Potassium Output Research Articles

Вплив альтерації гомеостазу глюкози на водно-електролітний баланс та кислотно-основний стан у пацієнтів із цукровим діабетом

Незважаючи на успіхи в терапії цукрового діабету, частота виникнення ускладнень, зокрема порушення водно-електролітного та кислотно-основного стану, останніми роками не зменшилась. Цікаво відмітити той факт, що клінічні прояви такого грізного ускладнення, як діабетичний кетоацидоз, уперше описав Дрешфельд у 1886 році. Відтоді і до початку застосування інсуліну (в 1922 р.) смертність від цього ускладнення сягала 100 %. Широке впровадження в практику інсулінотерапії знизило смертність до 30 %, а з удосконаленням методів лікування, зокрема інфузійної терапії, відбулось подальше її зниження. На сьогодні рівень летальності пацієнтів із порушеннями водно-електролітного та кислотно-основного стану залишається високим (близько 5 % у спеціалізованих центрах). Тільки в США щорічно від цього ускладнення помирає близько 4000 хворих на цукровий діабет. Прогноз перебігу захворювання значно погіршується з віком, при розвитку коми та артеріальної гіпотензії. Поширеність цукрового діабету стрімко зростає і на сьогодні становить від 20 до 50 % випадків вперше виявленого захворювання в молодих людей. Порушення електролітів є частими в пацієнтів із даною патологією і можуть бути результатом зміненого розподілу електролітів, пов’язаного з індукованою гіперглікемією осмотичних зрушень рідини, або загального дефіциту, спричиненого осмотичним діурезом. Ускладнення від пошкодження органів-мішеней і методи лікування цукрового діабету можуть також сприяти електролітним порушенням. Порушення регуляції гомеостазу глюкози призводить до великої кількості прямих і непрямих впливів на електролітний і кислотно-основний баланс, оскільки велика поширеність діабету гарантує, що лікарі практично кожної спеціальності мають справу з пацієнтами, хворими на цукровий діабет, а знання, пов’язані зі змінами електролітів, є необхідними. У статті розглянуто, як впливають зміни гомеостазу глюкози при цукровому діабеті на водно-електролітний баланс та кислотно-основний стан пацієнта.

Nutrient Budget in Indian Agriculture During 1970–2018: Assessing Inputs and Outputs of Nitrogen, Phosphorus, and Potassium

Nutrient Budget in Indian Agriculture During 1970–2018: Assessing Inputs and Outputs of Nitrogen, Phosphorus, and Potassium

Abstract 10795: Adam10 Gene Deficiency Impairs Kidney Function via Suppressing Klotho Shedding

A Disintegrin and Metalloproteinase 10 (ADAM10) is a member of the ADAM family of cell membrane-anchored proteins which processes and influences the functions of its substrates by in-/activating them or by liberating biologically active fragments. ADAM10 is primarily expressed in kidney epithelial cells. Thus, the objective of this study is to investigate whether ADAM10 is involved in the regulation and maintenance of normal kidney function. Tamoxifen-inducible kidney-specific cre (Ksp) and ADAM170-floxed mice were cross-bred for generating Ksp/ADAM10-floxed mice. Injection of tamoxifen initiated deletion of the ADAM10 gene and led to a significant reduction in ADAM10 protein expression in renal distal and proximal tubule cells. Notably, knockout of the ADAM10 gene largely decreased soluble Klotho levels in urine, indicating that ADAM10 is a critical enzyme in shedding Klotho. We found that renal sodium excretion was decreased in kidney-specific ADAM1 0 knockout mice (ADAM10 -/-), suggesting that ADMA10 deficiency results in an increase in Na reabsorption or Na retention. Urinary potassium output tended to increase in ADAM10 -/- mice although it did not reach a significant level. It is interesting that ADAM10 gene deficiency compromises renal tubular function leading to Na retention. Glomerular filtration rate (GFR) was dramatically decreased in ADAM10 -/- mice, indicating that ADAM10 deficiency impairs glomerular function. Interestingly, treatment with recombinant Klotho improved renal glomerular function. Therefore, ADAM10 gene knockout impairs kidney function likely via suppressing Klotho shedding.

