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PubMed1995

Addition of carbonic anhydrase augments extracellular pH buffering in rat cerebral cortex.

1. The ability of the extracellular space to buffer rapid alkaline shifts was studied in rat cortex in vitro and in vivo. Alkaline shifts were generated by iontophoresis of OH- or were evoked by pressure ejection of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). 2. In cortical slices, alkaline shifts induced by OH- were enhanced by the carbonic anhydrase (CA) inhibitor benzolamide (83 +/- 16%, mean +/- SE), and were decreased by superfusion of 10 mg/l CA (-59 +/- 4%). CA had no effect at 1 mg/l, and no additional effect at 100 mg/l. 3. In slices, and in vivo, alkaline shifts induced by AMPA were similarly enhanced by benzolamide and decreased by superfusion of CA. 4. These data indicate that extracellular CA activity is less than that required for maximum buffering. This suggests that equilibrium between CO2 and bicarbonate may not be attained during rapid extracellular pH shifts.

Aging↗
PubMed1977

Ferritin immune complex deposits in the choroid plexus.

Mice injected intraperitoneally with 20 mg of ferritin twice weekly for more than 4 weeks developed proteinuria due to the deposition of ferritin-antiferritin antibody complexes in renal glomeruli. Deposits of ferritin, immunoglobulin G (IgG) and third complement component (C3) also accumulated in the perivascular, extracellular space of the choroid plexus as demonstrated by immunofluorescence and electron microscopy. The findings confirm previous observations on immune complex deposits in the choroid plexus in spontaneous autoimmune disease and persistent viral infections. The occurrence of similar deposits in the human choroid plexus and the possibility of an associated disturbance of the blood-spinal fluid barrier are discussed.

Animals↗
PubMed1981

[Mode of action of pentetrazole at the cellular level (author's transl)].

The question of the origin of the paroxysmal depolarization shifts which can be recorded from neurones within an experimental epileptogenic focus is still controversial. In this paper, a special reference is made to data obtained in thin hippocampal slices in vitro during intra- and extracellular recordings from CA1 pyramidal cell somas before and after pentylenetetrazole (PTZ) application onto the slice surface. It is shown that PTZ can decrease inhibitory potentials, increase membrane input resistance and increase action potential duration. Using calcium-selective microelectrodes, it is shown that PTZ can enhance the lowering of calcium ion concentration in extracellular space, which is normally induced by repetitive stimulations. These data, as well as those from others, support the hypothesis that paroxysmal depolarization shifts seen in hippocampus could result from the facilitation of a slow depolarizing calcium current through the cell membrane uncovered by a depression of repolarizing potassium current produced by the convulsants. The observed depression of inhibitory potential would further facilitate the development of long-lasting depolarizing potentials.

Action Potentials↗
PubMed2000

Synthesis and release of L-serine by rat astroglia-rich primary cultures.

L-serine is known to have important functions in the mammalian CNS other than being a constituent of proteins. It is the metabolic precursor of the neuroactive substances D-serine and glycine, serves as a building block for phospholipid biosynthesis and is likely to be a neurotrophic factor. Based on the observation that rat astroglia-rich primary cultures release L-serine into their culture medium, the biosynthesis and release of L-serine in these cultures has been investigated. Release of L-serine is due to both biosynthesis from glucose and to proteolysis. Amino groups for L-serine synthesis originate from transamination of amino acids that are either taken up from the extracellular space or produced intracellularly by proteolysis. The enzymes of the "phosphorylated pathway" of serine biosynthesis, i.e., 3-phosphoglycerate dehydrogenase, phosphoserine aminotransferase and phosphoserine phosphatase are present in rat brain as well as in rat astroglia-rich primary cultures and their specific activities have been determined. The presence of these enzymes indicates the operation of the "phosphorylated pathway" of L-serine biosynthesis in brain.

Amino Acids↗
PubMed1972

Human intracranial atherosclerosis. A histochemical and ultrastructural study of gross fatty steak lesions.

