Impact of Dietary Factors on Brugada Syndrome and Long QT Syndrome.

A healthy regime is fundamental for the prevention of cardiovascular diseases (CVD). In inherited channelopathies, such as Brugada syndrome (BrS) and Long QT syndrome (LQTS), unfortunately, sudden cardiac death could be the first sign for patients affected by these syndromes. Several known factors are used to stratify the risk of developing cardiac arrhythmias, although none are determinative. The risk factors can be affected by adjusting lifestyle habits, such as a particular diet, impacting the risk of arrhythmogenic events and mortality. To date, the importance of understanding the relationship between diet and inherited channelopathies has been underrated. Therefore, we describe herein the effects of dietary factors on the development of arrhythmia in patients affected by BrS and LQTS. Modifying the diet might not be enough to fully prevent arrhythmias, but it can help lower the risk.

Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review.

Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid-base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride-bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2-4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a "mendicant" ion, plays a crucial role in acid-base and salt balance.

Benefits of peritoneal ultrafiltration in HFpEF and HFrEF patients.

BACKGROUND: Peritoneal ultrafiltration (pUF) in refractory heart failure (HF) reduces the incidence of decompensation episodes, which is of particular significance as each episode incrementally adds to mortality. Nevertheless, there are insufficient data about which patient cohort benefits the most. The objective of this study was to compare pUF in HFrEF and HFpEF, focusing on functional status, hospitalizations, surrogate endpoints and mortality. METHODS: This study involves 143 patients, who could be classified as either HFpEF (n = 37, 25.9%) or HFrEF (n = 106, 74.1%) and who received pUF due to refractory HF. RESULTS: Baseline eGFR was similar in HFrEF (23.1 ± 10.6 mg/dl) and HFpEF (27.8 ± 13.2 mg/dl). Significant improvements in NYHA class were found in HFpEF (3.19 ± 0.61 to 2.72 ± 0.58, P <  0.001) and HFrEF (3.45 ± 0.52 to 2.71 ± 0.72, P <  0.001). CRP decreased in HFrEF (19.4 ± 17.6 mg/l to 13.7 ± 21.4 mg/l, P = 0.018) and HFpEF (33.7 ± 52.6 mg/l to 17.1 ± 26.3 mg/l, P = 0.004). Body weight was significantly reduced in HFrEF (81.1 ± 14.6 kg to 77.2 ± 15.6 kg, P = 0.003) and HFpEF (86.9 ± 15.8 kg to 83.1 ± 15.9 kg, P = 0.005). LVEF improved only in HFrEF (25.9 ± 6.82% to 30.4 ± 12.2%, P = 0.046). BCR decreased significantly in HFrEF and HFpEF (55.7 ± 21.9 to 34.3 ± 17.9 P > 0.001 and 50.5 ± 68.9 to 37.6 ± 21.9, P = 0.006). Number of hospitalization episodes as well as number of hospitalization days decreased significantly only in HFpEF (total number 2.88 ± 1.62 to 1.25 ± 1.45, P <  0.001, days 40.4 ± 31.7 to 18.3 ± 22.5 days, P = 0.005). CONCLUSIONS: pUF offers various benefits in HFpEF and HFrEF, but there are also substantial differences. In particular, hospitalization rates were found to be significantly reduced in HFpEF patients, indicating a greater medical and economical advantage. However, LVEF was only found to be improved in HFrEF patients. While pUF can now be regarded as an option to supplement classical HF therapy, further studies are desirable to obtain specifications about pUF in HFpEF, HFmEF and HFrEF patients.

Effect of the methanol extract of the red cultivar Allium cepa L. on the serum biochemistry and electrolytes of rats following sub-chronic oral administration.

