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PubMed1983

Regulation of the acid-base status during environmental hypercapnia in the marine teleost fish Conger conger.

Specimens of Conger conger (L.) were exposed to environmental hypercapnia in a closed recirculating seawater system. Arterial plasma pH, PCO2 and bicarbonate concentration, as well as the net transfer of bicarbonate and ammonia between fish and ambient seawater, were monitored for 30 h of hypercapnia. The initial hypercapnia-induced reduction of arterial pH by about 0.4 pH units was restored to near control values within 10 h of hypercapnia by compensatory elevation of plasma bicarbonate concentration. The continuous rise in extracellular bicarbonate from about 5 to 22 mM during this time was the result of two different mechanisms. Initially, there was a net bicarbonate transfer from the intracellular space to the extracellular compartment until the net uptake of bicarbonate from the seawater started. The amount of bicarbonate originally transferred to the extracellular space was then returned to the intracellular compartment and finally the changes in both extracellular and intracellular pH were compensated by bicarbonate taken up from the environmental seawater. Since the ammonia excretion was not increased during hypercapnia and the pattern of plasma electrolyte concentrations does not favour the H+/Na+ ion exchange mechanism, it is concluded that the additional bicarbonate is gained by active HCO3-/Cl- ion exchange against the electrochemical gradient between fish and seawater.

Acid-Base Imbalance↗

PubMed2004

[PGD(2)/L-PGDS system in hypertension and renal injury].

Prostaglandin D(2) (PGD(2)) and its metabolites bind to the intracellular PPARs to regulate vasoactive substances involved in vascular remodeling through regulation of mRNAs transcription as well as through receptor-mediated mechanisms. PGD(2) decreases inducible NO, PAI-1, endothelin, and VCAM expression through inhibition to NF kappa B, STAT, or AP-1 transcription factors, which are regulated by cytokines/immune system. Moreover, transfer of L-PGDS (PGD(2) synthase) into the intracellular space of EC or SMC increases intracellular PGD(2), thereby decreasing these substances. PGD(2) attenuates in vivo organ injury mediated by cytokines and the immune system. The pretreatment with PGD(2) attenuates the liver damage and hemodynamic collapse following LPS. Dahl salt-sensitive rats, with decreased PGD(2) in the outer medulla of the kidney, are prone to hypertensive kidney injury. Serum L-PGDS level is increased in renal dysfunction through a decrease in glomerular filtration. L-PGDS in urine may be derived from a failure of tubular reabsorption or from in situ synthesis. Urinary L-PGDS excretion markedly increases in the early stage of kidney injury, and urinary L-PGDS is a useful predictor of the forthcoming renal injury. Indeed, urinary L-PGDS precedes clinically overt proteinuria or other parameters indicating renal dysfunction in hypertension, primary renal diseases, and diabetes in humans. PGD(2)/L-PGDS system is a Cinderella of vascular biology.

Animals↗

PubMed1985

Permeability of materials in postglomerular capillary bed and distribution to interstitium of kidney in rats.

Extracellular reference materials are necessary to estimate tubular transport parameters for drugs which are secreted in the kidney. They must set up the flow-limited distribution between plasma and interstitial space, not be distributed to the intracellular space, and be nondegradable in the extracellular space. The capillary permeability of various molecular weight markers in the post glomerular circulation was investigated by performing pulse-injection multiple indicator dilution experiments on isolated rat kidney, using simultaneous injection of T1824-labeled albumin (the plasma reference) and creatinine (or inulin) as the extracellular reference materials. The permeability constants and the gamma values (ratio of the volume in the space of interstitium to that of capillary plasma) for creatinine and inulin were calculated by a nonlinear least squares regression. The gamma values for creatinine were greater than those for inulin, implying that the volume of distribution for creatinine is different from that for inulin. The capillary permeability clearance (CLinflux) for creatinine was 4 times higher than that of inulin, and was 3 times greater than the perfusion rate. Thus, creatinine satisfies the qualification for the flow-limited distribution between plasma and interstitial space. These findings suggest that in the rat kidney creatinine is more suitable for the extracellular reference material than inulin.

Animals↗

PubMed1998

Hypomagnesemia: renal magnesium handling.

