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PubMed1991

Acid-base regulation in the toad Bufo marinus during environmental hypoxia.

Gas exchange and the correlated changes in blood and tissue metabolic and acid-base status were investigated during long term exposure of the toad Bufo marinus to graded levels of hypoxia. During hypoxia, PCO2 values in blood and tissues fell, leading to a transient alkalosis in the extracellular but not in the intracellular space. A reduction in blood perfusion of the skin during hypoxia may explain why PCO2 was low in sartorius muscle under normoxia, but approached the PCO2 values found in other tissues (gastrocnemius muscle, ventricle) under hypoxia. At PO2 values below the critical PO2, lactate was formed and the decrease in total CO2 was accelerated. Lactate levels in the plasma were higher than in the intracellular space of the skeletal muscles, a finding attributed to the pH-dependent distribution of lactic acid across the cell membrane. The comparison of metabolic proton quantities with those found in the extra- and intracellular acid-base status suggests that CO2 release was accelerated by anaerobic proton formation. The alkalizing effect of decreasing PCO2 in the skeletal musculature was compensated for by a release of base equivalents into the blood. The resulting alkalosis in the blood was probably compensated for by the release of base equivalents into the environment.

Acid-Base Equilibrium↗
PubMed1985

Penetration of C8 and C9 in the C5b-9 complex across the erythrocyte membrane into the cytoplasmic space.

We have developed a technique in which transglutaminase is used to measure the penetration of terminal complement proteins across the erythrocyte membrane into the cytoplasmic space. Penetration of a given terminal complement protein into the cytoplasmic space was assessed by labeling the protein of interest with radioactive iodine, forming the complement channel using the labeled protein, adding transglutaminase to only one side of the membrane, and allowing the enzyme to cross-link the susceptible proteins on that side of the membrane. Cross-linking was assessed by measuring the increase in molecular weight of the appropriate molecule on sodium dodecyl sulfate gels under reducing conditions. The results of these experiments indicate that C8 and C9 are rapidly cross-linked to high molecular weight from either the interior or the exterior of the membrane. In order to determine whether the cross-linking mediated by enzyme on the interior was occurring from within the ghosts and not via enzyme that had leaked into the extracellular medium, experiments were performed with dimethylcasein in the extracellular medium. In the presence of this protein, cross-linking of C8 and C9 from outside was negligible. Hence, if cross-linking occurs when transglutaminase is trapped inside the ghosts, it cannot be due to leakage of enzyme, but must be attributable to cross-linking from the inside. The results show that C9 definitely penetrated across the membrane into the intracellular space. With respect to C8, statistical evaluation indicates that C8 probably penetrated into the intracellular space.

Acyltransferases↗
PubMed2005

Biomedical applications of 133Cs NMR.

133Cs NMR is a valuable tool for non-invasively probing biological systems. As a congener of potassium, it accumulates in the intracellular space, primarily through the action of the Na+-K+ pump (ATPase). In addition, it is possible to resolve the MR signal of 133Cs in different tissue compartments on the basis of chemical shift or MR relaxation properties. This compartmental resolution applies not only to the intra- and extracellular spaces, but to subcellular compartments as well. In this review, we discuss the studies defining the ion transport, chemical shift and relaxation characteristics of 133Cs in living systems. We also review the application of 133Cs NMR to evaluation of ion transport across membranes and the kinetic/chemical environment of the intracellular space in systems ranging from red blood cells to rat brain.

Animals↗
PubMed2001

Phosphate removal and hemodialysis conditions.

Hyperphosphatemia is frequently found in hemodialysis patients, and the association with an increased risk of mortality has been demonstrated. Other authors have linked hyperphosphatemia to increased cardiovascular mortality. The normalization of phosphate plasma levels is therefore an important goal in the treatment of end-stage renal disease patients. Absorption of phosphate from the food exceeds the elimination through a hemodialysis treatment, and this leads to a chronic phosphate load for the majority of hemodialysis patients. This imbalance should be improved by either a reduction of phosphate absorption or an increased removal of phosphate. A reduction of phosphate absorption can be achieved by reducing the amount of phosphate in the diet or by the administration of phosphate binders. Unfortunately, these measures imply practical difficulties, for example, a lack of patient compliance or other side effects. When considering modifications of the hemodialysis treatment, an essential understanding of the kinetics of dialytic phosphate removal is mandatory. Phosphate is unevenly distributed in different compartments of the body. Only a very small amount of phosphate is present in the easily accessible plasma compartment. The major part of phosphate removed during hemodialysis originates from the cytoplasm of cells. A transfer from intracellular space to the plasma and further from the plasma to the dialysate is necessary. However, if we consider improvement to phosphate removal by dialysis procedures, full dialyzer clearance is effective in only the initial phase of the dialysis treatment. After this initial phase, the transfer rate for phosphate from the intracellular space to the plasma becomes the rate-limiting step for phosphate transport. Attempts to improve this transfer rate have recently been investigated by acidosis correction, but turned out not to be consistently successful. Furthermore, modifications of the treatment schedule have been described in the literature as measures to influence the phosphate balance consistently. Successful improvements of the phosphate balance can be achieved specifically through increasing the frequency of the dialysis treatments.