Twenty six-week repeat dose oral rat toxicity study of cizolirtine, a substance-P and calcitonin gene-related peptide release modulator

Cizolirtine, a substance-P and calcitonin gene-related peptide release modulator developed for the treatment of pain and urinary incontinence, was orally administered for 26-weeks to rats at dosages of 20, 60 and 200 mg/kg/day. Clinical signs were limited to post-dosing salivation and brown staining on head and muzzle. There were slight decreases in bodyweight gain and slight increases in water consumption among cizolirtine-treated animals. Slight increases in plasma alkaline phosphatase activity, and cholesterol and phospholipid concentrations were observed in mid- and/or high-dose animals. Low urinary volume, pH and sodium and potassium outputs were observed after 12-weeks, and low urinary pH, low sodium and high potassium outputs at end of treatment. Increased relative (to bodyweight) liver weight was observed in high-dose animals. Treated males and high-dose females showed a dose-related increase in the incidence and severity of periacinar hepatocytic hypertrophy and midzonal/periacinar hepatocytic fat vacuolization. Increased incidences of hepatic clear cell foci were observed in all cizolirtine-treated male groups and, to a lesser extent, in treated females. Ovaries of treated females showed a dose-dependent increased incidence of absent corpora lutea and, occasionally, follicular cysts. The dosages of 20 and 60 mg/kg/day were considered as the No-Observed-Adverse-Effect Levels for males and females, respectively.

The furosemide stress test, electrolyte response and Renal Index in critically ill patients.

Acute kidney injury (AKI) is a common syndrome in critically ill patients. The diagnostic ability of traditional markers such as serum creatinine has recently been questioned, and the use of newer tests such as the furosemide stress test or the ultrasound assessment of renal resistive index have been proposed. Aim of the present study was to compare the response to a furosemide stress test, the Renal Index in mechanically ventilated patients with and without acute kidney injury at admission, and who did or did not develop AKI at day three, among those with normal renal function at the CIU admission. Prospective observational study in consecutive mechanically ventilated patients admitted in a general intensive care. Furosemide stress test and ultrasonographical Renal Index were performed at the admission and clinical and laboratory data were collected before and two hours after the furosemide stress text. The urine output after the first and the second hours was recorded. Forty patients were enrolled, 19 of whom had AKI at admission. The Renal Index was significantly higher in patients with AKI (0.77±0.07 vs. 0.72±0.08, P=0.027); patients with AKI had a significantly lower urine output after the furosemide stress test (400 [340; 1400] vs.1525 [400; 2550] mL; P=0.013). The plasma concentrations of sodium, potassium and chloride were not different before and after the furosemide stress test in patients with and without AKI, whereas in patients with AKI, the total urine output of sodium, potassium and chloride were significantly lower compared to patients without AKI. Similar results were found in patients without AKI at admission and who developed AKI at day three as compared to those who did not develop AKI. The response to the furosemide stress test and the Renal Index could be used as additional tools to evaluate the kidney function in critically ill patients.

Soil acidification and basic cation use efficiency in an integrated no-till crop–livestock system under different grazing intensities

Under integrated crop–livestock production system (ICLS), the animal acts as a catalyzer, modifying and accelerating fluxes by ingesting forage nutrients (grazing) and returning them to the soil as urine and dung in a continuous process whose magnitude and direction depend on grazing intensity. Thus, ICLS may change soil acidification processes and rates. The objective of this research was to verify the influence of grazing intensities on soil acidification through measurements of the soil chemical attributes in the soil profile and the efficiency of basic cation use in a soybean–beef cattle integration system nine years after surface liming under long-term no-till conditions in southern Brazil. An experiment established in 2001 in a Rhodic Hapludox with soybean (summer) and a mix of black oat+Italian ryegrass (winter) succession was used. Treatments consisted of different grazing intensities during the winter season: intensive grazing (IG), moderate grazing (MG), and no-grazing (NG). The experiment was set up in a randomized complete blocks design with three replicates. To evaluate soil chemical attributes, soil was sampled up to 40cm, in May 2010, nine years after lime application. To quantify basic cations budgets and efficiencies, the inputs and outputs of calcium, magnesium, and potassium, as well as their initial and final exchangeable soil stocks were evaluated. Areas under grazed treatments, regardless of the intensity (IG or MG), presented lower soil acidification. Calcium and magnesium budgets were negative under NG and positive under MG. Potassium budgets were always negative, regardless of the management system, due to soybean grain harvest exportation and non-productive outputs. The soybean–beef cattle integrated system, with either IG or MG, was more efficient in calcium and magnesium utilization to produce protein; however, grazing does not affect potassium use efficiency.