A descriptive study of atherosclerotic lesions in human intracranial arteries was undertaken using both light and electron microscopic technics. Arterial segments of human middle cerebral, internal carotid and basilar arteries with gross fatty streak lesions were obtained at autopsy within 4 hours after death, fixed and embedded in plastic. A new technic has been developed in which 0.5 mu-thick sections can be stained with PAS/alcian blue, thereby enabling clear differentiation, substantiated by simultaneous electron microscopic studies, between the lipid-filled smooth muscle cell, which is surrounded by a PAS-positive basement membrane, and the lipid-filled blood monocyte. These technics demonstrated that the gross fatty streak comprised a focal intimal thickening bordered on the lumen by a patent endothelial lining and on the media by a usually intact elastic membrane. The lesion contained smooth muscle cells and cells presumed to be blood monocytes, both filled with and devoid of lipid droplets. Although little fragmented or new elastica was found in the extracellular space, numerous foci of membranous material could be observed, believed to be cell debris and plasma lipoproteins. The similarity between the morphology of such lesions in intracranial arteries with those found in other arterial beds suggests that the documented differences in the prevalence of atherosclerosis in the various beds has no bearing on either the structure of each type of lesion or its progression.

Adult↗
PubMed1989

The rat liver microcirculation in alcohol-induced hepatomegaly.

It has been suggested that hepatocyte enlargement can lead to compression of the extracellular space (sinusoidal and interstitial) and induce portal hypertension. However, this hypothesis has never been tested by measuring the vascular and extravascular spaces in the intact liver. The aim of the present study was to investigate the effects of chronic alcohol intake on the hepatic microcirculation using Goresky's multiple-indicator dilution technique in the isolated perfused rat liver. Female rat littermates were pair-fed either ethanol (n = 7) or an isocaloric carbohydrate diet (n = 7) for 21 days. As expected, chronic alcohol intake produced a significant increase in liver/body weight ratio (+32%, p less than 0.01) and hepatocyte size (+45%, p less than 0.001), which was accompanied by a marked increase in the cellular water space (control: 3.3 +/- 0.6 ml; ethanol-fed: 4.9 +/- 0.9 ml; p less than 0.001). When expressing data per total liver, the sinusoidal space was similar in the two groups (control: 1.87 +/- 0.2; ethanol-fed: 1.95 +/- 0.2 ml; not significant), whereas the interstitial space was increased in alcohol rats compared to controls (albumin space +58%, p less than 0.01; sucrose space +51%, p less than 0.01). In alcoholic rats, the sinusoidal space was probably stretched, with an overall reduced transversal diameter, as suggested by the reduced values found when data were expressed per gm of liver weight. However, despite this finding and the enlargement of the liver and hepatocytes observed in alcoholic rats, similar values were obtained between the two groups for the portal perfusion pressure and thus the intrahepatic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholism↗
PubMed1986

The effect of urea synthesis on extracellular pH in isolated perfused rat liver.

In a non-recirculating system of isolated liver perfusion, stimulation of urea synthesis by NH4Cl is followed by a decrease of effluent pH by up to 0.2 pH unit. This effect is not observed when urea synthesis is inhibited by amino-oxyacetate or norvaline. When the urea formed by the liver is immediately hydrolysed with urease before the effluent perfusate reaches the pH electrode, the urea-synthesis-induced acidification is no longer observed. This indicates that accompanying alterations in hepatic metabolism after stimulation of urea synthesis, such as increased energy provision and consumption, are not responsible for the extracellular acidification, but that the effect is due to the formation of urea itself. The acidification of the extracellular space after stimulation of urea synthesis by NH4Cl is quantitatively explained by the consumption of 2 mol of HCO3-/mol of urea formed: 1 mol being incorporated into urea, the other being protonated to yield CO2 and H2O. The data match the theoretically predicted HCO3- consumption during ureogenesis and underline the role of hepatic urea synthesis for disposal of HCO3- by converting it into the excretable products CO2 and urea.

Ammonium Chloride↗
PubMed1977

Sodium cyanate-induced ocular lesions in the beagle.

