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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an open-label prospective study the safety, efficacy, and patient tolerance of an enterally administered isotonic intestinal lavage solution containing polyethylene glycol-3350 was evaluated in 20 pediatric patients (ages 1 1/2 to 19 years) undergoing diagnostic colonoscopy. After an oral dose of metoclopramide, lavage solution was administered by mouth or nasogastric tube at a rate of 40 ml/kg per hour until stools were clear. Emesis occurred in 4 patients, nausea in 11, and abdominal distension in 5. Clear stools were produced in a mean (+/- SE) time of 2.6 +/- 0.3 hours. The volume of lavage solution delivered, which ranged from 15.6 to 183.3 ml/kg, varied inversely with the weight (and age) of the patient. Preparation of the colon was considered optimal in 11 patients, satisfactory in 7, and suboptimal in 2. Small but significant decreases in urine osmolality, blood urea nitrogen, serum glucose, and potassium values were noted at the termination of perfusion. Postperfusion serum glucose concentration in the smallest patient (11.4 kg) was 61 mg/dL (3.4 mmol/L). Mean (+/- SEM) change in weight after perfusion was 0.14 +/- 0.05 kg (range -0.2 to +0.6 kg). Of 20 patients, 11 required or requested nasogastric administration of the lavage solution because of its unpleasant taste. We conclude that whole intestinal perfusion with a balanced electrolyte solution containing polyethylene glycol is safe, acceptable, and efficacious in children.
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PMID:Safety, efficacy, and tolerance of intestinal lavage in pediatric patients undergoing diagnostic colonoscopy. 206 47

The influence of postprandial-like plasma insulin levels on intestinal calcium absorption (CaA) was studied in 9 healthy men. On separate occasions, they received either an i.v. infusion of 40 mU/m2 minute synthetic human insulin as well as a variable glucose infusion in order to clamp the plasma glucose at the baseline level (= glucose clamp), or insulin- and glucose-free vehicle infusions (= vehicle). During these infusions, an oral load containing 326 mg Ca in the form of Ca chloride was administered and CaA was determined thereafter with a 47Ca/85Sr double tracer method. During glucose clamp, mean plasma insulin was 172 +/- (1 SEM) 10 as compared to 6 +/- 1 microU/ml during vehicle infusions. During the clamp, 3-hour cumulative CaA rose significantly by 14% as compared to vehicle (39.2 +/- 2.5 vs. 34.4 +/- 2%, P less than 0.02). AT the same time, serum potassium and phosphorus dropped significantly, whereas serum parathyroid hormone (PTH) and 1,25(OH)2D levels were unchanged as compared to vehicle. The urinary excretions of potassium, sodium, and inorganic phosphorus, as well as the urinary specific activity of 47Ca, dropped significantly during glucose clamp, whereas the urinary excretion of cAMP was unchanged as compared to vehicle. The results suggest that, under the conditions of euglycemic hyperinsulinemic clamp, insulin stimulates CaA of healthy humans in a PTH- and 1,25(OH)2D-independent manner. Insulin may thus possibly be regarded as a factor participating in the regulation of CaA in humans.
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PMID:Intestinal calcium absorption during hyperinsulinemic euglycemic glucose clamp in healthy humans. 210 52

The intracellular potassium content of perfused rat heart was measured by potassium-39 nuclear magnetic resonance (NMR) spectroscopy at 33 degrees C with an inversion recovery technique based on the fact that the spin-lattice relaxation time (T1) of the intracellular potassium (8.3 msec at 8.45 T) is much faster than that of the extracellular potassium (68 msec). Intracellular potassium decreased to 60.2 +/- 4.3% of the control level (mean +/- SEM, n = 6) at 40 minutes from the start of metabolic inhibition (2 mM cyanide, 0 mM glucose). Removal of cyanide restored intracellular potassium to 94.2 +/- 3.9% at 30 minutes from the restart of oxidative metabolism. The cumulative potassium loss was determined from the flow rate and potassium concentration of the coronary effluent, which reached 139 +/- 12 mumol/g dry wt during 40 minutes of metabolic inhibition. This value was calculated as 41.8% of intracellular potassium in the control heart and agreed with the decrement of intracellular potassium measured by NMR. During the metabolic inhibition and recovery period, a linear correlation was observed between the changes in 39K NMR-observed intracellular potassium and the cumulative potassium loss. The present results evaluate the inversion recovery technique as a method to successfully monitor the myocardial intracellular potassium.
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PMID:Potassium-39 nuclear magnetic resonance observation of intracellular potassium without chemical shift reagents during metabolic inhibition in the isolated perfused rat heart. 211 22