Thyrotoxic periodic paralysis: clinical and molecular aspects

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that most often affects young East Asian males but increasingly also in other ethnic groups. The typical presentation is acute attacks varying from mild weakness to total paralysis starting at night or in the early morning a few hours after a heavy meal, alcohol abuse or strenuous exercise with complete recovery within 72h. Signs and symptoms of hyperthyroidism may not be obvious. The hallmark is hypokalemia from increased cellular sodium/potassium-ATPase pump activity with transport of potassium from the extracellular to the intracellular space in combination with reduced potassium output. Recently, KCNJ18 gene mutations which alter the function of an inwardly rectifying potassium channel named Kir2.6 have been detected in 0-33% of cases. Hence, the pathophysiology in TPP includes a genetic predisposition, thyrotoxicosis and environmental influences and the relative impact from each of these factors may vary. The initial treatment, which is potassium supplementation, should be given with caution due to a high risk of hyperkalemia. Propranolol is an alternative first-line therapeutic option based on the assumption that hyperadrenergic activity is involved in the pathogenesis. If thyroid function tests are unobtainable in the acute situation the diagnosis is supported by the findings of hypokalemia, low spot urine potassium excretion, hypophosphatemia with hypophosphaturia, high spot urine calcium/phosphate ratio, and electrocardiographic abnormalities as tachycardia, atrial fibrillation, high QRS voltage, and atrioventricular block. Definitive treatment is cure of the hyperthyroidism. The underlying mechanisms of TPP remain, however, incompletely understood awaiting further studies.

Racial differences in potassium homeostasis in response to differences in dietary sodium in girls

Racial differences in the renal disposition of potassium may be related to mechanisms for the greater susceptibility to hypertension in blacks than in whites. Our objective was to study the racial differences in the renin-angiotensin-aldosterone system and in potassium balance in black and white girls consuming a controlled diet that was low in potassium with 2 amounts of sodium intake (low compared with high). The studies reported here were performed in 40 black and 28 white girls, aged 11-15 y, under highly controlled metabolic conditions. The studies comprised 2 sessions of 20-d metabolic balance sessions, at 2 amounts of dietary sodium intake (58 and 170 mmol . L(-1) . d(-1)), in a crossover design and with a constant dietary potassium intake of 50 mmol . L(-1) . d(-1). Repeated-measures analysis of variance was used to test for racial differences in potassium output and retention by sodium intakes. Thirty black and 20 white girls completed the study. Urinary potassium excretion was lower in blacks than in whites, regardless of sodium intake (P < 0.05), with no differences in fecal or sweat potassium excretion. Cumulative potassium retention was significantly higher in blacks while consuming the low sodium diet. Plasma aldosterone concentrations after upright posture were significantly lower in blacks than in whites but were similar when supine, as were urinary aldosterone excretion rates. On week 3, blood pressure, body weight, urinary volume, creatinine, and serum sodium and potassium were similar. The well-known racial difference in urinary potassium excretion appears to be at least in part due to greater renal retention of potassium in black girls.

Consequences of cerebroventricular insulin injection on renal sodium handling in rats: effect of inhibition of central nitric oxide synthase

In the present study, we investigated the effects of acute intracerebroventricular (icv) insulin administration on central mechanisms regulating urinary sodium excretion in simultaneously centrally NG-nitro-L-arginine methylester (L-NAME)-injected unanesthetized rats. Male Wistar-Hannover rats were randomly assigned to one of five groups: a) icv 0.15 M NaCl-injected rats (control, N = 10), b) icv dose-response (1.26, 12.6 and 126 ng/3 microL) insulin-injected rats (N = 10), c) rats icv injected with 60 microg L-NAME in combination with NaCl (N = 10) or d) with insulin (N = 10), and e) subcutaneously insulin-injected rats (N = 5). Centrally administered insulin produced an increase in urinary output of sodium (NaCl: 855.6 +/- 85.1 Delta%/min; 126 ng insulin: 2055 +/- 310.6 Delta%/min; P = 0.005) and potassium (NaCl: 460.4 +/- 100 Delta%/min; 126 ng insulin: 669.2 +/- 60.8 Delta%/min; P = 0.025). The urinary sodium excretion response to icv 126 ng insulin microinjection was significantly attenuated by combined administration of L-NAME (126 ng insulin: 1935 +/- 258.3 Delta%/min; L-NAME + 126 ng insulin: 582.3 +/- 69.6 Delta%/min; P = 0.01). Insulin-induced natriuresis occurred by increasing post-proximal sodium excretion, despite an unchanged glomerular filtration rate. Although the rationale for decreased urinary sodium excretion induced by combined icv L-NAME and insulin administration is unknown, it is tempting to suggest that perhaps one of the efferent signals triggered by insulin in the CNS may be nitrergic in nature.