Background In traditional medicine, Allium cepa Linnaeus is used for the treatment of several disease conditions. Whilst reports abound on the effects of several cultivars of A. cepa L on biochemical parameters, similar information on the red cultivar is scarce. This study examines the effects of the methanol extract of the red cultivar A. cepa L on some serum biochemical parameters in experimental Wistar rats. Materials and methods Fifty-five Wistar rats were divided into three groups (A, B and C), which include 25, 25 and 5 rats, respectively. The rats in Groups A and B were sub-divided into 5 groups of 5 rats. Each rat was administered a certain dose of methanol extract of the red cultivar A. cepa L for 14 days (Group A) or 28 days (Group B). Group C rats served as the control and were administered with distilled water (10 mL/kg). Results A. cepa L administration resulted in dyslipidaemia, hyponatremia, hypokalaemia and hyperchloraemia; a significant (p < 0.05) decrease in hepatic enzymes and a significant (p < 0.05) increase in serum bicarbonate, bilirubin and its fractions. Conclusions These biochemical results indicate that the excessive and prolonged medicinal consumption of A. cepa L products beyond 7 days may induce moderate hepatic injury and mild renal dysfunction and may complicate disease conditions, such as hypertension and diabetes. Thus, in order to minimize its toxic effects, it is recommended that A. cepa L products should not be used for more than seven consecutive days or beyond a dosage of 90 mg/kg.

Hyperemesis gravidarum followed by refeeding syndrome causes electrolyte abnormalities induced rhabdomyolysis and diabetes insipidus.

Although hyperemesis gravidarum (HG), an extreme form of morning sickness, is a common complication during pregnancy, HG associated simultaneous onset of rhabdomyolysis and diabetes insipidus due to electrolyte abnormalities are rare. A 34-year-old woman with severe HG at 17 weeks of gestation complicated with appetite loss, weight reduction by 17 kg, general fatigue, myalgia, weakness and polyuria was identified to have simultaneous hypophosphatemia (1.6 mg/dL) and hypokalemia (2.0 mEq/L). Appetite recovery and the improvement of the hypophosphatemia (3.2 mg/dL) were observed prior to the first visit to our department. At the admission, she presented polyuria around 7,000~8,000 mL/day with impaired concentrating activity (U-Osm 185 mOsm/L), and abnormal creatine kinase elevation (4,505 U/L). The electrolyte disturbances and physio-metabolic abnormalities in undernourished state due to HG let us diagnose this case as refeeding syndrome (RFS). In this case, abnormal loss by vomiting, insufficient intake and previous inappropriate fluid infusion as well as the development of RFS may accelerate the severity of hypokalemia due to HG. Thus, as her abnormalities were considered as results of rhabdomyolysis and diabetes insipidus due to severe HG associated hypokalemia based on RFS, oral supplementation of potassium chloride was initiated. After 6 days of potassium supplementation, her symptoms and biochemical abnormalities were completely resolved. Severe HG followed by RFS can be causes of electrolyte abnormalities and subsequent complications, including rhabdomyolysis and renal diabetes insipidus. Appropriate diagnosis and prompt interventions including adequate nutrition are necessary to prevent electrolyte imbalance induced cardiac, neuromuscular and/or renal complications.

Oestradiol effects on neuroendocrine responses induced by water deprivation in rats.

Water deprivation (WD) induces changes in plasma volume and osmolality, which in turn activate several responses, including thirst, the activation of the renin-angiotensin system (RAS) and vasopressin (AVP) and oxytocin (OT) secretion. These systems seem to be influenced by oestradiol, as evidenced by the expression of its receptor in brain areas that control fluid balance. Thus, we investigated the effects of oestradiol treatment on behavioural and neuroendocrine changes of ovariectomized rats in response to WD. We observed that in response to WD, oestradiol treatment attenuated water intake, plasma osmolality and haematocrit but did not change urinary volume or osmolality. Moreover, oestradiol potentiated WD-induced AVP secretion, but did not alter the plasma OT or angiotensin II (Ang II) concentrations. Immunohistochemical data showed that oestradiol potentiated vasopressinergic neuronal activation in the lateral magnocellular PVN (PaLM) and supraoptic (SON) nuclei but did not induce further changes in Fos expression in the median preoptic nucleus (MnPO) or subfornical organ (SFO) or in oxytocinergic neuronal activation in the SON and PVN of WD rats. Regarding mRNA expression, oestradiol increased OT mRNA expression in the SON and PVN under basal conditions and after WD, but did not induce additional changes in the mRNA expression for AVP in the SON or PVN. It also did not affect the mRNA expression of RAS components in the PVN. In conclusion, our results show that oestradiol acts mainly on the vasopressinergic system in response to WD, potentiating vasopressinergic neuronal activation and AVP secretion without altering AVP mRNA expression.

