do not lead to any cumulative effects on blood electrolytes. However, repeated hypoglycaemias are cumulative with respect to K(+) levels due to a very slow recovery following hypoglycaemia. These results suggest that recurring hypoglycaemic events may lead to progressively lower K(+) levels despite rapid re-establishment of euglycaemia. This warrants close monitoring of plasma K(+) levels combined with continuous glucose monitoring particularly in patients under intensive insulin therapy who are subject to repeated hypoglycaemic episodes. Clinicaltrial.gov NCT01060917.

Interactive effects of ammonia and oxygen on growth and physiological status of juvenile Atlantic cod (Gadus morhua)

In order to investigate the interactive effects of sublethal ammonia concentrations and oxygen saturation on the growth and physiological status of Atlantic cod juveniles (Gadus morhua), 877 specimens (mean initial weight 20.8 g, SD=5.6) were exposed to nine different combinations of ammonia and oxygen concentrations for 64 days. The combinations applied were: control (1–2 μg L−1), low (31–34 μg L−1) and high (115–120 μg L−1) unionized ammonia-nitrogen (UIA-N) concentrations and hypoxia (57–69%), normoxia (83–88%) and mild hyperoxia (101–104%) oxygen saturations. High ammonia concentrations caused a significant decrease in growth throughout the experiment. An interactive effect of ammonia and oxygen on specific growth rates (SGR) was found in all periods, and was related to an increase and decrease in ammonia toxicity, respectively, in hypoxic and hyperoxic conditions. High ammonia concentrations caused some physiological disturbance in terms of an initial elevation of plasma K+ concentration, and a decrease in plasma Na+ and glucose concentration. Low ammonia concentrations did not cause any considerable change in weight, growth or physiological status, compared to controls. It is suggested that a mild hyperoxia may increase the tolerance of Atlantic cod juveniles to sublethal ammonia toxicity.

Mechanisms Controlling Feed Intake in Large-type Goats Fed on Dry Forage

An intracerebroventricular (ICV) infusion of somatostatin 1-28 (SRIF) was used as a thirst-controlling peptide antagonist to investigate whether or not thirst-controlling peptides are involved in the significant decrease in feed intake during the initial stages of feeding large-type goats on dry forage. A continuous ICV infusion of SRIF was conducted at a small dose of 4 μg/0.2 ml/h for 27 h from day 1 to day 2. Goats (n 5) were fed roughly crushed alfalfa hay cubes for 2 h twice daily and water was given ad libitum. Feed intake was measured during ICV infusion of artificial cerebrospinal fluid (ACSF) and SRIF. The feed intake during SRIF infusion increased significantly compared to that during ACSF infusion. In comparison to the ACSF treatment, plasma osmolality during the SRIF treatment significantly decreased during the first half of the 2 h feeding period. The factor causing the decrease in plasma osmolality during the ICV infusion of SRIF was a decrease in plasma Na, K, Cl, and Mg concentrations. In comparison to the ACSF infusion treatment, parotid saliva secretion volumes during the 2 h feeding period in the SRIF infusion treatment were significantly larger. While there was no significant difference in cumulative water intake (thirst levels) between the SRIF and the ACSF treatments upon conclusion of the 2 h feeding period, based on the plasma osmolality results it is thought that thirst level increases brought about by alfalfa hay cube feeding in the first half of the feeding period were reduced. It is thought that the somatostatin-induced increases in feed intake during the 2 h feeding period in the present experiment were caused by decreases in plasma osmolality brought about by the somatostatin infusion. As a result, it is suggested that the significant decrease in feed intake during the initial stages of feeding in large-type goats given roughly crushed alfalfa hay cubes, was due to the actions of thirst-controlling peptides.

Integrative approach to osmoregulatory action of atrial natriuretic peptide in seawater eels