1. To examine the metabolic effects of increases in circulating endogenous plasma catecholamines, we measured plasma glucose, potassium and magnesium in 14 patients undergoing elective coronary artery bypass grafting. The patients were randomized into two groups and received either sodium nitroprusside (a direct-acting vasodilator) or trimetaphan camsylate (a ganglion-blocking agent) for routine control of blood pressure during the operation. 2. There were significant differences between the two groups in the levels of all three metabolic variables studied. Plasma glucose levels rose in both groups, but were significantly higher in the sodium nitroprusside group [peak levels 9.14 (SEM 0.72)mmol/l compared with 6.71 (0.88) mmol/l, P less than 0.001, analysis of variance]. The cardioplegia solution caused a large increase in plasma magnesium in both groups but in the sodium nitroprusside group the level rose higher [to 1.59 (0.12)mmol/l compared with 1.34 (0.06)mmol/l] and fell faster (P less than 0.05, analysis of variance). In the group receiving sodium nitroprusside, plasma potassium fell, by a mean of 0.34mmol/l, as plasma catecholamine levels rose; no such fall was seen in the group receiving trimetaphan camsylate (P less than 0.05, analysis of variance). 3. It is concluded that the sympathoadrenal system is important in causing metabolic changes during cardiopulmonary bypass and may be relevant in other conditions such as acute myocardial infarction.
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PMID:Effects of circulating endogenous catecholamines on plasma glucose, potassium and magnesium. 215 47

1. We have used n.m.r. spectroscopy to measure rubidium concentrations in the skeletal muscle of live intact rats. Using a 1.9 T superconducting magnet and an ear-phone coil tuned to both protons (1H) and rubidium (87Rb), it was possible to make measurements of both tissue rubidium content and water content, and from these measurements to obtain the rubidium concentration. 2. The n.m.r. estimate of rubidium concentration in muscle in vivo was found to be a constant 31% (SEM 4%) of that estimated by flame atomic absorption spectroscopy in an extract of excised muscle. This is close to the predicted theoretical n.m.r. visibility of 33%. The visibility was constant for muscle rubidium concentrations ranging between 10 and 34 mmol/l. 3. Rubidium concentration measurement by this method is unaffected by variations in sample geometry, sample volume, tissue conductivity, coil tuning and amplifier gain. 4. By using this method to measure changes in tissue rubidium concentration with time in the same animal, it should now be possible to assess the activity of ion transport systems, such as sodium- and potassium-activated adenosine triphosphatase in vivo, by measuring the rates of change of tissue rubidium concentrations during the administration of rubidium salts. 5. This method could also be used to measure the absolute concentration of any n.m.r.-visible nucleus and could be applied to man.
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PMID:A non-invasive method of measuring concentrations of rubidium in rat skeletal muscle in vivo by 87Rb nuclear magnetic resonance spectroscopy: implications for the measurement of cation transport activity in vivo. 215 50

Little information is known regarding caffeine's effect on the substrate supporting sustained ventricular arrhythmias. This prospective study evaluated the effect of coffee (275 mg of caffeine) on this substrate with programmed ventricular stimulation in 22 patients with a history of symptomatic nonsustained ventricular tachycardia, ventricular tachycardia, or ventricular fibrillation. Patients underwent electrophysiological testing before and 1 hour after coffee ingestion. Mean (+/- SEM) plasma caffeine level achieved after coffee consumption was 6.2 +/- 0.5 mg/L. Mean plasma catecholamine and potassium values were not altered significantly 1 hour following caffeine ingestion. The number of extrastimuli required to induce an arrhythmia was unchanged in 10 patients (46%), increased in six (27%), and decreased in six (27%). Rhythm severity was unchanged in 17 patients (77%), more severe in two (9%), and less severe in three (14%). In those patients with clinical ventricular arrhythmias, caffeine did not significantly alter inducibility or severity of arrhythmias, suggesting little effect on the substrate supporting ventricular arrhythmias.
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PMID:Caffeine and ventricular arrhythmias. An electrophysiological approach. 221 1