Magnesium is an important constituent of the intracellular space that affects a number of intracellular and whole body functions. Magnesium balance depends on intake and renal excretion, which is regulated mainly in the thick ascending limb of the loop of Henle. The complex hormonal modulation that responds to changes in plasma concentration of other ions such as calcium and potassium is lacking for magnesium. As a result, negative magnesium balance results in a prompt decrease in plasma magnesium concentration, and hypermagnesemia accompanies renal failure with magnesium accumulation. Hypomagnesemia may result from gastrointestinal losses or renal losses, the latter due to primary renal magnesium wasting or in association with sodium loss. Hypomagnesemia may arise together with and contribute to the persistence of hypokalemia and hypocalcemia. The major direct toxicity of hypomagnesemia is cardiovascular. When urgent correction of hypomagnesemia is required, as with myocardial ischemia, post cardiopulmonary bypass, and torsades de pointes, intravenous or intramuscular magnesium sulfate should be used. Oral magnesium preparations are available for chronic use.

Animals↗

PubMed1994

Health and infarcted brain tissues studied at short diffusion times: the origins of apparent restriction and the reduction in apparent diffusion coefficient.

The significance of NMR water diffusion measurements performed at short diffusion times (< 10 ms) for brain tissue is examined. An apparent restriction to diffusion for both healthy and cytotoxically edematous tissue is shown: cytotoxic edema lengthens the diffusion time at which this phenomenon is visible. The dramatic reduction in apparent diffusion coefficient (ADC) observed in the core of cytotoxic edema is explained in terms of the enclosure of extracellular water in non-contiguous pockets in conjunction with the shift of water from the extra-to the intracellular space. The model presented provides an explanation for the ADC reduction without recourse to changes in the cell membrane permeability to water, or unrealistic values for the extra- and intracellular diffusion coefficients.

Animals↗

PubMed1990

Fluid and ion redistribution in skeletal muscle in an animal sepsis model.

The redistribution of fluid and electrolytes was investigated in a hyperdynamic sepsis animal model using cecal ligation and puncture (CLP) in Wistar rats. Hyponatremia was not observed. There was a significant shift of sodium, chloride, and water from the extracellular into the intracellular space as early as 12 hours following CLP. These data suggest that the mechanism by which hyponatremia occurs in clinical sepsis is not caused by shift of fluid from the intracellular to the extracellular space as proposed by the sick cell theory. This is more likely to result from fluid retention and dilution of the extracellular space possibly on the basis of antidiuretic hormone secretion.

Animals↗

PubMed1996

Nutritional state and the swelling-induced inhibition of proteolysis in perfused rat liver.

Recent work indicates that cell volume is an important regulator of proteolysis in liver. The antiproteolytic effects of insulin and some amino acids (e.g., glutamine and glycine) are mediated by increases in cell volume. The purpose of the present study was to assess the role of nutritional state in the cell volume-dependent regulation of proteolysis in isolated perfused rat liver. In rats that had been prelabeled by an intraperitoneal injection of L-[4,5-3H]leucine 16-20 h prior to the perfusion experiment, hepatic proteolysis was studied by determination of [3H]label release into effluent perfusate. In separate perfusion experiments [3H]inulin and [14C]urea, acting as markers for extracellular and the sum of extra- plus intracellular space, were employed for determination of effector-induced cell volume changes. Proteolysis in the perfused rat liver was inhibited by insulin-like growth factor-I (IGF-1) and taurocholic acid. Both agonists increased the intracellular water space. The nutritional state of the livers had marked influence on the hormone- and amino acid-dependent regulation of proteolysis. In livers from food-deprived rats for 24 h, the swelling responses to glycine, glutamine and alanine were enhanced, whereas the insulin- and IGF-1-induced increases of cell volume were diminished. A stronger inhibition of proteolysis was observed in livers from food-deprived rats upon addition of the amino acids, whereas the insulin- and IGF-1-mediated inhibition of proteolysis was attenuated. Independent of the nutritional state, a close relationship between the cellular hydration state and the corresponding inhibition of proteolysis was observed, regardless of whether cell volume was modified by amino acids, hormones, hypoosmotic exposure or bile acids. We conclude that the nutritional state markedly modifies the swelling potency of amino acids and hormones in liver and by this means affects proteolysis.

Amino Acids↗

PubMed1998

Depletion of intracellular Ca2+ stores or lowering extracellular calcium alters intracellular Ca2+ changes during cerebral energy deprivation.