Atrial natriuretic peptide (ANP) reduces plasma Na + concentration and promotes seawater (SW) adaptation in SW eels. However, little is known about the mechanisms for the hyponatremic effect of ANP. In order to evaluate the role of ANP in the whole-body Na + homeostasis of marine teleost, we reviewed previous in vivo experiments using exogenously administered ANP and present additional experiments to assess the role of endogenous ANP in Na + homeostasis in conscious SW eels. The Na + influx and efflux rate across the body surfaces including the gills measured with isotopic 22Na were not altered by the hyponatremic dose (5 pmol kg −1 min −1) of ANP infusion in SW eels. ANP infusion also had no effect on renal Na + excretion in SW eels. In contrast, ANP strongly inhibited drinking, and the inhibition was quantitatively correlated with the hyponatremic effect of ANP. Further, intestinal absorption of Na + was inhibited by ANP as examined in situ using intestinal sac in conscious SW eels. The combined inhibitory actions of ANP on drinking and intestinal absorption were sufficient to explain the decrease in plasma Na + concentration. In addition, removal of endogenous circulating ANP by immunoneutralization increased plasma Na + concentration with a concomitant increase in drinking rate in SW eels. These results strongly suggest that endogenous ANP is involved in the hyponatremic regulation through actions on drinking, and probably on intestine, in SW eels.

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT(1) and AT(2)) change in relation to maternal water-electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na(+)-restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT(1) and AT(2) mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na(+) restriction decreases Na(+) excretion without altering plasma volume, plasma Na(+) concentration or the expression of AT(1) and AT(2) mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT(1) mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT(1) protein decreases in the kidney and AT(2) mRNA declines in the adrenal cortex. In pregnant rats, Na(+) restriction induces a decrease in plasma Na(+), an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT(1) and AT(2) in the pituitary and AT(2) mRNA in the adrenal cortex are lower in the Na(+)-restricted pregnant group when compared to normally fed pregnant animals. Na(+) restriction also induces a decrease in AT(1) protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na(+) depletion by the tissue-specific modulation of ANGII receptors. Finally, these receptors may be implicated in the IUGR response to low Na(+).

Effects of waterborne complexing agents on silver uptake and depuration in rainbow trout

Rainbow trout Oncorhynchus mykiss(c. 60 g) were exposed for 1 week to 0·1 μM silver as AgNO3 in ion poor water (Ca c. 150 μM, pH c. 8, water temperature 13° C) with or without waterborne organic matter (27 mg C l−1 as Aldrich humic acid), thiosulphate (5 μM Na2S2O3) or chloride (4 mM KCl). Organic matter decreased Ag accumulation by the gills initially, but did not decrease Ag accumulation by plasma or liver. Thiosulphate decreased the amount of Ag accumulated by the gills for the entire 1 week exposure but had no effect on Ag concentrations in the plasma, liver or bile. Chloride had no effect on Ag uptake in any of the tissues examined. All three complexing agents reduced the decreases in plasma Na and Cl concentrations caused by Ag. To study the effects of waterborne complexing agents on Ag depuration, rainbow trout were exposed to 0·1 μM AgNO3 for 1 week then placed for 8 days in Ag‐free, ion poor water with or without waterborne organic matter (55 mg C l−1) or thiosulphate (5 μM). These complexing agents did not alter depuration of Ag from the gills, plasma, liver or bile. Thus, once Ag has entered a fish, subsequent elimination of internal Ag is not affected by external complexing agents.

Influence of brain angiotensin on thermoregulation and hydromineral balance during pregnancy in rats

During mammalian pregnancy, body temperature decreases and there are changes in fluid and electrolyte balance. Angiotensin signaling mechanisms in the brain have been shown to influence thermoregulation and body fluid balance in the nonpregnant state. We hypothesized that brain angiotensin is also implicated in adjusting these physiological systems in the pregnant rat. We compared core temperature and fluid regulation in three groups of pregnant rats: untreated rats, rats receiving continuous infusion of an AT(1) antagonist candesartan (5 microg.kg(-1).day(-1)) into a lateral cerebral ventricle to block brain AT(1) receptors, and rats receiving vehicle [artificial cerebrospinal fluid (aCSF)] vehicle. Untreated and aCSF-treated rats showed a decrease in colonic temperature (-0.5 and -0.8 degrees C respectively) by day 20 of gestation. However, rats treated with candesartan had increased colonic temperature compared with baseline (+0.9 degrees C), and their temperature was significantly higher on days 7 (P < 0.05), 17 (P < 0.05), and 20 (P < 0.001) compared with the other groups (aCSF and untreated). Daily food and water intakes and body weight were not different between the three groups. Similarly, litter sizes and pup weights were equal in all groups. Finally, the expected decreases in plasma Na(+) and osmolality during pregnancy were equivalent in all groups. This study suggests that brain angiotensin mediates the progressive decrease in body temperature that occurs during pregnancy. However, the changes in fluid balance associated with pregnancy are not dependent on brain angiotensin.