Acidosis↗
PubMedDate not supplied

[Body composition in chronic renal insufficiency in the primary anuric phase and after dialysis].

Bioelectric impedance was analysed before and after dialysis to assess the body composition of 36 patients suffering from chronic kidney failure in fair nutritional condition: resistance values were used to quantify total body water and reactance values as dimensional indices of the intracellular spaces and cell mass. Before dialysis, total body water was significantly higher than that of healthy subjects comparable for height, sex, age and weight, while it was not possible to obtain direct data on the dimensions of the cell mass. After dialysis, total body water values normalised and the dimensions of the intracellular spaces and cell mass became almost comparable to those of the controls: data analysis shows that during treatment, weight loss occurs almost exclusively in the extracellular compartments of the organism. Notwithstanding the fact that the absolute values are similar to those of the controls, body composition did not normalise as relationships between the dimensions of the various sectors remain altered.

Adult↗
PubMed1978

Alloxan uptake by isolated rat islets of Langerhans.

Alloxan inhibits subsequent glucose-induced insulin release from isolated rat islets of Langerhans maintained in vitro. Several agents (D-glucose, D-mannose, 3-0-methyl-D-glucose, caffeine, and cytochalasin B) when present during the alloxan exposure protect against alloxan inhibition of insulin release. To examine the mechanism of alloxan inhibition, the uptake of [2-14C]alloxan was measured in isolated islets. [2-14C]Alloxan was rapidly accumulated by the islets in a time- and temperature-dependent manner. The radio-activity from islets incubated with [2-14C]alloxan was isolated and shown by thin layer chromatography to comigrate with alloxan and alloxanic acid, an alloxan decomposition product. As no uptake of radioactivity occurred in the presence of medium containing the radioactive decomposition product, it was concluded that alloxan enters the intracellular space of the islet and undergoes a subsequent internal decomposition. Some of the protective agents (3-0-methyl-D-glucose, caffeine, and cytochalasin B) partially inhibited alloxan uptake, whereas others (D-glucose and D-mannose) increased the uptake of alloxan. These and other results suggest that the experimental agents do not provide protection against alloxan inhibition by preventing the entry of alloxan into the intracellular space of the islet. The possibility of D-glucose and alloxan competing for a common binding site on the cell membrane is discussed.

Alloxan↗
PubMed1992

Localization of binding sites for epidermal growth factor (EGF) in rat kidney: evidence for the existence of low affinity EGF binding sites on the brush border membrane.

We investigated the renal distribution of 125I-EGF in the filtering perfused rat kidney using an acid washing technique. Trichloroacetic acid-precipitable 125I-EGF radioactivity was eluted from both the renal vein and the urinary cannulae, the former regarded as representing the antiluminal, and the latter the luminal, cell surface bound 125I-radioactivity. The addition of excess unlabeled EGF (20 nM) to the perfusate completely inhibited the binding of 125I-EGF to the antiluminal membrane but did not inhibit that of 125I-EGF to the luminal membrane. On the other hand, the order of relative density of 125I-EGF binding sites in the in vivo kidney determined by autoradiography was cortex > inner medulla > outer medulla. After the i.v. administration of excess unlabeled EGF together with 125I-EGF, the renal uptake of 125I-EGF was inhibited completely in the inner medulla, but only by 50% in the cortex and outer medulla, suggesting the presence of nonsaturable luminal uptake of EGF in the cortex and outer medulla. After i.v. administration of 125I-EGF, a change in position of silver grains from the luminal cell surface membrane to the intracellular space was observed in the proximal convoluted tubules. In conclusion, in addition to the previously identified uptake mechanisms of circulating EGF through high-affinity binding sites on the antiluminal cell surface membrane, the reabsorption mechanism of filtered EGF through low-affinity binding sites on the luminal cell surface membrane was demonstrated. In vivo autoradiography showed the gradual internalization of EGF from the luminal cell surface membrane to the intracellular space of the proximal convoluted tubule.