Consequences of cerebroventricular insulin injection on renal sodium handling in rats: effect of inhibition of central nitric oxide synthase

In the present study, we investigated the effects of acute intracerebroventricular (icv) insulin administration on central mechanisms regulating urinary sodium excretion in simultaneously centrally NG-nitro-L-arginine methylester (L-NAME)-injected unanesthetized rats. Male Wistar-Hannover rats were randomly assigned to one of five groups: a) icv 0.15 M NaCl-injected rats (control, N = 10), b) icv dose-response (1.26, 12.6 and 126 ng/3 µL) insulin-injected rats (N = 10), c) rats icv injected with 60 µg L-NAME in combination with NaCl (N = 10) or d) with insulin (N = 10), and e) subcutaneously insulin-injected rats (N = 5). Centrally administered insulin produced an increase in urinary output of sodium (NaCl: 855.6 ± 85.1 Δ%/min; 126 ng insulin: 2055 ± 310.6 Δ%/min; P = 0.005) and potassium (NaCl: 460.4 ± 100 Δ%/min; 126 ng insulin: 669.2 ± 60.8 Δ%/min; P = 0.025). The urinary sodium excretion response to icv 126 ng insulin microinjection was significantly attenuated by combined administration of L-NAME (126 ng insulin: 1935 ± 258.3 Δ%/min; L-NAME + 126 ng insulin: 582.3 ± 69.6 Δ%/min; P = 0.01). Insulin-induced natriuresis occurred by increasing post-proximal sodium excretion, despite an unchanged glomerular filtration rate. Although the rationale for decreased urinary sodium excretion induced by combined icv L-NAME and insulin administration is unknown, it is tempting to suggest that perhaps one of the efferent signals triggered by insulin in the CNS may be nitrergic in nature.

Effects of nonsteroidal anti-inflammatory drugs on postoperative renal function in adults with normal renal function

Nonsteroidal anti-inflammatory drugs (NSAIDs) can play a major role in the management of acute pain in the peri-operative period. However, there are conflicting views on whether NSAIDs are associated with adverse renal effects. The primary objective of this review was to determine the effects of NSAIDs on postoperative renal function in adults with normal preoperative renal function. Electronic searches for relevant randomised and quasi-randomised controlled trials in Cochrane Central Register of Controlled Trials, MEDLINE and EMBASE were performed. Attempts were also made to identify trials from citation lists of relevant trials, review articles and clinical practice guidelines. Handsearching of conference abstracts published in major anaesthetic journals was also performed. Date of most recent search: May 2006 The inclusion criteria were randomised or quasi-randomised comparisons of individual NSAIDs with either each other or placebo for treatment of postoperative pain, with relevant postoperative renal outcome measures, in adult surgical patients with normal renal function. The data were extracted independently by two authors. The primary outcome measure was creatinine clearance within the first two days after surgery. Secondary outcome measures included serum creatinine, urine volume, urinary sodium level, urinary potassium level, fractional excretion of sodium, fractional excretion of potassium and need for dialysis. Weighted mean differences for continuous outcomes and relative risk (RR) and risk difference (RD) for dichotomous outcomes were estimated with 95% confidence intervals (CI). Twenty-three trials (1459 patients) fulfilled the selection criteria for this review. NSAIDs reduced creatinine clearance by 16 mL/min (95%CI 5 to 28) and potassium output by 38 mmol/day (95%CI 19 to 56) on the first day after surgery compared to placebo. There was no significant difference in serum creatinine on the first day (0 umol/L, 95%CI -3 to 4) compared to placebo. No significant reduction in urine volume during the early postoperative period was found. There was no significant difference in serum creatinine in the early postoperative period between patients receiving diclofenac, ketorolac, indomethacin, ketoprofen or etodolac. No cases of postoperative renal failure requiring dialysis were described. The trials were not heterogeneous for the primary outcome. NSAIDs caused a clinically unimportant transient reduction in renal function in the early postoperative period in patients with normal preoperative renal function. NSAIDs should not be withheld from adults with normal preoperative renal function because of concerns about postoperative renal impairment.

Effects of Norepinephrine and a Combined Norepinephrine and Dobutamine Infusion on Systemic Hemodynamics and Indices of Renal Function in Normotensive Neonatal Thoroughbred Foals

