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Intravenous rehydration is required only in patients with severe diarrhea due to V. cholerae who are in shock, with absent peripheral pulse and blood pressure; when the shock has been corrected, rehydration can be completed using an oral rehydration solution. The intravenous solution to be used is 5:4: 1 (5g of sodium chloride, 4g of sodium bicarbonate and 1g of potassium chloride per liter) or a comparable commercial alkaline solution. For oral rehydration a solution is used containing 3.5 g sodium chloride, 2.5g sodium bicarbonate, 1.5g potassium chloride and 20g of glucose (or 40g of sucrose) per liter. These fluids are administered in a volume replacing the amount lost before treatment was initiated and the fluids lost in the continuing diarrhea. With this management, a case fatality rate of 50% in the untreated falls to less than 1%. The addition of antibiotics such as tetracycline and furazolidone reduces the duration of diarrhea and the need for continuing fluid balance observation. Intravenous rehydration of severe diarrhea cases with normal saline solution or with 5% glucose solution increases the acidosis with resulting veno-constriction, which favors the pooling of blood in the heart and the pulmonary circulation leading to cardiac overload and then failure and circulatory peripheral collapse. When acidosis is corrected by the sodium bicarbonate solution and with adequate fluid replacement, normal hemodynamics are reestablished and the patient immediately recovers from the collapse. In cases of mild or moderate diarrhea, replacement entirely by oral rehydration of the estimated volume of lost fluid alone is usually sufficient. This management of diarrhea is applicable for diarrhea from any cause, including enterotoxigenic Escherichia coli, Rotavirus, Salmonella and Shigella as well as Vibrio cholerae.
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PMID:[Development of a rehydration therapy in diarrheic disease. 1980]. 176 34

Injection of scolicidal solution into the hydatid cysts has been used to sterilize the cyst and to prevent intra-abdominal dissemination of the parasite during surgery. We report six cases of complications of this measure. Intraoperative collapse in one patient and an immediate postoperative death occurring after injection of 10% H202. Postoperative sclerosing cholangitis occurred in 4 patients in whom 2% formalin or 20% sodium chloride was injected into the cyst. Cholangiography showed strictures affecting the intrahepatic biliary tree in 2 and both the intra and extra biliary tree in 3. Sclerosing cholangitis in these patients was likely to result from the caustic effect of the scolicidal solution having diffused from the cyst into the biliary tree. Jaundice developed in 3 patients from 2 to 5 months after operation. The intra-operative collapses is related to the injection of H202 into the cyst. The dramatic increasing of the volume of the cyst may fissure of the cyst-wall and allows the passage of gaz into the circulation. As the efficacity of intracystic injection of a scolicidal solution in preventing the dissemination of the parasite is still unproven, we recommend the rejection of this maneuver in the surgical treatment of hydatid disease of the liver.
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PMID:[Complications of peroperative sterilization of hydatid cysts of the liver. Apropos of 6 cases]. 181 31

Recent studies have shown that potentially fatal hyponatremia can develop during prolonged exercise. To determine the incidence of hyponatremia in athletes competing in ultradistance events, we measured serum sodium levels in 315 of 626 (50%) runners who were treated for collapse after two 90 km ultramarathon footraces (total starters 20,335; total finishers 18,031) and in 101 of 147 (69%) finishers in a 186 km ultratriathlon. In both races the athletes drank fluids with low sodium chloride content (less than 6.8 mmol.l-1). Hyponatremia (serum sodium level less than 130 mmol.l-1) was identified in 27 of 315 (9%) collapsed runners in the 90 km races and in none of the triathletes. In response to diuretic therapy, the runner with the most severe hyponatremia (serum sodium level = 112 mmol.l-1) excreted in excess of 7.5 l dilute urine during the first 17 h of hospitalization. These data suggest that, although symptomatic hyponatremia occurs in less than 0.3% of competitors during prolonged exercise even when they ingest little sodium chloride, it is found in a significant proportion (9%) of collapsed runners. A regulated contraction of the extracellular fluid volume would explain why the majority of athletes maintain normal serum sodium levels even though they develop a significant sodium chloride deficit during prolonged exercise. Alternatively, sodium chloride losses during prolonged exercise may be substantially less than are currently believed. Physicians treating collapsed ultradistance athletes need to be aware that as many as 10% or more of such patients may be hyponatremic.
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PMID:The incidence of hyponatremia during prolonged ultraendurance exercise. 228 68