Reproduction, blood and plasma parameters and gill histology of vendace ( Coregonus albula L.) in long-term exposure to acidity and aluminum

Vendace were exposed to pHs 4.75 and 5.25 with or without added aluminum (200 μg=7.4 μmol Al L −1) from late endogenous vitellogenesis in July through the spawning period. At the normal time of spawning, when 48% of the control females had already released their eggs, 50% of females at pH 4.75+Al had completely unovulated oocytes. The final proportions of completely ovulated females were 14%, 36%, 25%, 61%, and 81% at pH 4.75+Al, pH 4.75, pH 5.25+Al, pH 5.25, and in the control group, respectively. Delayed testes regression was seen in males at pH 4.75+Al. A clear decrease in plasma Na + and Cl − and an increase in blood glucose concentration was detected only near spawning time, from October to November, coincident with Al accumulation inside the gill tissue. It is concluded that seasonal changes, probably related to reproductive physiology or to the decrease in water temperature, are associated with the increase in Al toxicity in vendace.

Effects of feeding on waterborne silver uptake and depuration in rainbow trout (Oncorhynchus mykiss)

Rainbow trout (Oncorhynchus mykiss, ~50 g) were exposed to 0.1 µM AgNO3in ion-poor water (Ca ~300 µM, pH ~7, 13°C) with or without being fed 2% of their body weight daily. Gills, plasma, livers, and bile were sampled after 4 h, 24 h, and 1 week. Feeding did not alter Ag uptake by trout, and did not prevent decreases in plasma Na and Cl caused by Ag. To study Ag depuration, trout were exposed to 0.1 µM AgNO3for one week and then were placed in Ag-free, ion-poor water with or without being fed 1% of their body weight daily. Plasma Ag decreased over the 15-day depuration period (elimination rate, ke= 0.085 day–1), but there were no effects of feeding on Ag depuration. There were no physiological differences between fed and unfed fish except for slightly higher plasma glucose concentrations and higher condition factors in fed fish by the end of the Ag depuration period. Thus, once Ag has entered a fish, subsequent elimination (e.g., from the plasma) is not affected by food-related processes such as biliary excretion or increased metabolic rate, or by external factors like food debris in the water.

Plasma volume and ions during exercise in cool, dry; hot, dry; and hot, humid conditions.

We studied the effects of heat and relative humidity (RH) on plasma volume (PV) and ion responses to submaximal exercise and 60 min recovery in Thoroughbreds. Five horses were exercised at 50% of peak VO2 in cool, dry (CD, T = 22 degrees C, RH = 45-55%), and hot, humid (HH, T = 30-34 degrees C, RH = 80-85%) conditions until a pulmonary artery temperature of 41.5 degrees C was reached. Blood was obtained from the carotid artery. Body mass was measured at rest and after 30 min of recovery. The thermal conditions had no effect on the PV and ion responses during exercise and initial 30 min of recovery. Exercise resulted in an 8.5% decrease in PV within the first 2 min and, in the absence of changes in plasma [Na+] and [Cl-], was responsible for a 150 to 185 mmol decrease in plasma Na+ and Cl- contents. The decrease in PV was responsible for about 50% of the increase in packed cell volume (37% at rest; 51% at 2 min of exercise). Plasma [K+] and K+ content increased rapidly during the first 2 min of exercise. With cessation of exercise, plasma [K+] declined with a half time of about 2 min; recovery of PV and plasma Na+ and Cl- contents occurred with a half time of 10-15 min, with nearly complete recovery by 30 min. In the HD trial, between 30 and 60 min of recovery there were further decreases in PV and ion contents. It is concluded that with this exercise protocol, thermal stress had minimal influence on the rate and magnitude of exercise-induced changes in PV and ion contents. However, thermal stress during recovery from exercise may impede the restoration of PV and ion contents.

Neuroendocrine control of blood volume, blood pressure and cardiovascular function in horses