Animals↗
PubMed1995

Electrophysiologic changes in ischemic ventricular myocardium: I. Influence of ionic, metabolic, and energetic changes.

Myocardial ischemia leads to significant changes in the intracellular and extracellular ionic milieu, high-energy phosphate compounds, and accumulation of metabolic by-products. Changes are measured in extracellular pH and K+, and intracellular pH, Ca2+, Na+, Mg2+, ATP, ADP, and inorganic phosphate. Alterations of membrane currents occur as a consequence of these ionic changes, adrenergic receptor stimulation, and accumulation of lactate, amphipathic compounds, and adenosine. Changes in the volume of the extracellular and intracellular spaces contribute further to the ultimate perturbations of active and passive membrane properties that underlie alterations in excitability, abnormal automaticity, refractoriness, and conduction. These characteristic changes of electrophysiologic properties culminate in loss of excitability and failure of impulse propagation and form the substrate for ventricular arrhythmias mediated through abnormal impulse formation and reentry. The ability to detail the changes in ions, metabolites, and high-energy phosphate compounds in both the extracellular and intracellular spaces and to correlate them directly with the simultaneously occurring electrophysiologic changes have greatly enhanced our understanding of the electrical events that characterize the ischemic process and hold promise for permitting studies aimed at developing interventions that may lessen the lethal consequences of ischemia.

Animals↗
PubMed1993

Effects of insulin on fatty acid reesterification in healthy subjects.

The effects of insulin on triacylglycerol/fatty acid cycling (fatty acid reesterification) were studied in 12 normal subjects during euglycemic hyperinsulinemia with the use of stable isotope dilution analysis ([2H5]glycerol and [1-13C]palmitate) in combination with indirect calorimetry. During basal conditions, 5.6 +/- 0.6 mumol.kg-1 x min-1 of fatty acid were released of which approximately 3.3 mumol.kg-1 x min-1 were oxidized and approximately 2.2 mumol.kg-1 x min-1 were reesterified. A minority of the recycled fatty acid, (0.8 +/- 0.4 mumol.kg-1 x min-1) never left the intracellular space before being reesterified (intracellular triacylglycerol/fatty acid cycling), whereas the majority (1.2 +/- 0.4 mumol.kg-1 x min-1) were first released into the extracellular space and then reesterified in various organs (extracellular triacylglycerol/fatty acid cycling). In response to insulin, fatty acid release declined by 71% (from 5.6 +/- 0.6 to 1.6 +/- 0.2 mumol.kg-1 x min-1). Fatty acid oxidation (measured by indirect calorimetry) declined by 55% (from 3.3 +/- 0.3 to 1.5 +/- 0.3 mumol.kg-1 x min-1) and total triacylglycerol/fatty acid cycling was completely suppressed (from 2.2 to 0.0 mumol.kg-1 x min-1). Fatty acid release, oxidation, total and extracellular triacylglycerol/fatty acid cycling all correlated positively with plasma fatty acid concentrations. These data showed that insulin profoundly suppressed fatty acid release, oxidation as well as reesterification of those fatty acids that had entered the extracellular compartment. They suggested that physiological concentrations of insulin suppressed extracellular fatty acid reesterification primarily by inhibiting lipolysis.

Adult↗
PubMed1996

Sodium-dependent carnitine transport in human placental choriocarcinoma cells.

The JAR human placental choriocarcinoma cells were found to transport carnitine into the intracellular space by a Na(+)-dependent process. The transport showed no requirement for anions. The Na+-dependent process was saturable and the apparent Michaelis-Menten constant for carnitine was 12.3 +/- 0.5 microM. Na+ activated the transport by increasing the affinity of the transport system for carnitine. The transport system specifically interacted with L-carnitine, D-carnitine, acetyl-DL-carnitine and betaine. 6-N-Trimethyllysine and choline had little or no effect on carnitine transport. Of the total transport measured, transport into the intracellular space represented 90%. Plasma membrane vesicles prepared from JAR cells were found to bind carnitine in a Na(+)-dependent manner. The binding was saturable with an apparent dissociation constant of 0.66 +/- 0.08 microM. The binding process was specific for L-carnitine, D-carnitine, acetyl-DL-carnitine, and betaine. 6-N-Trimethyllysine and choline showed little or no affinity. It is concluded that the JAR cells express a Na(+)-dependent high-affinity system for carnitine transport and that the Na(+)-dependent high-affinity carnitine binding detected in purified JAR cell plasma membrane vesicles is possibly related to the transmembrane transport process.