Norepinephrine is a potent vasopressor that increases arterial blood pressure but may have adverse effects on renal blood flow. The combination of norepinephrine and dobutamine may lead to improved renal perfusion compared to an infusion of norepinephrine alone. The effects of these drugs in the normotensive neonatal foal have not been reported. Norepinephrine increases arterial blood pressure. Adding dobutamine to a norepinephrine infusion will change the renal profile during the infusions without changing the arterial blood pressure. Eight conscious Thoroughbred foals were used in this study. Each foal received norepinephrine (0.1 microg/kg/min), combined norepinephrine (0.1 microg/kg/min) and dobutamine (5 microg/kg/min), and a control dose of saline in a masked, placebo-controlled study. Heart rate, arterial blood pressure (direct), and cardiac output (lithium dilution) were measured, and systemic vascular resistance, stroke volume, cardiac index, and stroke volume index were calculated. Urine output, creatinine clearance, and fractional excretion of sodium, potassium, and chloride were measured. Norepinephrine and a combined norepinephrine and dobutamine infusion increased arterial blood pressure and systemic vascular resistance and decreased heart rate and cardiac index as compared to saline. The combination resulted in higher arterial pressure than norepinephrine alone. There was no significant difference in urine output, creatinine clearance, or fractional excretion of electrolytes with either infusion as compared to saline. These data suggest that norepinephrine and a combined norepinephrine and dobutamine infusion cause unique hemodynamic effects without affecting indices of renal function, and this effect warrants further investigation.

Cause and management of high volume output salt-depleting ileostomy

Ileostomy function was studied in 12 patients with an established ileostomy following proctocolectomy, in 6 of whom minimal amounts (less than 9 cm) and in 6 significant amounts (30-120 cm, mean 60 cm) of terminal ileum had been removed. Patients who had undergone significant ileal resection had daily faecal volumes considerably greater than those with minimal ileal resection (1202 +/- 284 ml versus 401 +/- 92 ml, P less than 0.001), and also greater daily outputs of sodium (146 +/- 53 mEq versus 43 +/- 12 mEq) and potassium (12.7 +/- 9.0 mEq versus 4.0 +/- 0.99 mEq). The percentage water content of the ileostomy fluid was greater in patients who had had the ileum resected (93.1 +/- 1.8% versus 89.8 +/- 2.5%). In addition, the sodium/potassium ratio in the urine in patients with a properly acting ileostomy after ileal resection was low. It is concluded that when recurrent inflammatory bowel disease, partial small bowel obstruction and intraperitoneal sepsis have been excluded there remains a number of patients whose high ileostomy output is due entirely to the amount of ileum resected. The management of patients with a high output ileostomy with codeine phosphate, Lomotil and oral administration of sodium chloride tablets is discussed.

Adenosine A1 Receptor Antagonist Blunts Urinary Potassium Excretion, but Not Renal Hemodynamic Effects, Induced by Carbonic Anhydrase Inhibitor in Rats

Acetazolamide (AZ) is a carbonic anhydrase inhibitor with diuretic actions at the proximal tubule. Clinical use of AZ is limited, in part, because of the urinary potassium loss and decrease of renal hemodynamic function that accompanies the drug. There is recent interest in A1 adenosine receptor (A1AR) antagonists, a novel class of diuretic agents that do not cause loss of potassium or tubuloglomerular feedback- (TGF) mediated reductions of renal hemodynamics. We tested whether the A1AR antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) could attenuate the adverse effects normally associated with use of AZ. Renal blood flow (RBF) and urine output were measured during two consecutive 40-min periods in anesthetized rats. In the first period, vehicle or DPCPX was infused. DPCPX alone increased urine output and sodium excretion but did not significantly alter potassium output or RBF. In the second period, the initial infusion of vehicle or DPCPX was continued, and either AZ or its vehicle was administered. AZ alone increased urinary excretion of both sodium and potassium and decreased RBF. DPCPX significantly attenuated the AZ-induced increase of potassium excretion by 50% but did not blunt the renal hemodynamic response to AZ. In a separate study, angiotensin II type 1 (AT1) receptor blockade also failed to blunt the renal hemodynamic response to AZ. In summary, A1AR antagonists may be useful diuretic agents alone or in combination with other conventional diuretic agents. The decrease of RBF that occurred in response to carbonic anhydrase inhibition was not attenuated by either A1AR blockade or AT1 receptor blockade and does not seem to be mediated by a TGF-dependent mechanism.

Stimulated Active Potassium Secretion in a Patient With Colonic Pseudo-Obstruction: A New Mechanism of Secretory Diarrhea