Eghindi among Sahrawi refugees of Western Sahara.

Eghindi is an illness built around a set of pathological states experienced by Sahrawi in the desert environment of Western Sahara. Its core symptoms are caused by osmotic imbalances related to salt consumption. In 1975, many Sahrawi were exiled into refugee camps, and they have since experienced radical sociocultural changes, which are reflected in changing explanatory models of eghindi. Older and conservative refugees, attached to traditional Sahrawi culture, have expanded its conceptualization to include new pathogenic factors, while younger and progressive refugees, acculturated with Western culture, began challenging its existence. Eghindi became embodied within a broader process of negotiation of Sahrawi cultural identity. Our findings provide a framework for thinking about the evolution of illness in response to displacement, and highlight that when explanatory models evolve, intracultural tensions can arise within a population.

Genistein affects parathyroid gland and NaPi 2a cotransporter in an animal model of the andropause.

This study aimed to examine the effects of genistein on the structural and functional changes in parathyroid glands (PTG) and sodium phosphate cotransporter 2a (NaPi 2a) in orchidectomized rats. Sixteen-month-old Wistar rats were divided into sham-operated (SO), orchidectomized (Orx) and genistein-treated orchidectomized (Orx+G) groups. Genistein (30 mg/kg/day) was administered subcutaneously for 3 weeks, while the controls received vehicle alone. PTG was analyzed histomorphometrically, while the expressions of NaPi 2a mRNA/protein levels from kidneys were determined by real time PCR and Western blots. Serum and urine parameters were determined biochemically. The PTG volume in Orx rats was increased by 30% (p<0.05), compared to the SO group. Orx+G treatment increased the PTG volume by 35% and 75% (p<0.05) respectively, comparing to Orx and SO animals. Orchidectomy led to increment of serum PTH by 27% (p<0.05) compared to the SO group, Orx+G decreased it by 18% (p<0.05) comparing to Orx animals. NaPi 2a expression in Orx animals was reduced in regards to its abundance in SO animals, although it was increased in Orx+G group compared to the Orx. Phosphorus urine content of Orx animals was raised by 12% (p<0.05) compared to that for the SO group, while Orx+G induced a 17% reduction (p<0.05) in regards to Orx animals. Our study shows that Orx increases PTG volume and serum PTH level, while protein expression of NaPi 2a is reduced. Application of genistein attenuates the orchidectomy-induced changes in serum PTH level, stimulates the expression of NaPi 2a and reduces urinary Pi excretion, implying potential beneficial effects on andropausal symptoms.

Clinical relevance and utility of cetuximab-related changes in magnesium and calcium serum levels.

Hypomagnesemia and hypocalcemia are common adverse events during cetuximab treatment. The influence of the chemotherapeutic combination on serum levels is unknown and the predictive value is currently under discussion. This analysis investigated 79 patients who had received cetuximab for at least 6 weeks in the day clinic of the Comprehensive Cancer Center, University of Munich. Calcium and magnesium serum levels were analyzed weekly; tumor response and adverse events were followed. Thirty-eight patients had metastatic colorectal cancer (mCRC) and the predictive value of hypomagnesemia was tested in these patients. During therapy, calcium serum levels decreased to about 97% of the baseline levels and were maintained for the duration of treatment. Magnesium levels showed a significant time-dependent decrease. Serum levels of magnesium were lower when cetuximab was combined with a platinum derivative. After a treatment duration of 12 weeks, magnesium levels decreased to 70% in platinum-treated patients, whereas they decreased to only 90% of baseline in patients who did not receive platinum therapy. In patients treated for mCRC, a decrease of serum magnesium below 95% of the baseline levels 14 days after initiating treatment separated patients significantly in terms of survival times. Magnesium levels decrease in a time-dependent manner during cetuximab therapy. As hypomagnesemia was more prominent in patients receiving platinum agents, magnesium measurements may be advised in these patients. In mCRC patients treated with cetuximab, day-14 magnesium serum levels correlated with treatment efficacy.