1. The interactions between cytochrome c (native and [(14)C]carboxymethylated) and monolayers of phosphatidylcholine, phosphatidic acid and cardiolipin at the air/water interface was investigated by measurements of surface radioactivity, pressure and potential. 2. On a subphase of 10mm-or m-sodium chloride, penetration of cytochrome c into egg phosphatidylcholine monolayers, as measured by an increase of surface pressure, and the number of molecules penetrating, as judged by surface radioactivity, were inversely proportional to the initial pressure of the monolayer and became zero at 20dynes/cm. The constant of proportionality was increased when the cytochrome c was carboxymethylated or decreased when the phospholipid was hydrogenated, but the cut-off point remained at 20dynes/cm. 3. Penetrated cytochrome c could be removed almost entirely by compression of the phosphatidylcholine monolayer above 20dynes/cm. 4. With phosphatidic acid and cardiolipin monolayers on 10mm-sodium chloride the binding of cytochrome c was much stronger and cytochrome c penetrated into films nearing the collapse pressure (>40dynes/cm.). The penetration was partly electrostatically facilitated, since it was decreased by carrying out the reaction on a subphase of m-sodium chloride, and the relationship between the surface pressure increment and the initial film pressure moved nearer to that observed with phosphatidylcholine. 5. Surface radioactivity determinations showed that [(14)C]carboxymethylated cytochrome c was still adsorbed on phosphatidic acid and cardiolipin monolayers after the cessation of penetration. This adsorption was primarily electrostatic in nature because it could be prevented and substantially reversed by adding m-sodium chloride to the subphase and there was no similar adsorption on phosphatidylcholine films. 6. The penetration into and adsorption on the three phospholipid monolayers was examined as a function of the pH of the subphase and compared with the state of ionization of both the phospholipid and the protein, and the area occupied by the latter at an air/water interface. 7. It is concluded that the binding of cytochrome c to phospholipids can only be partially understood by a consideration of the ionic interaction between the components and that subtle conformational changes in the protein must affect the magnitude and stability of the complex. 8. If cytochrome c is associated with a phospholipid in mitochondria then cardiolipin would fulfil the characteristics of the binding most adequately.
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PMID:Interactions of cytochrome c and [14C]. 538 43

When spread from organic solvents onto electrolyte solutions, the Ca2+ ionophores A23187 (I) and X537A (II) formed films with relatively high surface pressures potentials. Ionophores I had collapse pressures between 16 and 19 dynes/cm and nearly equal surface activity on distilled water and on 1000 mEq of either sodium chloride or calcium chloride. Film pressure did not reveal appreciable ion selectivity. However, the surface potential of I on calcium chloride solution was higher than that on sodium chloride, and the potential difference, delta(deltaV), of 40 mv was independent of the electrolyte concentration. In contrast, the ion selectivity of II was dependent on the electrolyte concentrations since the delta(deltaV) value between calcium chloride and sodium chloride was maximal (130 mv) on 1000 mEq and negligible on 500- and 2000-mEq salt solutions. The isotherms of phospholipid-ionophore films were markedly different from those of the individual components, although they revealed ionophore characteristics at low film pressures and phospholipid behavior at high film pressures. The magnitude of the surface potential indicated that dipalmitoyl phosphatidylcholine enhanced, whereas mitochondrial lipid and cardiolipin reduced, the preference of the two ionophores for Ca2+ over Na+. Since the ion selectivity was manifested most at both high electrolyte and high lecithin concentrations, the ionophore probably prefers the low dielectric constant of neutral lipid membranes to complex with the selected cation.
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PMID:Surface properties of membrane systems: interaction of electrolyte and lipid with Ca2+ ionophores. 676 74

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41

Annexins, Ca2+- and phospholipid-binding proteins are known to bind to artificial and biological membranes in a calcium-dependent manner. However, the precise mechanism of the annexin-membrane interactions still remains to be studied in detail. In this paper we describe the results of studies on the interactions of the annexin/Ca complexes with phospholipids, obtained by the Wilhelmy balance method of assessing the surface pressure of a phospholipid monolayer. We show that the annexin IV/Ca as well as annexin VI/Ca complexes significantly reduce the surface pressure of a phosphatidylserine monolayer, when its initial value is close to collapse pressure. The effect is highly specific for monolayers composed of phosphatidylserine and strongly sensitive to pH and ionic strength. The most pronounced changes have been observed at pH 7.0-7.5, at a protein/Ca molar ratio of 1:2 for annexin IV and 1:4 for annexin VI. In the presence of sodium chloride at concentrations exceeding 400mM this effect was almost completely abolished. The obtained results point to the mainly electrostatic character of the annexin/phosphatidylserine interactions. In addition, using large multilamellar lipid vesicles and serine proteases, we demonstrate that annexins, when bound in a ternary complex with phospholipids and calcium ions, are partially protected against proteolysis. Our observation that annexin molecules, complexed with calcium ions, are protected against proteolytic attack in the presence of PS liposomes does not have to be necessarily explained in terms of partial penetration of protein within the membrane bilayer.
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PMID:Interaction of annexins IV and VI with phosphatidylserine in the presence of Ca2+: monolayer and proteolytic study. 911 63