Secretory diarrhea is caused by inhibition of intestinal active sodium absorption and stimulation of active chloride secretion. The resulting increase in fecal sodium salts causes an isotonic increase in fecal water output. Abnormalities in potassium transport are not known to be a cause of secretory diarrhea. The aim of our report is to describe a patient with secretory diarrhea that was mediated by excess intestinal secretion of potassium. A 78-year-old woman developed colonic pseudo-obstruction, complicated by severe diarrhea and hypokalemia. Her stools were collected quantitatively on 11 occasions and analyzed for electrolyte concentrations. Rectosigmoid potential difference was measured. The diarrheal fluid had a very high potassium concentration (130-170 mEq/L) and a very low sodium concentration (4-15 mEq/L). Stool potassium losses were as high as 256 mEq/day (normal, 9 mEq/day), and fecal sodium losses were never higher than 13 mEq/day. Potential difference between colonic lumen and a peripheral reference electrode was -14 mV (lumen side negative). Fecal potassium salts were the exclusive driving force for severe secretory diarrhea in a patient with colonic pseudo-obstruction. The high fecal output of potassium was due to stimulation of active colonic potassium secretion, possibly because of changes in autonomic nervous system activity and distention of the colon in association with colonic pseudo-obstruction. The extremely low fecal excretion of sodium indicates that active sodium absorption was not inhibited. This case study reveals an ion transport mechanism of secretory diarrhea that has not been previously appreciated.

Effects Of Preexercise Rehydration Beverages On Fluid Balance And Exercise Tolerance

Decreases in plasma and intracellular water volumes during exercise may decrease sweat rate, promote hyperthermia, and increase the rate of glycogen utilization. Rehydration beverages containing electrolytes and carbohydrates may increase water intake during exercise and limit water excretion in urine. PURPOSE To study the efficacy of 4 preexercise beverages on fluid balance during submaximal exercise and subsequent exercise performance. METHODS Twenty healthy people (10 male, 10 female; 24±3 y) exercised at 57±4% (mean±SD) VO peak in a thermoneutral environment (WBGT= 16.2±1.6 °C) for 90 min, 45 min after ingesting 355 ml of either chicken noodle soup (SOUP), a carbohydrate/electrolyte beverage (CE), or water (WATER). Water intake during exercise was allowed ad libitum except in a second soup trial (SOUPCON) where water was given at times and volumes equal to CE. After 90 min of steady state exercise subjects performed a time trial in which they accumulated as rapidly as possible the amount of work equal to 30 min at ∼60% VO2peak. Results: Total body mass lost and urine output were similar between trials. The additional water ingested during SOUP, CE, and SOUPCON (p<0.01) compared to WATER resulted in enhanced fluid balance in SOUP and SOUPCON compared to WATER and CE (−268±414 g and −328±500 g vs. −654±577 g and −477±596 g respectively, p<0.05). The percent change in plasma volume was not different in any trial. Plasma sodium was similar in all trials (p=0.8). Plasma osmolality (p=0.01) was higher during SOUPCON compared to CE and WATER at before and during exercise (P<0.05) and was higher in SOUP compared to WATER and CE at the end of exercise (p<0.05). Urine specific gravity increased in CE, WATER, and SOUPCON (p<0.05 for all). Urine osmolality decreased in CE and increased in SOUPCON (p<0.05), and total urinary output of sodium and potassium was higher in SOUPCON compared to CE (p<0.05). Heart rate, systolic and diastolic blood pressures, rectal temperature, and thirst responses were not different between trials. No performance differences were observed in the time trial (p=0.4). CONCLUSIONS Higher electrolyte concentrations associated with chicken noodle soup (S and SOUPCON) resulted in better maintenance of fluid balance due to increased water intake and less urinary water loss. Fluid balance differences did not result in significant differences in percent plasma volume, heart rate, blood pressure, body temperature regulation, or subsequent exercise performance. Supported Campbell Soup Co, Inc.

Dietary habits and nutritional biomarkers in Italian type 1 diabetes families: evidence of unhealthy diet and combined-vitamin-deficient intakes.

Nutritional status and lifestyle can have profound effects on health. To analyse behaviour patterns in population subgroups of public health importance, we compared lifestyle, dietary intake of energy and selected nutrients, and nutritional biomarkers of type 1 diabetes (T1DM) patients and nondiabetic first-degree relatives against control subjects with no family history of T1DM. A cross-sectional study. Department of Internal Medicine, University of Pisa, Italy. A total of 209 individuals including 38 type 1 patients, 76 relatives, and 95 healthy subjects. We used the European Prospective Investigation of Cancer and Nutrition questionnaires to assess dietary intake and lifestyle. Anthropometric indices and nutritional biomarkers (such as plasma levels of albumin, iron, lipids, homocysteine, vitamin B9 and vitamin B12 as well as urinary outputs of nitrogen, sodium and potassium) were evaluated. Emerging health issues: (1) In total, 45% of controls were overweight. Increasing age was associated with increasing body mass and decreasing activity in sport in front of an unchanged energy intake. (2) The distribution of energy sources was incorrect. The proportion of caloric intake derived from total fat and cholesterol did not match general guidelines. Total dietary fibre consumption was assessed to be adequate (25 g/day) in only 27% of all the participants. (3) Estimated daily intakes of water-soluble vitamin B9 and fat-soluble vitamin D and vitamin E were deficient in comparison with dietary reference intakes. (4) The prevalence of adoption and maintenance of healthful eating and physical activity habits was higher in women and T1DM patients (probably as a consequence of the medical educational intervention). On the contrary, supportiveness of the family in term of changing the undesirable behaviours at home seemed to fail. This study provides first evidence indicating unhealthy dietary behaviours, which could even predispose to the development of diabetes and cardiovascular complications, in subjects living in Pisa. The combination of vitamin B9 and vitamin E deprivation could be deleterious for endothelial function, since these antioxidants have been implicated in the modulation of nitric oxide and eicosanoid signalling.