Binding Sites↗
PubMed1999

A mechanistic analysis to characterize oramucosal permeation properties.

The hypotheses of this study are that the permeation of ionizable molecules follows the pH-partition theory, that the preferred transport pathway for penetrants depends on their charge status and that transport resistance is related to the membrane-coating granules (MCG). Transcellular resistance is believed to be proportional to the volume of MCG in the intracellular space while paracellular resistance is believed to result from the extrusion of the lipid contents of the MCG into the intercellular space. Nicotine, an ionizable model compound with two pK(a) values (3.4 and 8.2), was chosen as a molecular probe to investigate the pH-partition theory on permeation through porcine oramucosae, to characterize the differences in permeability among various oramucosae, and to explore the preferred transport pathways of each nicotine species through oramucosae. The pH-partition theory was proved from the observations that permeability, partition coefficient and diffusivity of nicotine varied as a function of pH. The keratinized gingiva was found to have greater permeability than the non-keratinized buccal and sublingual mucosae. The neutral nicotine species had a higher permeability than the ionized species due to its higher partition coefficient and diffusivity. A mechanistic analysis (permeability ratio-pH profile) was conducted to determine the preferred transport pathway of each nicotine species. The permeability of neutral nicotine was found to be proportional to the occupied volume of MCG in the intracellular space. This indicates that the preferred transport pathway for neutral nicotine is transcellular. As the solution pH was decreased, and a greater fraction of nicotine became protonated, the transport of hydrophilic, charged nicotine species along the intercellular pathway was preferred.

Animals↗
PubMed1994

Cerebral blood flow and effects of cerebrospinal fluid on calcium transport in patients with cerebral infarction.

BACKGROUND AND PURPOSE: In this study we investigated whether cerebrospinal fluid in patients with brain infarction possesses an activity that contributes to the evolution of brain ischemia. As a test, the effect of cerebrospinal fluid on Ca2+ influx into the intracellular space was chosen because this process is a mechanism for vasospasm, platelet aggregation as thrombi, and neuron damage. METHODS: Effects of cerebrospinal fluid taken from 48 patients with cerebral hemispheric infarction on the concentration of cytosolic free Ca2+ in platelets were studied using the fluorescent probe quin-2. Hemispheric cerebral blood flow was measured using 133Xe intravenous injection. RESULTS: Cerebrospinal fluid in 19 of 48 patients with cerebral hemispheric infarction increased the level of cytosolic free Ca2+ in platelets. The course of the disease in the patients who showed a positive effect of cerebrospinal fluid on Ca2+, when compared with that of patients who showed a negative effect, was characterized by a more severe clinical manifestation and mortality. The decrease in hemispheric cerebral blood flow was more marked in both ischemic and contralateral hemispheres in patients with positive effects of cerebrospinal fluid on the level of Ca2+. CONCLUSIONS: These data suggest that the ability of cerebrospinal fluid to evoke Ca2+ influx into the intracellular space in patients with brain infarction is a factor that aggravates ischemic brain damage.

Biological Transport↗
PubMed1992

Stimulation of hepatocyte System y(+)-mediated L-arginine transport by an inflammatory agent.