SummarySeveral body systems make critical contributions to the defence of blood volume, mean arterial pressure and plasma tonicity. These mechanisms ensure adequate blood flow to the working muscles and vital tissues along with the provision of adequate fluid volume for sweating and thermoregulation. The present paper integrates data from several recent studies that examined the neuroendocrine control of cardiovascular function in exercising horses. These studies focused on the effects of exercise on plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), plasma renin activity (PRA) and aldosterone (ALDO), hormones associated with the regulation of blood pressure, the distribution of blood flow and the long term control of vascular fluid volume. Data were collected during incremental and endurance exercise, following frusemide administration and after splenectomy. Increases in ANP during exercise were associated with increased atrial pressure and stretching of the atrium. Increases in PRA and ALDO are correlated with increases in sympathetic activity during incremental exercise and with decreases in plasma Na+ and CI− concentrations. Plasma AVP increases later in exercise in response to fluid losses, increases in plasma osmolality, and decreases in right atrial pressure. AVP has a minimal effect on renal function during exercise and may be more important during recovery, when it stimulates thirst and drinking. Frusemide and splenectomy decrease atrial pressure, resulting in lower plasma ANP and greater plasma AVP concentrations during steady‐state submaximal exercise. The ANP and AVP responses are part of the neuroendocrine action of the cardiopulmonary baroreflex which appears to mediate the accommodation of the mobilised splenic reserve in the horse. In summary, exercise induced increases in ANP, AVP, PRA and ALDO in the horse appear to play an important role in cardiovascular homeostasis.

Seasonal Variation in the Physiological Response of Atlantic Cod (Gadus morhua) to Low Salinity

Plasma Na+, Cl−, K+, osmotic pressure, Cortisol, glucose, and protein, blood hemoglobin and hematocrit, and water content of skeletal muscle were measured at regular intervals during a 28-d period following the transfer of Atlantic cod (Gadus morhua) to waters of 7, 14, 21, and 28‰ (control) salinity. These experiments were repeated four times at 3-mo intervals under natural photoperiod and temperatures (0–10 °C). Exposure to 7‰ salinity caused large decreases in plasma Na+ in winter (25 mmol/L over 14 d) and in spring (32 mmol/L over 7 d) when the lowest value for the year was reached (156 mmol/L). Transfer to 14 and 21‰ salinity resulted in a slight decrease (maximum 4%) in plasma Na+ which was much smaller than the seasonal variation (14%) observed in controls. Hydration of skeletal muscle occurred only at 7‰ (2.3% maximum), but these changes were small compared with the seasonal variation (3.9%) observed in the controls. Principal components and clustering analyses showed that all ionic and osmotic variables measured were highly correlated while being only weakly associated with the condition or reproductive status of the fish. There were no indications that acclimation to low salinity was stressful for cod.

Physiological disturbances in rainbow trout (Salmo gairdneri) during acid and aluminum exposures in soft water of two calcium concentrations

Rainbow trout (Salmo gairdneri) fitted with dorsal aortic cannulae were exposed in a flow-through soft water system to three acidities (pH 5.2, 4.8, or 4.4) and two concentrations of Ca (45 or 410 μequiv.∙L−1), in the presence (105 μg∙L−1) or absence of Al. Blood was sampled for respiratory gases, ions, metabolites, and hematology before and at 4, 18, 28, 42, and 66 h exposure. Two toxic mechanisms of Al and acidity were seen: (i) ionoregulatory toxicity, which was caused by Al at pH 5.2 and 4.8 and by acidity at pH 4.4, and (ii) respiratory toxicity, which was caused solely by Al, and was greatest at higher pH. Ionoregulatory toxicity involved decreases in plasma Na+ and Cl−, red cell swelling, and hemoconcentration. Respiratory toxicity involved reduced blood oxygen tension, elevated blood carbon dioxide tension, and increases in blood lactate. Blood acidosis was a combination of respiratory acidosis (due to CO2 accumulation in the blood; higher pH exposures) and metabolic acidosis (probably due to differential Na+ and Cl− loss into the external, acidic environment; lower pH exposures). Higher water Ca reduced ionoregulatory disturbances due to acidity alone but not those due to Al at higher pH. Higher water Ca also reduced respiratory disturbances at lower pH but not at higher pH. The results are discussed with reference to the chemistry of Al and changes in the gill epithelium associated with acid and Al exposure.

Do Rainbow Trout (Salmo gairdneri) Acclimate to Low pH?