[A case of hypomagnesemia linked to refractory hypokalemia and hypocalcemia with short bowel syndrome].

We report a case of a 59-year old Japanese woman with short bowel syndrome, whose hypokalemia and hypocalcemia were successfully treated with magnesium (Mg) supplementation. Two years previously, she underwent Mile's operation for advanced rectal cancer, which could have been the cause of subsequent extensive resection of the small intestine by strangulation. After serial resection, she gradually developed chronic diarrhea and anorexia. Three weeks before admission, she developed general fatigue and tetany, and was hospitalized at another hospital. On admission, her serum K and Ca were 2.5 mEq/L and 4.3 mg/dL, respectively, hence regular fluid therapy containing potassium (K) and calcium (Ca) was provided following admission. However, her hypokalemia and hypocalcemia persisted, and she also displayed renal dysfunction and thereafter was transferred to our department for further evaluation and treatment. Since the laboratory tests revealed severe hypomagnesemia (0.4 mg/dL), we started intravenous Mg supplementation together with fluid therapy containing K and Ca. After the combination therapy, her clinical symptoms and electrolyte disorders were remarkably improved within a week. As Mg is essential for PTH secretion in response to hypocalcemia and to inhibit the K channel activity that controls urinary K excretion, hypomagnesemia can cause hypocalcemia and hypokalemia, which is refractory to repletion therapy unless Mg is administered. Therefore, for patients who present with signs of Mg deficiency, early and accurate diagnosis of Mg deficiency should be made and corrected.

Posterior pituitary (PP) evaluation in patients with anterior pituitary defect associated with ectopic PP and septo-optic dysplasia.

OBJECTIVE: Controversies exist about posterior pituitary (PP) function in subjects with ectopic PP (EPP) and with cerebral midline defects and/or their co-occurrence. We investigate water and electrolyte disturbances in patients at risk for PP dysfunction. DESIGN: The study was conducted in a single Pediatric Endocrinology Research Unit. METHODS: Forty-two subjects with childhood-onset GH deficiency were subdivided into five groups: normal magnetic resonance imaging (n=8, group 1); EPP (n=15, group 2); septo-optic dysplasia (SOD) with normal PP (n=4, group 3); EPP and SOD without (n=7, group 4), and with additional midline brain abnormalities (n=8, group 5). At a mean age of 16.0±1.1 years, they underwent a 120 min i.v. infusion with hypertonic 5% saline and evaluation of plasma osmolality (Posm), arginine vasopressin (AVP), thirst score (in groups 1 and 2), and urinary osmolality were performed. RESULTS: Mean Posm and AVP significantly increased from baseline scores (284.7±4.9 mosm/kg and 0.6±0.2 pmol/l) to 120 min after saline infusion (300.5±8.0 mosm/kg and 10.3±3.3 pmol/l, P<0.0001). Group 5 showed higher mean Posm and lower mean AVP at all time points (P<0.0001). Mean thirst score did not show a significantly different trend between the groups 1 and 2. Urine osmolality was above 750 mosm/kg in all but seven patients after osmotic challenge. CONCLUSIONS: Patients with midline brain abnormalities and EPP have defective osmoregulated AVP. Patients with EPP and congenital hypopituitarism have normal PP function.

Water in health and disease: new aspects of disturbances in water metabolism.

Vasopressin is a critical regulator of water homeostasis. There are two major receptors for vasopressin: V1 and V2 receptors. Disturbances in water balance are commonly encountered in clinical practice and can be divided into disorders of urinary dilution and concentration. The major representatives of such disorders are diabetes insipidus and the syndrome of inappropriate secretion of antidiuretic hormone (SI ADH). Recent studies show that genetic forms of nephrogenic diabetes insipidus are due to mutations in the genes coding for the vasopressin V2 receptor (V2R) or aquaporin-2 (AQP2). Identification of the genes involved and analysis of the cellular fate of the V2R and AQP2 mutants are relevant for understanding the functioning of the V2R and AQP2 protein. These developments also have implications for future therapeutic options. The development of nonpeptide vasopressin receptor antagonists (VRAs) offers prospects for the treatment of euvolaemic (SI ADH) or hypervolaemic hyponatraemia (congestive heart failure or cirrhosis). Several nonpeptide VRAs are now in various stages of clinical trials. At present, only conivaptan is registered by the FD A for intravenous treatment of euvolaemic and hypervolaemic hyponatremia. A recent long-term study comparing tolvaptan with placebo in patients with chronic heart failure showed no reduction in risk of death and hospitalisation.

