Search

Na and Cl fluxes and short-circuit current (Isc) in rabbit ileum have been studied as a function of ionic concentrations in HCO3-free solutions. Both net Na flux (JnetNa) andIscshow similar saturation functions of [Na] at fixed [Cl]. They show no significant difference between zero and 112mmNa but at 140mmNaIscis significantly greater than theJnetNa. Net Cl transport, secretion, is observed only at 140mmNa and is approximately equivalent to the difference between theIscandJnetNa. The transcellular mucosa-to-serosa Na fluxes measured at 140 and 70mmNa do not differ significantly from the correspondingIsc. The net Cl flux varies with [Cl] at fixed [Na] whileIscis virtually not affected by [Cl]. These results suggest that the absorptive Na transport process is electrogenic and responsible for theIscand that the secretory fluxes of Na and Cl are coupled, require high [Na], vary with [Cl], and do not contribute toIsc. K-free solution abolishes theIscafter a prolonged lag. Finally, the effect of a low resistance shunt pathway on active Na absorption is examined with a four-compartment model.Na and Cl fluxes and short-circuit current (Isc) in rabbit ileum have been studied as a function of ionic concentrations in HCO3-free solutions. Both net Na flux (JnetNa) andIscshow similar saturation functions of [Na] at fixed [Cl]. They show no significant difference between zero and 112mmNa but at 140mmNaIscis significantly greater than theJnetNa. Net Cl transport, secretion, is observed only at 140mmNa and is approximately equivalent to the difference between theIscandJnetNa. The transcellular mucosa-to-serosa Na fluxes measured at 140 and 70mmNa do not differ significantly from the correspondingIsc. The net Cl flux varies with [Cl] at fixed [Na] whileIscis virtually not affected by [Cl]. These results suggest that the absorptive Na transport process is electrogenic and responsible for theIscand that the secretory fluxes of Na and Cl are coupled, require high [Na], vary with [Cl], and do not contribute toIsc. K-free solution abolishes theIscafter a prolonged lag. Finally, the effect of a low resistance shunt pathway on active Na absorption is examined with a four-compartment model.

Among the many treatments for acute diarrhea, oral ingestion of glucose has received much attention. However, this treatment may have opposite effects in different situations. Simple ingestion of an electrolyte solution containing glucose has proved to be an efficient and simple treatment for the acute diarrhea associated with cholera and appears to be a usable alternative to the intravenous infusion of water and electrolytes to maintain fluid balance.1-5 The favorable socioeconomic consequences of such an approach have been apparent to many pediatricians.6 In contrast, glucose is one of the many substances known to aggravate acute diarrhea in some situations that are not always well defined.7-10 In these clinical situations, glucose ingestion may have been the direct cause of infant death.10.11 Similarly, in the rare congenital glucose-galactose malabsorption syndrome, the extensive intestinal fluid loss is clearly caused by ingestion of glucose and galactose.Water absorption or

The reaction of a variety of substituted thiophenes, under Friedel–Craft conditions, leading to acetylthiophenes is described. Some of the by-products obtained are isolated and their mode of formation rationalized. The bromination, the reduction of the bromoketones, and their transformation to thienylethanolamines is reported. The degradation products of bromohydrin as well as isomeric amines obtained in the final substitution reaction are characterized and a possible mechanism for the formation of these compounds is proposed.

Reaction of 2-amino-3-nitropyridine with acid chlorides in the presence of dimethyl sulfoxide and a tertiary base, such as pyridine, unexpectedly yielded the aminal N,N′-bis(3-nitro-2-pyridinylimino)methylene 5. A similar aminal 6formed when 2-amino-5-nitropyridine was treated under the same conditions. However, simple aminopyridines such as 2-aminopyridine or 2-amino-6-methylpyridine gave only the 2-N-methylenethiomethyl derivatives. It was proved that the aminals are formed by the attack of a suitable base on the N-methylenethiomethyl intermediates with expulsion of methyl mercaptan. The formation of these unusual aminals may be explained to be taking place via a Pummerer type rearrangement.

Sodium flux from serosa to mucosa, JsmNa in rabbit ileum in vitro has been studied as a function of applied electrical potential at equal sodium concentrations in the bathing solutions. The results indicate that JsmNa involves two pathways, a diffusional flux through a paracellular shunt pathway and a flux that is independent of applied potential and presumably involves a transcellular pathway. The latter pathway comprises approximately 25 % of JsmNa in Ringer's solution containing 10 mM glucose and 25 mM bicarbonate. It is stimulated significantly by theophylline unaffected by removal of glucose or addition of ouabain but is reduced to negligible values by anoxia, dinitrophenol, and replacement of all chloride and bicarbonate by isethionate. Thus this component of JsmNa has a number of characteristics consistent with involvement in a specific secretory process mediating an electrically neutral secretory transport of sodium plus anion from serosa to mucosa. In addition to stimulating this process, theophylline significantly reduced the permeability of the paracellular shunt pathway to sodium.

This paper describes a total synthesis of a biogenetically possible, hitherto unknown macrolide 4. Starting with 3,5-dimethoxybenzaldehyde, ketone 5awas generated in five steps. Alkylation of this compound by bromopentene followed by decarboxylation yielded pentenyl ketone 6. Oxymercuration–demercuration followed by dehydration gave cyclic enol ether 8. Oxidation with m-chloroperbenzoic acid led to the macrolide 4.

not available

Massive secretion of fluid and electrolytes into the intestinal lumen is observed in cholera but, in normal intestine, more than 50 per cent of Na transepithelial flux involves an extracellular route. This study was, therefore, undertaken to determine the role of the epithelial cells in the Na secretion observed in cholera. From measurements of flux as a function of electrical potential, the transcellular Na fluxes (Jc) were estimated, in vitro, on ileum treated with cholera toxin (CT) for 60 minutes and compared with Jc from unchallenged control (C) intestine from the same rabbit. In absence of electrochemical potential, in Ringer's solution, CT caused a net Na secretion (−1.35 ± 0.21 μeq/hr cm2), without statistical change in short circuit current. The net secretion appears to be due to a decrease of transcellular Na flux from mucosa to serosa (Jcms) (−0.94 ± 0.35 μeq/hr cm2) and an increase of flux from serosa to mucosa (Jcsm) (+0.75 ± 0.64 μeq/hr cm2). The Na addition of lOmM glucose caused an increase (p<0.01) of Jnet, Isc and Jems almost identical in C and CT intestine. However, Jcsm did not change significantly with glucose. These results indicate that CT caused an active cellular Na secretion which is most easily explained by posttulating that CT stimulates an electrically neutral (Na+Anion) transport process from serosa to mucosa but does not change the “electrogenic” Na absorption.