BACKGROUND: Arginine participates in several distinct metabolic pathways, including polyamine and nitric oxide biosynthesis. Normally, arginine is effectively sequestered from the hepatocyte intracellular space by the low basal activity of membrane transport system y+. This has implications for the subsequent metabolism of arginine and for hepatic arginine requirements during a septic insult. We investigated the influence of tumor necrosis factor (TNF) on the activity of System y(+)-mediated hepatocyte arginine transport employing hepatic plasma membrane vesicles (HPMVs). METHODS: Rats were treated with a single intraperitoneal injection of TNF (50 or 150 micrograms/kg body weight) for 2, 4, or 24 hours, and HPMVs were prepared by Percoll density gradient centrifugation. Vesicle purity was established by assay of enzyme markers. Vesicle arginine transport activity was evaluated by measurement of tritiated arginine uptake employing a rapid mixing-filtration technique. RESULTS: Arginine transport by HPMVs was entirely independent of sodium and consisted of saturable and nonsaturable components. Prior treatment with TNF resulted in a time- and dose-dependent stimulation of saturable transport within 2 hours and a return to basal levels after 24 hours. Nonsaturable uptake was unchanged. Inhibition analysis indicated that the TNF-induced increase in saturable arginine transport activity was mediated by an increase in System y+. Kinetic analysis revealed that accelerated transport was caused by a 78% increase in the maximal velocity of transport without alteration in transport affinity. CONCLUSIONS: In vivo treatment with TNF results in a rapid stimulation of saturable, System y(+)-mediated arginine transport in the liver. This TNF-induced stimulation of hepatic arginine transport may serve to increase the normally restricted availability of extrahepatic arginine to the hepatocyte intracellular space during a septic insult to support important arginine-dependent pathways in the liver.

Animals↗
PubMed2004

Invasion of chicken embryo fibroblast cells by avian Pasteurella multocida.

Invasion of chicken embryo fibroblast (CEF) cells by the virulent encapsulated Pasteurella multocida strains P-1059 (serovar A:3) and X-73 (serovar A:1) and an avirulent noncapsulated derivative P-1059B (serovar -:3) was investigated. The number of intracellular bacteria increased for all the strains after 2, 4 and 6 h post-inoculation to CEF cells. By 6 h post-inoculation, the number of invaded bacteria of encapsulated strains was significantly higher than noncapsulated strain and reached 150- and 112-fold for strains P-1059 and X-73, respectively, while it was 9-fold for strain P-1059B as compared to the number of invaded bacteria recovered after 2 h post-inoculation. Electron microscopy of invasion by encapsulated strains showed that the bacteria were adhering to CEF cells membrane after 1 h of inoculation. By 4-h, one or two bacteria were detected within membrane-bound vacuoles of the intracellular space. The number of intracellular bacteria markedly increased at 14 h post-inoculation. Invasion of all strains was inhibited significantly when the monolayers were treated with periodic acid (P<0.001) or trypsin (P<0.05). The treatment of bacteria with hyaluronidase did not affect invasion. The present results indicate that avian P. multocida capsular type A strains are invasive and that the receptor on CEF cell surface might be glycoprotein.

Animals↗
PubMed2001

Toxic effects of subconjunctival 5-fluorouracil and mitomycin C on ciliary body of rats.

PURPOSE: The effects of subconjunctival injection of mitomycin C and different concentrations of 5-fluorouracil on the epithelium of the ciliary body of twenty Sprague Dawley SD rats was studied. METHODS: Twenty rats were divided into four treatment groups. The first three groups received 0.2 ml of 5, 10, and 30 mg of 5-fluorouracil subconjunctivally respectively, and the fourth group 0.2 ml of 0.4 mg/ml mitomycin C subconjunctivally. The right eye received 0.2 ml of the antimetabolite, while the left eye was injected with 0.2 ml of saline subconjunctivally, as a control. The eyes were examined histologically, in a masked fashion, by light and by transmission electron microscopy. In each treatment group, two eyes were examined after one week, and three eyes were examined one month after the subconjunctival injection. RESULTS: Electron microscopy revealed toxic effects in the epithelium of the ciliary body of all treatment groups. The 5-fluorouracil group revealed focal mitochondrial edema, enlargement of intercellular spaces, and dilatation of intracellular spaces. The mitomycin C group showed pyknotic nuclei, enlargement of intercellular spaces, and irregular flattened epithelial cells. The severity of changes correlated with concentration and length of exposure. No pathology was found by light microscopy in all groups. CONCLUSIONS: This study demonstrates that subconjunctival antimetabolites mitomycin C and 5-fluorouracil can penetrate the sclera and exert toxic effects on the epithelium of the ciliary body, even in low doses. These changes were only apparent by electron microscopy and were still present one month after the injection. These findings may contribute to the theory that the application of antimetabolites during or after surgery has a direct effect on the epithelium of the ciliary body, besides its known effect on the conjunctiva. Further studies are needed to evaluate its effect on intraocular pressure.

Animals↗