Cytoplasmatic calcium concentrations are elevated two to three fold during cerebral ischemia. In order to determine the role of calcium-release from intracellular stores vs. calcium entry from the extracellular space, intracellular stores were depleted by the use of thapsigargin and calcium was removed from the incubation fluid prior to energy deprivation (ED). CA 1 pyramidal neurons in hippocampal rat slices were filled with a 1:2 mixture of Fluo-3 and Fura Red by intracellular injection. The neurons were visualized in a Confocal Laser Scanning Microscope (CLSM) and the fluorescence ratio from the probe mixture was used to quantify the calcium concentration. Intracellular calcium concentration was monitored before and during ED. The intracellular calcium concentration was 55 nM prior to ED and increased to 25 microM during ED. The resting levels were the same in the experimental groups, but the increase during ED was significantly lower in the intervention groups. The increase in the calcium free group was to 1 microM and in the thapsigargin group to 5 microM. In the last experimental group, thapsigargin treatment and removal of extracellular calcium, the intracellular calcium increased to 630 nM. These results demonstrate that the increased intracellular calcium seen during ED originates from several sources. Calcium-release from intracellular stores may be of major importance in calcium-related neuronal injury during cerebral ischemia.

Aniline Compounds↗

PubMed1985

Spinal cord injury and protection.

Subsequent to traumatic injury of the spinal cord, a series of pathophysiological events occurs in the injured tissue that leads to tissue destruction and paraplegia. These include hemorrhagic necrosis, ischemia, edema, inflammation, neuronophagia, loss of Ca2+ from the extracellular space, and loss of K+ from the intracellular space. In addition, there is trauma-initiated lipid peroxidation and hydrolysis in cellular membranes. Both lipid peroxidation and hydrolysis can damage cells directly; hydrolysis also results in the formation of the biologically active prostaglandins and leukotrienes (eicosanoids). The time course of membrane lipid alterations seen in studies of antioxidant interventions suggests that posttraumatic ischemia, edema, inflammation, and ionic fluxes are the result of extensive membrane peroxidative reactions and lipolysis that produce vasoactive and chemotactic eicosanoids. A diverse group of compounds has been shown to be effective in ameliorating spinal cord injury in experimental animals. These include the synthetic glucocorticoid methylprednisolone sodium succinate (MPSS); the antioxidants vitamin E, selenium, and dimethyl sulfoxide (DMSO); the opiate antagonist naloxone; and thyrotropin-releasing hormone (TRH). With the exception of TRH, all of these agents have demonstrable antioxidant and/or anti-lipid-hydrolysis properties. Thus the effectiveness of these substances may lie in their ability to quench membrane peroxidative reactions or to inhibit the release of fatty acids from membrane phospholipids, or both. Whatever the mode of action, early administration appears to be a requirement for maximum effectiveness.

Animals↗

PubMed1971

The osmotic behavior of rod photoreceptor outer segment discs.

The permeability properties of frog rod photoreceptor outer segment discs were investigated in preparations of purified, dark-adapted, outer segment fragments by the techniques of direct volume measurement and electron microscopy. Outer segment discs were found to swell and contract reversibly in response to changes in the osmotic pressure of the bathing medium in accordance with the Boyle-van't Hoff law. By use of the criterion of reversible osmotic swelling, the disc membrane is impermeable to Na(+), K(+), Mg(+2), Ca(+2), Cl(-), and (PO(4))(-3) ions, whereas it is freely permeable to ammonium acetate. The disc membrane is impermeable to sucrose, although its osmotic behavior towards this substance is different from its behavior towards impermeable ions. Electron microscopy showed that the osmotic effects on the rod outer segment fragments represent changes in the intradiscal volume. Fixation with glutaraldehyde did not abolish the permeability properties of the disc membrane, and fixed membranes were still capable of osmotic volume changes. It is concluded from this study that the frog's rod photoreceptor outer segment discs are free-floating membranous organelles with an inside space separate and distinct from the photoreceptor intracellular space.

Acetates↗

PubMed1986

Distribution of tris buffer between intracellular and extracellular space as a function of plasma pH in the rat.