Prostaglandin E2 (PGE2) impairs the hydrosmotic effect of vasopressin in toad bladder and mammalian kidney. Because some studies in animals have suggested that potassium depletion enhances renal PGE2 production, the present study examined whether the renal concentrating defect of potassium depletion in humans is mediated by PGE2. Five normal volunteers were studied before and after moderate potassium depletion achieved by 10 days of dietary potassium restriction and administration of a polystyrene sulfonate potassium exchange resin (Kayexalate). Maximal urinary osmolality (Umax) decreased from 1,094 +/- 58 (mean +/- SEM) to 820 +/- 26 mmol/kg (mOsm/kg) (P less than 0.01) following potassium depletion, but urinary PGE2 excretion did not change (496 +/- 145 and 435 +/- 186 ng/d, respectively). Indomethacin suppressed PGE2 excretion significantly, but failed to increase Umax in either the normal or the potassium-depleted state (1,094 +/- 34 and 825 +/- 56 mmol/kg, respectively). It is concluded that the renal concentrating defect produced by moderate potassium restriction in humans is not mediated by PGE2.
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PMID:The renal concentrating defect associated with potassium depletion is independent of prostaglandin E2. 223 40

A modified synaptosomal superfusion apparatus is described which uses less than 10 micrograms of tissue per replicate sample and facilitates the routine separation of 3H-DA, 3H-DOPAC, and 3H-HVA. A flow rate of 1.5 ml/min allows superfusion without the use of reuptake or monoamine oxidase inhibitors. Superfusate samples are collected directly onto alumina columns for the separation of 3H-DA and its acid metabolites. Total recovery of authentic 3H-DA applied via superfusion was 87.63(1.10) percent [Mean(SEM)]. Contamination of the acetic acid eluate fraction, containing 80.98(1.15)% of the total DA, by DOPAC and HVA was less than 0.1%. To illustrate the utility of this technique, the relative proportions of 3H-DA and 3H-metabolites released from synaptosomes by 6 mM potassium and 1 microM reserpine were compared.
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PMID:A microassay for measuring synaptosomal 3H-dopamine and 3H-metabolite release. 229 40

As plasma potassium concentrations, whether normal or elevated, can be reduced by intravenous administration of either epinephrine or ritodrine, the effects of these drugs were examined during acute hyperkalemia. Six anesthetized dogs were studied every 2 wk, on 18 separate occasions. Hyperkalemia was induced by intravenous infusion of potassium chloride, resulting in plasma potassium concentrations of 9.6 +/- 0.3 mEq/L (mean +/- SEM), bradycardia, and idioventricular rhythm. Dogs were then given slow intravenous injections every 30 min of either saline (controls), epinephrine, or ritodrine. Epinephrine doses were 0.01, 0.1, 1.0, 10, or 100 micrograms/kg; ritodrine doses were 0.1, 1.0, 10, 100, or 1000 micrograms/kg. At the highest does, both epinephrine and ritodrine caused clinically important decreases in plasma potassium, reducing concentrations to below 7.0 mEq/L. Ritodrine had a significantly greater effect than epinephrine. Side effects included hypertension and dysrhythmias with epinephrine, serious hypotension with ritodrine, and tachycardia with both drugs. For both drugs, the doses that caused a decrease in plasma potassium also caused an increase in heart rate and there was a correlation between plasma potassium levels and heart rate. Epinephrine and ritodrine may be useful in treating acute hyperkalemia, but cardiovascular side effects may occur. Increased heart rate could be used as an indicator of therapeutic effect and the magnitude of the increase in heart rate may be helpful in predicting the level of response.
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PMID:Effects of epinephrine and ritodrine in dogs with acute hyperkalemia. 231 82

The perilymphatic space was perfused with artificial perilymph containing 5 x 10(-3)M potassium canrenoate. The EP, K+ and Na+ activities in the scala media were measured with double barrelled K+ or Na+ selective microelectrode. Following the onset of the perfusion, the EP gradually declined and was stable after about 20 minutes. K+ activity also declined gradually but Na+ activity was unchanged. When the EP became stable, the artificial ventilation was stopped. The EP dropped to a large negative potential and K+ activity decreased gradually, but Na+ activity increased by degrees. The same results were observed in the untreated animals when the ventilation was stopped. There are no pathological changes both in the TEM view of the stria vascularis and in the SEM view of the hair cell. These results suggest that this drug may affect K+ conductance of the stria vascularis specifically.
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PMID:[Effect of potassium canrenoate on the EP and Na+, K+ activities in endolymph]. 235 44


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