Ocular lesions secondary to sodium cyanate administration in the beagle are described. Fifteen dogs were given sodium cyanate at doses of 30 to 170 mg/kg/day, 5 days per week. Fourteen developed cataracts which were generally posterior and subcapsular. Five animals developed corneal lesions. Control beagles and cyanate-treated rats and monkeys did not develop lesions. The one drug-treated beagle without ocular lesions received a maximum dose of 30 mg/kg/day of sodium cyanate for 19 months and achieved a mean carbamylatin of 0.39 residue of cyanate per mol of hemoglobin. Animals developing cataracts received a maximum dose of 119+/-23 mg/kg/day for 28+/-10 months and achieved a mean carbamylation of 0.69+/-0.13 residue/mol. Animals developing corneal lesions received a maximum dose of 113+/-22 mg/kg/day for 36+/-7 months and achieved a mean carbamylation of 0.78+/-0.09 residue/mol. Younger animals appeared more susceptible to the cataractogenic effects of the drug than older ones. Lens intracellular sodium was increased by 100% in the cataractous lenses while potassium was significantly decreased in the lenses with the greatest opacity. Extracellular space was increased in the cataractous lenses by 61%. Reduced glutathione levels were decreased by 34% and lactate leakage into the medium was increased by 12%. Rubidium-86 uptake was increased by 26% in the cataractous lenses, probably reflecting an inadequate compensatory response to increased passive fluxes of cations resulting from a structural or enzymatic lesion.

Age Factors↗
PubMed1998

An increase in extracellular glutamate is a sensitive method of detecting ischaemic neuronal damage during cranial base and cerebrovascular surgery. An in vivo microdialysis study.

All patients undergoing neurological surgery are at risk for serious complications. Ischaemic damage presenting with hemiparesis or speech difficulties occurs in up to 6% of patients undergoing cerebral bypass procedures and other complicated neurosurgical procedures. Currently available methods for detection of such damage include the use of somatosensory evoked potentials (SSEPs) and electro-encephalography (EEG). Unfortunately, these techniques have false positives and may remain normal in the presence of severe focal neurological deficits. Early detection of potential deficits may prevent or minimize damage through a change in operative or anaesthetic strategy. With the availability of several potential neuroprotective compounds, it is also possible to treat patients at risk of developing ischaemic complications if the individuals are identified early. The excitatory neurotransmitter glutamate is not only a metabolic product, but is also thought to promote ischaemia induced cell injury if released into the extracellular space. It may be a significant parameter for ischaemic brain metabolism. In this report we describe 10 patients who underwent extracranial-intracranial (EC-IC) high flow bypass procedures with routine intra-operative monitoring (IOM) as well as intra-operative in-vivo microdialysis measurement of glutamate. Our aim was to compare intra-operative microdialytic findings and IOM findings with respect to patients' early postoperative clinical courses. Three patients had significant intra-operative glutamate increases indicating ischaemia. Two of these patients awoke with a new neurological deficit (hemiparesis). Routine IOM findings were either normal or showed only transient changes during the time the glutamate levels were high. Our study shows that an increase in extracellular glutamate, as monitored by in-vivo microdialysis, is an excellent early market of neuronal damage. While our glutamate measurements were done off-line, it may be possible to get in future continuous on-line measurements to serve as an early warning system for potential ischaemic damage.

Adult↗
PubMed1972

Accumulation and apparent active transport of prostaglandins by some rabbit tissues in vitro.