Severe electrolyte disorders following cardiac surgery: a prospective controlled observational study.

INTRODUCTION: Electrolyte disorders are an important cause of ventricular and supraventricular arrhythmias as well as various other complications in the intensive care unit. Patients undergoing cardiac surgery are at risk for development of tachyarrhythmias, especially in the period during and immediately after surgical intervention. Preventing electrolyte disorders is thus an important goal of therapy in such patients. However, although levels of potassium are usually measured regularly in these patients, other electrolytes such as magnesium, phosphate and calcium are measured far less frequently. We hypothesized that patients undergoing cardiac surgical procedures might be at risk for electrolyte depletion, and we therefore conducted the present study to assess electrolyte levels in such patients. METHODS: Levels of magnesium, phosphate, potassium, calcium and sodium were measured in 500 consecutive patients undergoing various cardiac surgical procedures who required extracorporeal circulation (group 1). A total of 250 patients admitted to the intensive care unit following other major surgical procedures served as control individuals (group 2). Urine electrolyte excretion was measured in a subgroup of 50 patients in both groups. RESULTS: All cardiac patients received 1 l cardioplegia solution containing 16 mmol potassium and 16 mmol magnesium. In addition, intravenous potassium supplementation was greater in cardiac surgery patients (mean +/- standard error: 10.2 +/- 4.8 mmol/hour in cardiac surgery patients versus 1.3 +/- 1.0 in control individuals; P < 0.01), and most (76% versus 2%; P < 0.01) received one or more doses of magnesium (on average 2.1 g) for clinical reasons, mostly intraoperative arrhythmia. Despite these differences in supplementation, electrolyte levels decreased significantly in cardiac surgery patients, most of whom (88% of cardiac surgery patients versus 20% of control individuals; P < 0.001) met criteria for clinical deficiency in one or more electrolytes. Electrolyte levels were as follows (mmol/l [mean +/- standard error]; cardiac patients versus control individuals): phosphate 0.43 +/- 0.22 versus 0.92 +/- 0.32 (P < 0.001); magnesium 0.62 +/- 0.24 versus 0.95 +/- 0.27 (P < 0.001); calcium 1.96 +/- 0.41 versus 2.12 +/- 0.33 (P < 0.001); and potassium 3.6 +/- 0.70 versus 3.9 +/- 0.63 (P < 0.01). Magnesium levels in patients who had not received supplementation were 0.47 +/- 0.16 mmol/l in group 1 and 0.95 +/- 0.26 mmol/l in group 2 (P < 0.001). Urinary excretion of potassium, magnesium and phosphate was high in group 1 (data not shown), but this alone could not completely account for the observed electrolyte depletion. CONCLUSION: Patients undergoing cardiac surgery with extracorporeal circulation are at high risk for electrolyte depletion, despite supplementation of some electrolytes, such as potassium. The probable mechanism is a combination of increased urinary excretion and intracellular shift induced by a combination of extracorporeal circulation and decreased body temperature during surgery (hypothermia induced diuresis). Our findings may partly explain the high risk of tachyarrhythmia in patients who have undergone cardiac surgery. Prophylactic supplementation of potassium, magnesium and phosphate should be seriously considered in all patients undergoing cardiac surgical procedures, both during surgery and in the immediate postoperative period. Levels of these electrolytes should be monitored frequently in such patients.

Subarachnoid haemorrhage and vasospasm: using physiological theory to generate nursing interventions.