A strain of Bacillus designated TA2.A1, isolated from a thermal spring in Te Aroha, New Zealand, grew optimally at pH 9.2 and 70 degrees C. Bacillus strain TA2.A1 utilized glutamate as a sole carbon and energy source for growth, and sodium chloride (>5 mM) was an obligate requirement for growth. Growth on glutamate was inhibited by monensin and amiloride, both inhibitors that collapse the sodium gradient (DeltapNa) across the cell membrane. N, N-Dicyclohexylcarbodiimide inhibited the growth of Bacillus strain TA2.A1, suggesting that an F1F0-ATPase (H type) was being used to generate cellular ATP needed for anabolic reactions. Vanadate, an inhibitor of V-type ATPases, did not affect the growth of Bacillus strain TA2.A1. Glutamate transport by Bacillus strain TA2.A1 could be driven by an artificial membrane potential (DeltaPsi), but only when sodium was present. In the absence of sodium, the rate of DeltaPsi-driven glutamate uptake was fourfold lower. No glutamate transport was observed in the presence of DeltapNa alone (i.e., no DeltaPsi). Glutamate uptake was specifically inhibited by monensin, and the Km for sodium was 5.6 mM. The Hill plot had a slope of approximately 1, suggesting that sodium binding was noncooperative and that the glutamate transporter had a single binding site for sodium. Glutamate transport was not affected by the protonophore carbonyl cyanide m-chlorophenylhydrazone, suggesting that the transmembrane pH gradient was not required for glutamate transport. The rate of glutamate transport increased with increasing glutamate concentration; the Km for glutamate was 2.90 microM, and the Vmax was 0.7 nmol. min-1 mg of protein. Glutamate transport was specifically inhibited by glutamate analogues.
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PMID:Sodium-dependent glutamate uptake by an alkaliphilic, thermophilic Bacillus strain, TA2.A1. 1032 19

During ultra-endurance exercise, both increase in body temperature and dehydration due to sweat losses, lead to a decrease in central blood volume. The heart rate drift allows maintaining appropriate cardiac output, in order to satisfy both muscle perfusion and heat transfer requirements by increasing skin blood flow. The resulting dehydration can impair thermal regulation and increase the risks of serious accidents as heat stroke. Endurance events, lasting more than 8 hours, result in large sweat sodium chloride losses. Thus, ingestion of large amounts of water with poor salt intake can induce symptomatic hyponatremia (plasma sodium < 130 mEq/L) which is also a serious accident. Heat environment increases the thermal constraint and when the air humidity is high, evaporation of sweat is compromise. Thus, thermal stress becomes uncompensable which increases the risk of cardiovascular collapse. Cold exposure induces physiological responses to maintain internal temperature by both limiting thermal losses and increasing metabolic heat production. Cold can induce accidental hypothermia and local frost-bites; moreover, it increases the risk of arrhythmia during exercise. Some guidelines (cardiovascular fitness, water and electrolyte intakes, protective clothing) are given for each extreme condition.
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PMID:[Sports and extreme conditions. Cardiovascular incidence in long term exertion and extreme temperatures (heat, cold)]. 1150 64

The objective of this article was to study the mechanism by which annealing increases the primary drying time in mannitol-trehalose-sodium chloride-based formulations. The thermal events occurring during annealing and the glass transition of the frozen solutions were monitored with differential scanning calorimetry (DSC). Manometric temperature measurement was used to evaluate the dry layer resistances during primary drying. The morphologies of the freeze-dried cakes were examined by scanning electron microscopy (SEM). The degrees of crystallinity of mannitol and sodium chloride (NaCl) in freeze-dried cakes were determined by powder X-ray diffraction (XRD). DSC results indicated that annealing during freezing did not increase the glass transition temperature (Tg') significantly, but there was a distinct decrease of deltaCp at Tg' with annealing, suggesting a decrease in amorphous content. SEM revealed that most mannitol crystallized as the delta-form during annealing at -23 degrees C, and further crystallized as the alpha-form, together with NaCl crystallization, during subsequent annealing at -33 degrees C. The powder XRD results demonstrated that annealing caused crystal growth of mannitol and NaCl, and thus prevented the partial collapse observed without annealing. However, the highly crystallized mannitol blocked the pathways for water vapor escape, contributing to the increase in the dry layer resistance and thus the longer times for primary drying. Freeze-dried cakes without annealing had lower dry layer resistances because partial collapse created larger channels for water vapor escape. Therefore, two-step annealing in freezing makes mannitol-trehalose-sodium chloride-based formulations robust in freeze-drying, but annealing increases the dry layer resistances, thereby extending primary drying.
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PMID:Freeze-drying of mannitol-trehalose-sodium chloride-based formulations: the impact of annealing on dry layer resistance to mass transfer and cake structure. 1500 Apr 69


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