1. Slices or bits of rabbit tissues, not exceeding 100 mg, were incubated in tissue culture medium containing tritium-labelled prostaglandin ([(3)H]PG). In some experiments, incubation medium also contained saturating concentrations of an unlabelled prostaglandin (PG), or [(14)C]-sucrose for determination of extracellular space. At the end of the incubation period, usually 1 hr, the tissues were removed and weighed, and their (3)H (and (14)C) content were determined along with that of a unit volume of medium.2. Tissues known to play a central role in PG metabolism (lung and liver) and in its excretion (kidney cortex) and tissues which have a known function in blood-brain and blood-ocular barriers (choroid plexuses and ciliary processes) show a large accumulation of (3)H when incubated in a medium containing [(3)H]PGE(1). In addition, tissues of the female reproductive tract, and the aorta of the rabbit show similar (3)H accumulation. When uncorrected for tissue solid content or extracellular water volume, the extent of this accumulation is two- to sixfold. Calculated on the basis that all excess (3)H is present in the free form in the intracellular water, the accumulation ratio for ciliary processes, for example, indicates an over fortysix-fold gradient of PGE(1) across the cell membrane.3. Tissues which accumulate [(3)H]PGE(1) also accumulate [(3)H]PGA(1), [(3)H]PGF(1alpha) and [(3)H]PGF(2alpha). In some tissues specificity is, however, apparent; in the lung accumulation of [(3)H]PGA(1) was significantly greater than that of [(3)H]PGF(1alpha).4. The extent of [(3)H]PGE(1) accumulation was decreased, or in some tissues completely inhibited, by incubation at 2 degrees C, or by addition of large concentrations of unlabelled PG.5. Accumulation of [(3)H]PGE(1) by the foetal liver is not apparent on the 20th day of gestation, but is fully developed by the 30th day of gestation. The foetal lung does not accumulate [(3)H]PGE(1) at any stage of gestation.6. In some tissues, most notably muscle, there appears to be full equilibrium of [(3)H]PGE(1) between tissue water and medium within 1 hr of incubation.7. PGs are partially excluded from the intracellular volume of some other tissues, most notably the spleen and subcutaneous connective tissues. This apparent exclusion cannot be blocked by incubation in the cold, or by the addition of saturating levels of unlabelled PG.8. The simplest explanation for all observed results is that cell membranes are, in general, impermeable to PGs. However, there are specific, carrier-mediated mechanisms across some membranes which facilitate the entry of PGs. In some cells these transport mechanisms are linked to a source of metabolic energy, and/or to the counter-transport of some other substance, thus allowing net accumulation of PGs against a concentration gradient. Alternatively, (3)H accumulation may represent adsorption of [(3)H]PGs or one of their labelled metabolites on to specific adsorption sites.

Animals↗
PubMed1986

Superoxide production in experimental brain injury.

The appearance of superoxide anion radicals in cerebral extracellular space during and after experimental fluid-percussion brain injury was investigated in anesthetized cats equipped with cranial windows. Superoxide was detected by demonstrating the presence of superoxide dismutase (SOD)-inhibitable reduction of nitroblue tetrazolium (NBT). The SOD-inhibitable rate of reduction of NBT was 3.52 +/- 0.72 nM/min/sq cm during brain injury and 4.11 +/- 0.74 nM/min/sq cm 1 hour after injury. No significant superoxide production was detected in control animals. The sustained arteriolar dilation and reduced responsiveness to the vasoconstrictor effects of arterial hypocapnia observed 30 minutes after brain injury were eliminated by after-treatment with topical SOD (60 U/ml) and catalase (40 U/ml). The results show that experimental brain injury causes the generation and appearance in extracellular fluid space of superoxide. Superoxide production continues for at least 1 hour following injury. The sustained dilation and abnormal responsiveness of cerebral arterioles after injury are due to the continued generation of superoxide and other radicals derived from it. These functional changes can be reversed by after-treatment with appropriate scavenging agents.

Animals↗
PubMedDate not supplied

The effect of selective destruction and regeneration of rat Leydig cells on the intratesticular distribution of testosterone and morphology of the seminiferous epithelium.

This study was designed to explore the relationship between the intratesticular distribution of testosterone and spermatogenesis by completely destroying the Leydig cells of mature male rats with injection of a single i.p. dose of ethane dimethanesulphonate. After such treatment, testosterone levels in serum, testicular interstitial fluid, seminiferous tubules, and whole testis declined significantly 6 to 24 hours after injection and fell below assay detection limits between 3 and 7 days. At 3 and 7 days, serum LH and FSH levels rose significantly and remained elevated up to 4 and 6 weeks, respectively, in comparison with vehicle-treated controls. Leydig cells disappeared from the interstitium by day 3, but between 2 and 4 weeks postinjection a new generation of fetal-like Leydig cells repopulated the testicular interstitium and, during weeks 6 to 10, were transformed into, or replaced by, Leydig cells with an adult type of morphology. Histologic examination of the seminiferous tubules showed progressive disruption of spermatogenesis between 3 and 14 days post-ethane dimethanesulphonate. The first histologic sign of spermatogenic damage was noted at day 3, with the occurrence of stage-specific degenerating pachytene primary spermatocytes at stages VII to VIII of the spermatogenic cycle. On day 7, these cells and degenerating round, or step 19, spermatids often were observed during stages VII to XI, although qualitatively normal spermatogenesis also was seen in these and all other stages of the cycle. Maximum impairment of spermatogenesis occurred 2 weeks post-ethane dimethane sulphonate, at which time the tubules commonly lacked one or more germ cell generations or, alternatively, showed accumulation of lipid inclusions, extracellular spaces, and variable numbers of degenerating germ cells. Following repopulation of the testis by Leydig cells during weeks 3 and 4, spermatogenesis recovered. By 10 weeks after treatment, qualitatively normal spermatogenesis was seen in the great majority of seminiferous tubules, although a few tubules still remained in which the germ cell complement was severely reduced, and contained only Sertoli cells and spermatogonia.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1977