English translation of abstracts of original articles published in German 50 years ago on the discovery of aldosterone

Chemical degradation of the new crystalline mineralocorticoid provisionally called electrocortin has shown that this compound is 11h,21-dihydroxy-3,20-diketo-4-pregnen18-al. In solution, this reacts mainly as the 11-hemiacetal. We suggest aldosterone as the definitive name for the compound. Simpson SA, Tait JF, Wettstein A, Neher R, von Euw J, Schindler O, Reichstein, T. Aldosteron, Isolierung und 0167-5273/$ see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2004.05.005 * Corresponding author. Tel.: +44 113 392 5401; fax: +44 113 392 5395. Eigenschaften. Ueber Bestandteile der Nebennierenrinde und verwandte Stoffe. 91. Mitteilung. Helv. Chim. Acta 1954;37:1163–200. Title: Aldosterone. Isolation and characteristics. The constituents of the adrenal cortex and related substances. Abstract: We previously described, in two brief reports, the isolation and chemical structure of a new crystalline corticoid with a particularly potent effect on mineralocorticoid metabolism. The hormone was provisionally called electrocortin. After identification of its chemical structure the name aldosterone was suggested as the definitive name, which is in keeping with the internationally accepted nomenclature classification. In the mean time, the same substance has also been isolated in crystalline form by Mattox and co-workers. We report here the details of its chemical structure, isolation and its characteristics. We previously described, in two brief reports, the isolation and chemical structure of a new crystalline corticoid with a particularly potent effect on mineralocorticoid metabolism. The hormone was provisionally called electrocortin. After identification of its chemical structure the name aldosterone was suggested as the definitive name, which is in keeping with the internationally accepted nomenclature classification. In the mean time, the same substance has also been isolated in crystalline form by Mattox and co-workers. We report here the details of its chemical structure, isolation and its characteristics. Simpson SA, Tait JF, Wettstein A, Neher R, von Euw J, Schindler O, Reichstein, T. Die Konstitution des Aldosterons. Ueber Bestandteile der Nebennierenrinde und verwandte Stoffe. 92. Mitteilung. Helv. Chim. Acta 1954;37:1200–23. Title: The chemical structure of aldosterone. Constituents of the adrenal cortex and related substances. Abstract: We previously described, in two brief reports, the isolation and chemical structure of aldosterone. Details ology 96 (2004) 497–498 We previously described, in two brief reports, the isolation and chemical structure of aldosterone. Details ology 96 (2004) 497–498 D. Schlosshan et al. / International Journal of Cardiology 96 (2004) 497–498 498 regarding its isolation and the characteristics and derivatives of this hormone were described in the 91st report of this series. Here, we would like to report the results of the identification of its chemical structure. Chemical degradation of aldosterone has shown that this compound is an 18oxo-corticosterone. In solution, it probably can be found predominantly in the cyclohemiacetal form. Simpson SA, Tait JF, Wettstein A, Neher R, von Euw J, Reichstein, T. Isolierung eines neuen kristallisierten Hormons aus Nebennieren mit besonders hoher Wirksamkeit auf den Mineralstoffwechsel. Experientia 1953:9;333–5. Title: Isolation of a new crystalline hormone from the adrenal gland with a particularly potent effect on electrolyte metabolism. Recently, a new, highly sensitive method was described allowing rapid measurement of the effects of steroids on the ratio of urinary sodium and potassium output using only tracer amounts of substrate. With the help of this test, it was possible to demonstrate unequivocally that adrenal gland extracts indeed contain a specific substance with high activity that can also be detected after paper chromatographic separation and in the blood. It was also possible to purify this substance to a high degree. Using the method described above, the concentrates were 60–80 times more potent than cortexone. We have now been able to isolate this substance in a pure crystalline form from several concentrates prepared by our two research groups working in parallel in Basel. Methods and results: Extracts prepared from 500 kg of beef adrenals using the method described by Cartland and Kuizenga served as starting material. A total of 167 g of this material was purified using partition chromatography on large kiesleguhr columns with aqueous methanol:benzene solvent systems. Further purification using paper chromatography and repeated partition chromatography yielded 22 mg of the raw crystalline compound. Using the Na42/K42 method by Simpson and Tait, the compound described was around 100 times, and using the modified sodium retention method of Kagawa et al. around 50 times more potent than Cortexone. In (maintenance tests) in adrenalectomised dogs the compound appeared 30 times more potent than cortexone– acetate. Conclusion: We therefore consider that we have found a new important hormone of the adrenal cortex. We will report later about experiments leading to the chemical identification and synthesis of this compound as well as other more detailed biological experiments. We reserve the right to suggest a new name for the new compound at that time.