Rats were anaesthetized with halothane and artificially ventilated. After bilateral nephrectomy and implantation of arterial and venous catheters, arterial plasma pH (pHe) was adjusted by infusion of HCl or sodium bicarbonate to 7.2, 7.4, or 7.5 and kept constant throughout the experiment. The distribution of tris between intra- and extracellular compartments was determined as a function of time up to 24 h after infusion of 14C-labelled tris and 3H inulin in five skeletal muscle groups, heart, liver, spleen, and brain tissue. The following results were obtained: Tris diffuses very slowly into the intracellular space of the investigated tissues. For different arterial plasma pH, the intracellular tris concentration is quite different. It rises more rapidly and reaches higher levels in alkalemia. Five different skeletal muscle groups showed the same rates of rise of intracellular tris at the same pHe. Tris diffuses almost immediately into liver cells, the rates being slower in spleen, heart, skeletal muscle and brain, in that order. Only in the liver did intracellular tris concentration reach a steady state, at levels higher than theoretically predicted, suggesting that ionic tris also is permeable. In other tissues, lack of steady states at the end precluded similar conclusions. It can be concluded that the clinical importance of tris therapy is in its elimination of H+ ions from the extracellular space and in the generation of bicarbonate that then penetrates the intracellular compartment.

Animals↗

PubMed1978

[Metabolic unit in the microcirculatory system of the exocrine part of the pancreas].

Metabolism between exocrine pancreocytes and blood is mediated with the participation of the metabolic section of the microcirculatory system. It includes: blood capillaries, pericapillary space, intracellular gaps and metabolite distributional complex (basal-lateral folds of pancreocytic plasmolemma). As demonstrated morphological and histochemical changes developed in exocrine pancreocytes and in the metabolic section of the pancreatic gland at different stages of the secretory cycle, interconnections between them are complex and dynamical. All the elements of the metabolic section undergo a certain reconstruction adequate to functional state of pancreocytes. Metabolism between glandular cells and the vascular bed is regulated by structural reconstruction of pancreocytic plasmolemma. A certain functional specialization in plasmolemmic folds is noted: basal-lateral folds regulate transport between pericapillary space and intracellular gaps, while the main function of the lateral folds is to transport substances by means of pinocytosis.

Animals↗

PubMed1990

Multiple quantum filtered 23Na NMR spectroscopy in the perfused heart.

It has been proposed that multiple quantum filtered (MQF) 23Na NMR spectroscopy may distinguish between sodium in the intra- and extracellular spaces, in vivo, and without the requirement for toxic shift reagents. We have investigated the origin of such signals in perfused rat hearts, using shift reagents to discriminate between NMR signals from the two compartments. We find that the observed MQF signal arises predominantly from the extracellular space in the normal heart, and from the intracellular space in the ischaemic heart. However, the quenching effect of the shift reagent may hide some of the extracellular MQF signal, especially during ischaemia. Estimates of intracellular and extracellular relaxation times are obtained and possible mechanisms of the interaction discussed.

Animals↗

PubMed2003

A mathematical study of volume shifts and ionic concentration changes during ischemia and hypoxia.

The response of tissue to ischemia (cessation of blood flow and deprivation of oxygen) includes swelling of the intracellular space, shrinkage of the extracellular space, and an increase in the extracellular potassium concentration. The responses of cardiac and brain tissue to ischemia are qualitatively different in that cardiac tissue shows a rise in extracellular potassium over several minutes from about 5 to 10-12 mM followed by a plateau, while brain tissue shows a similar initial rise followed by a very rapid increase in extracellular potassium to levels of 50-80 mM. During hypoxia the flow of blood (or perfusate) is maintained and, while there is a substantial efflux of potassium from cells, there is little accumulation of potassium in the interstitium. A mathematical model is proposed and studied to try to elucidate the mechanism(s) underlying the increase in extracellular potassium, and the different time courses seen in neural and cardiac tissue. The model involves a Hodgkin-Huxley-type description of transmembrane ion currents, allows for ion concentrations as well as volumes to change for both the intracellular and extracellular space, and includes coupling of damaged tissue to nearby healthy tissue. The model produces a response to ischemia much like that seen in neural tissue, and the mechanism underlying this response in the model is determined. The same mechanism is not present in cardiac ion models, and this may explain the qualitative difference in response shown in cardiac tissue.

Animals↗

PubMed1975

In vivo studies on the metabolism of hexanedioic acid.