[Ultrastructural morphometric analysis of the spiral ganglion in guinea pigs (author's transl)].

This is the first morphometric analysis of the cochlear spiral ganglion. Therefore the ganglion was subdivided in precisely defined compartments. We found that the normal, untreated spiral ganglion in guinea pigs contains 58% ganglion cells of the granular type, 26% satellite cells and Schwann cells, 8.6% extracellular space, 6.4% myelinated nerve fibers and 1% ganglion cells of the filamentous type. The granular ganglion cell consists in 83% out of cytoplasm and in 17% out of nuclei. The cytoplasm is containing 13% ribosomes, 12% mitochondria, 10% RER, 2.1% Golgi apparatus, 1.3% lysosomes. Based on these quantitative datas we expect to detect alterations of the normal structure earlier and more precisely under pathophysiological conditions as before.

Animals↗
PubMed1979

Changes in fluid compartments and ionic composition in the isolated chick retina during SD.

Total content of water, extracellular spaces (ES), na+, K+, and C1- in the isolated chick retina were measured in the presence (test) or absence (control) of spreading depression (SD). During SD in medium with 0.5 mM or 2 mM MgSO4, there is an increase in the intracellular concentration of Na+ and C1- and a decrease in the intracellular concentration of K+. A decrease in the ES was only found in the medium with 2 mM MgSO4 together with a diminished outmovement of K+. We suggest that a decrease in the ES is due to an increased absorption of K+ by the Muller cells, causing its swelling and consequently a decrease of the ES. The addition of sucrose (17 mM) to the incubation medium as the extracellular marker markedly decreased the intracellular concentration of C1- in control retinas, blocked the inward movement of this ion to the tissue during SD and also changed the K+ movement during the phenomenon in medium with 2 mM MgSO4. We suggest that C1- is an important ion in the ionic balance of the Muller cells and that sucrose must have its site of action at these cells.

Animals↗
PubMed1995

Dynamic analysis of ethanol effects on NMDA-evoked dopamine overflow in rat striatum.

This study was undertaken to dynamically examine the effects of ethanol on the striatal dopaminergic transmission, in terms of N-methyl-D-aspartate (NMDA)-evoked dopamine release and dopamine uptake. In the striatum of urethane-anesthetized Sprague-Dawley rats, extracellular dopamine was measured using in vivo electrochemical detection coupled with a nafion-coated carbon fiber working electrode. Micro-ejection of NMDA evoked a transient dopamine release from the dopamine-containing nerve terminals in striatum. Local application of ethanol by pressure ejection did not elicit significant changes in spontaneous dopamine release. However, with ethanol pretreatment, the time course of NMDA-induced dopamine release was markedly prolonged while the magnitude and the rate of clearance were significantly reduced. These effects were compared to those of nomifensine, a dopamine uptake blocker. Nominfensine pretreatment was found to augment the time course of NMDA-evoked dopamine release analogous to those by ethanol pretreatment. Furthermore, pretreatment with ethanol did not increase the time course parameters of dopamine signals if dopamine releases were induced by co-application of NMDA and nominfensine. These data suggest that in addition to the attenuation of NMDA-evoked dopamine release, ethanol inhibits dopamine uptake in a similar fashion to that observed with nomifensine in situ in the striatum. Indeed, ethanol altered the uptake of exogenous dopamine from the extracellular space of striatal cortex. The time course of dopamine signals was prolonged and the rate of clearance was reduced after ethanol treatment. Taken together, our data demonstrate that ethanol simultaneously inhibits NMDA-evoked dopamine release and dopamine uptake in the striatum, suggesting the importance of the interplay between release and uptake in ethanol effects on striatal dopaminergic transmission.