Effects of nonsteroidal anti-inflammatory drugs on postoperative renal function in adults with normal renal function.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can play a major role in the management of acute pain in the peri-operative period. However, there are conflicting views on whether NSAIDs are associated with adverse renal effects. The primary objective of this review was to determine the effects of NSAIDs on postoperative renal function in adults with normal preoperative renal function. Electronic searches for relevant randomised and quasi-randomised controlled trials in Cochrane Central Register of Controlled Trials, MEDLINE and EMBASE were performed. Attempts were also made to identify trials from citation lists of relevant trials, review articles and clinical practice guidelines. Handsearching of conference abstracts published in major anaesthetic journals was also performed. (Search date: 7 February 2003) The inclusion criteria were randomised or quasi-randomised comparisons of individual NSAIDs with either each other or placebo for treatment of postoperative pain, with relevant postoperative renal outcome measures, in adult surgical patients with normal renal function. The data was extracted independently by two reviewers. The primary outcome measure was creatinine clearance within the first two days after surgery. Secondary outcome measures included serum creatinine, urine volume, urinary sodium level, urinary potassium level, fractional excretion of sodium, fractional excretion of potassium, need for dialysis and need for diuretic or dopamine treatment for renal insufficiency. Weighted mean differences for continuous outcomes and relative risk for dichotomous outcomes were estimated. Nineteen trials ( n = 1204) fulfilled the selection criteria for this review. NSAIDs reduced creatinine clearance by 16 ml/min (95%CI 5 to 28) and potassium output by 38 mmol/day (95%CI 19 to 56) on the first day after surgery compared to placebo. There was no significant difference in serum creatinine on the first day (0 umol/L, 95%CI -5 to 4) compared to placebo. No significant reduction in urine volume during the early postoperative period was found. There was no significant difference in serum creatinine in the early postoperative period between patients receiving diclofenace and ketorolac (or indomethacin). No cases of postoperative renal failure requiring dialysis were described. The trials were homogeneous for the primary outcome. NSAIDs caused a clinically unimportant transient reduction in renal function in the early postoperative period in patients with normal preoperative renal function. NSAIDs should not be withheld from adults with normal preoperative renal function because of concerns about postoperative renal impairment.

Effect of intracerebroventricularly injected insulin on urinary sodium excretion by cerebroventricular streptozotocin-treated rats.

Recent evidence suggests that insulin may influence many brain functions. It is known that intracerebroventricular (icv) injection of nondiabetogenic doses of streptozotocin (STZ) can damage insulin receptor signal transduction. In the present study, we examined the functional damage to the brain insulin receptors on central mechanisms regulating glomerular filtration rate and urinary sodium excretion, over four periods of 30 min, in response to 3 microl insulin or 0.15 NaCl (vehicle) injected icv in STZ-treated freely moving Wistar-Hannover rats (250-300 g). The icv cannula site was visually confirmed by 2% Evans blue infusion. Centrally administered insulin (42.0 ng/ micro l) increased the urinary output of sodium (from 855.6 85.1 to 2055 310.6 delta%/min; N = 11) and potassium (from 460.4 100 to 669 60.8 delta%/min; N = 11). The urinary sodium excretion response to icv insulin microinjection was markedly attenuated by previous central STZ (100 micro g/3 micro l) administration (from 628 45.8 to 617 87.6 delta%/min; N = 5) or by icv injection of a dopamine antagonist, haloperidol (4 micro g/3 micro l) (from 498 +/- 39.4 to 517 +/- 73.2 delta%/min; N = 5). Additionally, insulin-induced natriuresis occurred by increased post-proximal tubule sodium rejection, despite an unchanged glomerular filtration rate. Excluding the possibility of a direct action of STZ on central insulin receptor-carrying neurons, the current data suggest that the insulin-sensitive response may be processed through dopaminergic D1 receptors containing neuronal pathways.