Adult rainbow trout (Salmo gairdneri) previously exposed to long-term sublethal acid stress (3 mo, pH 4.8) in artificial soft water (Ca2+ = 50, Na+ = 50, Cl− = 100 μeq∙L−1) were challenged with acute severe acid exposure (4.5–5 h, pH 4.0). Their response in terms of whole-body ionic exchanges and blood chemistry was compared with that of trout that had no previous history of acid exposure (naive fish). Acute pH 4.0 exposure caused significant ionoregulatory disturbances in both acid-preexposed and naive fish. Rates of net Na+ and Cl− body losses were twice as large in acid-preexposed fish as in naive fish. The two groups showed similar slight net uptake of acidic equivalents. However, the dynamics of acid–base exchange differed, especially with regard to ammonia excretion which was elevated in acid-preexposed fish and inhibited in naive fish. A larger decrease in plasma Na+, red blood cell swelling, and the maintenance of high-stress indicators (elevated plasma glucose and ammonia excretion, depressed osmolality) confirmed that osmo-ionoregulatory disturbances were more intense in acid-preexposed fish than in naive fish. Thus, long-term sublethal acid exposure did not improve but rather significantly decreased the ability of rainbow trout to respond to more severe acid stress. We conclude that acclimation to acid stress does not occur in rainbow trout.

低ナトリウム血症をきたした難治性下顎骨骨髄炎の１例

A case of hyponatremia associated with incurable mandibular osteomyelytis was reported in this paper. A 77-year-old male admitted to our hospital with a complaint of pus discharge from extraoral fistel of mental region on March, 1980. Resection and reconstruction of major portion of mandible using the rib bone graft, was performed under a diagnosis of chronic mandibular osteomyelitis. However, this operation did not cure him. He had been given heavy antibiotics chemotherapy and operated frequently during his 3 years stay in our hospital.Since September, 1983 his plasma Na+ concentration reached 130 mEq/l with no symptoms of hyponatremia. After his final operation on December, 1983 nausea, vomiting and drowsiness appeared with low concentration of plasma Na+ (120 mEq/l) and low plasma osmorality (260 mOsm/Kg. H2O). Clinical examination revealed that there were no abnormality in functions of liver, kidney, heart and adrenal glands. Plasma ADH was within normal limits. These symptoms were in accordance with hyponatremia, the so-called “sick cell syndrome”We had treated this patient with infusion of 3% NaC1 1, 000 ml/day, and medication of predonisolone 30 mg/day. G-I-K terapy was tried for 1 week, but it was not effective in this case. These therapies had continued a year and a half untill his death. The cause of death was airway obstraction by his own tongue while sleeping.Hyponatremia is common in severely ill patients. It has been reported that decrease in plasma Na+ concentration results from disturbances of cell function by illness. It seems to be important to think of sick cell syndrome, when hyponatremia appears in wasting disease patients such as incurable infection and terminal phase of cancer.

Adrenaline causes potassium influx in skeletal muscle and potassium efflux in cardiac muscle in rats: The role of NA/K ATPase

Previous in vitro evidence suggest that adrenaline causes K influx in skeletal muscle by stimulating a ouabain sensitive Na/K ATPase membrane pump. However in rabbits, adrenaline induced hypokalaemia was not significantly altered by pretreatment with digoxin (50μg/kg). Rats were infused with adrenaline or saline after being given a tracer dose of 42KCl. Adrenaline caused a highly significant uptake of 42K in skeletal muscle and a decrease in 42K uptake in ventricle. Rats were also studied after receiving a high dose of digoxin (1.4 mg/kg) which by itself produced a significant increase in plasma K, a decrease in plasma Na and a decreased uptake of 42K in ventricle and lung. These results suggest that adequate widespread Na/K ATPase inhibition had been achieved by this dose of digoxin but despite this, adrenaline still caused hypokalaemia and also still caused significant 42K tissue uptake by skeletal muscle. These results suggest that adrenaline causes K influx by skeletal muscle and K efflux by cardiac tissue. Furthermore the former mechanism was not inhibited by pretreatment with digoxin.

The effects of acid exposure on the ion regulation and seawater adaptation of coho salmon ( Oncorhynchus kisutch) parrs and smolts

1. 1. Smolts exhibited decreases in plasma Na + levels after 7 days and lower Na +, K +-ATPase activities 14 days after acid exposure. 2. 2. Parrs exhibited decreased plasma Na + after 24 hr acid exposure.li 3. 3. Plasma Na + increased and Na +, K +-ATPase decreased in smolts after transfer to seawater. 4. 4. Parrs exhibited increased plasma Na + as well as Na +, K +-ATPase activity immediately after transfer to seawater. 5. 5. It was concluded that acid exposure prior to entry into seawater was detrimental to coho salmon with regard to the length of acid exposure and stage of development. 6. 6. A possible mechanism by which fish die from acid stress is inhibition of gill Na +, K +-ATPase concomitant with decreases in plasma Na + levels.