Caring for critically ill patients with a subarachnoid haemorrhage and preventing its most prevalent and devastating complication, vasospasm, requires an in-depth understanding of the mechanisms which underpin the physiology of SAH. This is essential to provide appropriate nursing practice derived from theory. All too often practitioners are asked to follow unsubstantiated regimes without question of the origins of practices. This paper approaches the physiological theory underpinning the mechanisms surrounding subarachnoid haemorrhage and the altered cerebral and extracerebral dysfunction which can occur. Physiological theory is analysed to generate nursing interventions which may be individually tailored to provide comprehensive nursing care with a sound underpinning to its practice. The foundations of effective management of SAH lies within prevention, early diagnosis, and correction of complications [Neurosurg. Clin. North Am. 9 (3) (1998) 595]. In order for such identification to take place, it is essential to have an understanding of the physiological theory that underpins the basis of care interventions. These interventions should compliment all other theoretical input that influences patient care and nursing practice, contributing to a holistic, dynamically formulated plan of care.

[Aldosterone and cardiovascular diseases, more than water and salt retention]. / Aldosteron en cardiovasculaire ziekten, meer dan water- en zoutretentie.

The activation of the different neurohumoral system plays an important role in the different mechanisms of the development and progression of arterial hypertension and chronic heart failure. The renin-angiotensin II-aldosterone system is one of the key players in this process. With the use of ACE-inhibitors in the treatment of hypertension and heart failure, less attention has been paid to aldosterone. Aldosterone has been only considered as a humoral factor playing a role in salt and water homeostasis and as a consequence controlling arterial blood pressure. There is now evidence of vascular synthesis of aldosterone besides the secretion at the adrenal cortex as well that aldosterone is involved in the development of left ventricular hypertrophy in arterial hypertension, decreased arterial elasticity of the large arteries in chronic heart failure and is inversely correlated with venous capacitance in chronic heart failure. Moreover aldosterone plays a role in the disturbances of the vascular matrix, endothelial dysfunction as well as baroreflex dysfunction. This work has contributed indirectly in the unraveling of the mechanisms which could be partly explained the results of the RALES-trial. The new research project will be focused on the study of the cross-talk between the autonomic nervous system and aldosterone in normotension, arterial hypertension and heart failure.

[Malignant arrhythmias caused by hyperkalemia: a new area of drug-induced electrolyte abnormalities]. / Hyperkalaemia okozta malignus ritmuszavarok: a gyógyszer indukálta elektrolitzavarok új korszaka.

INTRODUCTION: High dose of angiotensin converting enzyme inhibitor is indicated in the treatment of heart failure and it is part of the treatment in the patients suffering from diabetes mellitus and nephropathy. The patients with preexisting renal insufficiency could have slowly elevated serum potassium level treated by angiotensin converting enzyme inhibitor. PATIENTS: Seven acute admitted cases is presented with severe hyperkalaemia and life threatening arrhythmias caused by ACEI administration. Wide QRS accelerated rhythm was detected in two cases and bradyarrhythmias in five cases. Two patients died among the bradyarrhythmias. CONCLUSIONS: The authors call the attention of danger of high dose angiotensin converting enzyme inhibitor in patients with preexisting renal insufficiency and concomittant drugs elevating serum potassium level.

Hypocalcemia and hypomagnesemia.

The occurrence of hypocalcemia is well documented in clinical veterinary medicine. In this article, we have attempted to provide an overview of the established causes as well as information on more recently recognized etiologies such as the ionized hypocalcemia seen in cats with urethral obstruction and the presence of the disorder in critically ill patient populations. Hypomagnesemia has been identified as the most common electrolyte abnormality in canine and feline critically ill patients. Magnesium depletion and experience with supplementation appear to have most significance in diabetic ketoacidotic patients with the development of associated refractory hypokalemia. (N. Dhupa, BVM, MRCVS, unpublished observations, 1997). Although cardiac arrythmias are associated with hypomagnesemia in human patients, documentation of this association in veterinary patients is lacking. Because hypomagnesemia has been associated with other electrolyte abnormalities in human and veterinary populations, the detection of hypokalemia (particularly if refractory to therapy), hyponatremia, hypophosphatemia, or hypocalcemia should indicate the possibility of coexisting hypomagnesemia.