Animals↗
PubMed1986

A program in BASIC for calculation of tissue ion flux rates, rate constants, and cellular ion contents and concentrations for a three compartmental serial model.

A BASIC program is presented to calculate tissue ion flux rates, rate constants, and cellular ion contents and concentrations from ion flux curves. For the purpose of this program, the biological tissue will be treated as a three compartmental series model. The program requires that eight experimentally determined variables be entered for each ion species to be analyzed: the experimental slope and intercept variables for each phase of the flux curve, the wet and dry tissue weights, the known or estimated value of extracellular space and the measured or known value of the cellular surface to volume ratio of the particular tissue being studied. All other required input data are obtained from the literature or experimental protocol and may be treated as constants. This program was designed for the in vitro determination of ion exchange in skeletal muscle but may be used with little or no modification for flux measurements in other tissues.

Animals↗
PubMed1984

Effect of chronic digoxin treatment on cardiac function, electrolytes and ATPase in failing heart due to pressure overload.

A decrease in the cardiac function and intracellular calcium, and an increase in the cardiac sarcolemmal ATPase have been reported in aortic stenosis of 6 to 9 months duration in dogs. The present investigation deals with the effect of 3 months of digoxin treatment on cardiac function, electrolytes and ATPase in dogs with 3 months of aortic stenosis in order to determine whether digoxin treatment gives only haemodynamic improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. There were no significant changes in any of the haemodynamic parameters of left and right ventricles except the left ventricular end-diastolic pressure which increased significantly at 3 months of aortic stenosis. All the hearts developed left ventricular hypertrophy. Concomitant with these changes, there was a tendency for a decrease in the total tissue Ca2+, intracellular Ca2+ and K+, and a tendency for an increase in the sarcolemmal ATPase. There were no significant differences in any of the haemodynamic parameters between the aortic stenotic and digoxin treated aortic stenotic dogs indicating that digoxin was at least maintaining the haemodynamics close to the pretreatment level. Although digoxin treatment prevented the changes in the sarcolemmal ATPase and extracellular space, it did not prevent the further decrease in the total or intracellular Ca2+. The total and intracellular Ca2+ was still significantly higher than previously observed after 6 to 9 months of aortic stenosis. These results suggest that digoxin treatment not only tended to prevent further deterioration of cardiac function but also tended to prevent further changes in the sarcolemmal ATPase and electrolytes.

Adenosine Triphosphatases↗
PubMed1987

Ionic changes induced by excitatory amino acids in the rat cerebral cortex.

The ionic mechanisms underlying the action of excitatory amino acids were investigated in the rat motor cortex. Ion-selective microelectrodes were attached to micropipettes such that their tips were very close and local changes in extracellular concentration of sodium, calcium, and potassium ions elicited through ionophoretic applications of glutamate (Glu) and of its agonists N-methyl-D-aspartate (NMDA), quisqualate (Quis), and kainate (Ka) were measured. These agents produced moderate increases in [K+]o (up to 13 mM) but, in contrast, substantial tetrodotoxin-insensitive decreases in [Na+]o (maximally of 60 mM). NMDA-induced sodium responses could be blocked by manganese, while the Quis- and Ka-induced responses were not. Quis and Ka produced increases in [Ca2+]o or biphasic responses while NMDA, even with small doses, induced each time drastic decreases in [Ca2+]o (maximally of 1.15 mM), which could be attenuated or blocked by manganese but not by organic calcium channel blockers. NMDA responses could be abolished by reduced doses of 2-amino-phosphonovalerate. The largest Glu- and NMDA-induced calcium responses were observed in the superficial cortical layers, but such maxima disappeared after selective degeneration of pyramidal tract neurons. All amino acids produced sizeable reductions in the extracellular space volume. The following can be concluded. (i) All the excitatory amino acids tested induce an increased permeability to sodium and potassium ions. (ii) In addition, the NMDA-operated channels have specifically a large permeability for calcium, although calcium ions contribute only by less than 10% to the NMDA-induced inward currents.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

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