1. Using the combined gas-liquid chromatography-mass spectrometry technique it was shown that ketotic patients excreted up to 273 mg of hexanedioic acid daily in their urine, whereas serum samples from these patients contained only trace amounts of this acid. Healthy humans excreted 2-5 mg daily. Hexanedioic acid was not detectable in normal serum. 2. An experiment with the infusion of large amounts of 3-hydroxybutyrate into a dog indicated that the increased urinary hexanedioic acid excretion in ketosis is not due to a competition between 3-hydroxybutyrate and hexanedioic acid for the same renal reabsorption mechanism. 3. [ 1,6-14-C]Hexanedioic acid intravenously injected into a dog was at first distributed in the extracellular space, followed by a partial equilibration with the intracellular space. About 11% of the injected dose was expired as 14-CO2 in 220 min. The maximal 14-CO2 production rate was obtained after about 20 min. In 240 min, 47% of the injected radioactivity was recovered in the urine. The large urinary excretion of labeled hexanedioic acid observed in the presence of only trace amounts in serum, showed that the high excretion by ketotic patients of the dicarboxylic acid may be explained without postulating an exclusive renal synthesis for hexanedioic acid.

Adipates↗

PubMed1987

Autoantibodies--a mechanism of microdebridement.

Antibodies to foreign debris are generally beneficial because they speed inflammation and debridement of tissue. Intracellular components are debris if they reach extracellular space. If not rapidly debrided from extracellular space, intracellular components stimulate autoantibody production. If not debrided, cellular constituents like other foreign material can initiate a chronic tissue response. Antibodies will speed removal of debris if an effective microdebridement mechanism is present. This is their general biologic significance. If the patient has a defective microdebridement system as in lupus erythematosus or rheumatoid arthritis, the autoantibodies occur to large numbers of intracellular substances and accumulate and contribute to tissue damage. Tissue damage occurs and autoantibodies accumulate in lupus erythematosus and rheumatoid arthritis because of inadequate microdebridement. This should not detract from the fact that autoantibodies are a common secondary phenomenon which plays an important part in maintaining tissue microdebridement.

Aging↗

PubMed2005

NMDA receptors are expressed in oligodendrocytes and activated in ischaemia.

Glutamate-mediated damage to oligodendrocytes contributes to mental or physical impairment in periventricular leukomalacia (pre- or perinatal white matter injury leading to cerebral palsy), spinal cord injury, multiple sclerosis and stroke. Unlike neurons, white matter oligodendrocytes reportedly lack NMDA (N-methyl-d-aspartate) receptors. It is believed that glutamate damages oligodendrocytes, especially their precursor cells, by acting on calcium-permeable AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid)/kainate receptors alone or by reversing cystine-glutamate exchange and depriving cells of antioxidant protection. Here we show that precursor, immature and mature oligodendrocytes in the white matter of the cerebellum and corpus callosum exhibit NMDA-evoked currents, mediated by receptors that are blocked only weakly by Mg2+ and that may contain NR1, NR2C and NR3 NMDA receptor subunits. NMDA receptors are present in the myelinating processes of oligodendrocytes, where the small intracellular space could lead to a large rise in intracellular ion concentration in response to NMDA receptor activation. Simulating ischaemia led to development of an inward current in oligodendrocytes, which was partly mediated by NMDA receptors. These results point to NMDA receptors of unusual subunit composition as a potential therapeutic target for preventing white matter damage in a variety of diseases.

Animals↗

PubMed2001

ESR detection of intraphagosomal superoxide in polymorphonuclear leukocytes using 5-(diethoxyphosphoryl)-5-methyl-l-pyrroline-N-oxide.

We applied a spin trap, 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO), to detect O2*- generation during phagocytosis in human polymorphonuclear leukocytes (PMNs). PMNs were activated with serum-opsonized zymosan (sOZ) in the presence of DEPMPO. The ESR spectra mainly consisted of Cu,Zn-SOD-sensitive DEPMPO-OOH spin adducts. To clarify where these spin-adducts were present, cells after stimulation were separated from extracellular fluid by brief centrifugation and resuspended in Hanks' balanced salt solution. ESR examination showed that DEPMPO-OOH adducts were present in both fractions. When cells were stimulated by phorbol myristate acetate (PMA), the DEPMPO-OOH was detected in extracellular fluid but not in the cell fraction. Furthermore, DEPMPO-OOH adducts were quickly converted into ESR-silent compounds by addition of cell lysate of PMNs. These results indicate that DEPMPO is useful to detect O2*- of extracellular space including the intraphagosome but not that of intracellular space in sOZ-stimulated phagocytes.

Cyclic N-Oxides↗