Approaches to diuretic therapy and electrolyte imbalance in congestive heart failure.

This review has summarized the current role of diuretic therapy in heart failure, emphasizing those aspects most relevant to this patient population. Recommended diuretic usage is as follows: Asymptomatic left ventricular dysfunction--establish moderate sodium intake, Mild sodium retention--thiazide-type diuretic or low-dose loop diuretic; continue moderate sodium intake; combine with an ACE inhibitor, Moderate sodium retention--loop diuretic, adjusting for renal function, if necessary; continue moderate sodium intake; combine with an ACE inhibitor, Severe sodium retention--large-dose loop diuretic combined with a thiazide-type diuretic; continue moderate sodium intake; ACE inhibitor, unless contraindicated; consider addition of a potassium-sparing diuretic Treatment measures for refractory sodium retention--intermittent intravenous loop diuretic; short-term infusion of a loop diuretic; intensified combination oral diuretic therapy; intravenous positive inotropic therapy; ultrafiltration or dialysis. In addition, the well-known adverse effect of electrolyte depletion and guidelines for electrolyte replacement have been discussed. It is evident that the diuretic class of pharmacologic therapy has not been as well assessed as both the positive inotrope and vasodilator classes. Limitations in this regard have been summarized recently. Even relatively simple parameters or instruments, such as the sodium retention score, when applied to clinical trials will yield a greater understanding of the utility and limitations of diuretic therapy for heart failure.

Differential regulation of melanin-concentrating hormone gene expression in distinct hypothalamic areas under osmotic stimulation in rat.

Melanin-concentrating hormone and associated peptides represent a novel peptide neuronal system that may be involved in the control of water homeostasis in mammals. We have examined the effect of 24 h dehydration or salt-loading over a period of six days, on melanin-concentrating hormone messenger RNA levels in rat brains by using complementary methods of Northern blotting and in situ hybridization histochemistry. In response to one to six day salt-loading regimen, hypothalamic melanin-concentrating hormone messenger RNA content in male or female rats decreased by two to three-fold. Levels of melanin-concentrating hormone messenger RNA in the hypothalamus were also dramatically decreased following dehydration in female rats whereas contrasting responses were noted in male rats. In addition, no significant variation in the low levels of melanin-concentrating hormone gene transcripts in medulla pons and cortex was found after osmotic stimulus. In agreement with Northern blot data, in situ hybridization studies revealed that the majority of the melanin-concentrating hormone-expressing neurons in the anterior part of the lateral hypothalamus of dehydrated or salt-loaded rats expressed lower amounts of melanin-concentrating hormone messenger RNAs than those found in control rats. Interestingly, less variation was found in the posterior part of the lateral hypothalamus. Furthermore few clusters of cells, located in zona incerta and near the internal capsula and fornix, increased their contents in melanin-concentrating hormone messenger RNA in salt-loaded but not in dehydrated rats suggesting that melanin-concentrating hormone gene expression may be regulated differently by various osmotic stimuli. Finally, diurnal variations in melanin-concentrating hormone messenger RNA contents were observed in normal and dehydrated rats with highest levels around 22.00 h and lowest levels during daylight hours. However, the up-regulation of melanin-concentrating hormone gene activity at night was found lower in dehydrated rats than in control animals suggesting that osmotic stress may interfere with the generation of the diurnal pattern of melanin-concentrating hormone messenger RNA expression. Altogether, our results indicate that osmotic stimulations lead to a selective and conspicuous inhibition of melanin-concentrating hormone gene activity in the whole hypothalamus of rat. We suggest that the melanin-concentrating hormone neuronal system plays an important role in integration processes relative to nocturnal regulation of water homeostasis and drinking behavior.

Distúrbios do equilíbrio hidroeletrolítico e insuficiência renal aguda / Hydroelectrolytic disturbances and acute renal insufficiency

Nesta revisäo säo apresentadas as bases fisiopatológicas e as condutas terapêuticas dos distúrbios do equilíbrio hidroeletrolítico e da insuficiência renal aguda. Säo discutidos os desequilíbrios dos íons sódio, potássio e cálcio, a necrose tubular aguda e a azotemia pré-renal