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PubMed1985

Morphological effects of streptomyces hyaluronidase treatment on the outgrowth of the nasal processes in mouse embryos.

The role of hyaluronic acid (HA) in embryonic mouse nasal process outgrowth was assessed following administration of Streptomyces hyaluronidase, an enzyme that degrades HA. Enzyme-treated and control embryos were compared morphologically 4 and 24 hr after treatment on day 11 of gestation. After 4 hr the nasal processes of treated embryos were reduced in volume compared to controls. This size reduction was associated with a decrease in the amount of extracellular space in the nasal processes and a change in mesenchymal cell shape. Extracellular matrix material observed in controls included collagenlike fibers, 25-30-nm granules, and a delicate meshwork of 3-4-nm filaments. Basal laminae exhibited filamentous and granular material that extended to the surface of underlying cells. Similar matrix constituents were observed in treated embryos with the exception of the 3-4-nm filaments, which probably represent HA. By 24 hr after treatment, embryonic circulation had ceased and heart beat was slow. The nasal processes of these embryos were very small, but their configuration was such that fusion had often begun. Thus the presence of HA appears to be important in maintenance of the normal volume of the nasal processes and in maintenance of normal mesenchymal cell morphology, but other factors appear to contribute to the change in process shape requisite for fusion.

Animals↗
PubMed1981

[Changes of extracellular potassium concentration in the cortex and brain stem during the acute phase of experimental closed head injury (author's transl)].

The high concentration of extracellular potassium ((K+)o) impedes neuronal activity by depolarizing the membrane potential and further causing depolarization block or conduction block, and also causes swelling of astrocytes, which may result in narrowing of extracellular space and affect the diffusion of metabolites. Thus, when high concentration of extracellular potassium prolongs, pathological changes of neurons may ensue. In such state as cerebral ischemia, contusion or spreading depression, marked elevation of extracellular potassium was reported by many authors. In order to reveal the changes of extracellular potassium during the acute phase of closed head injury, following experimental studies were performed. In the first experiment, closed head injury model of the mouse was used. Directly after the impact with 600 g.cm, spontaneous movement of the animal disappeared for about 5-6 minutes often accompanied by immediate epilepsy. In this state, cortical (K+)0 increased from the control level of 4.1 +/- 1.8 mM to 20-30 mM. The elevated (K+)0 recovered gradually within 10-30 minutes. Directly after the same impact, apnea, bradycardia and low voltage EEG also appeared. In the second experiment, closed head injury model of the rat was used. With the impact of 9000 g.cm, the same concussion-like symptoms appeared as those of mice. Directly after the impact, (K+)0 in the cortex and brain stem elevated but the change patterns of cortical (K+)0 and brain stem (K+)0 were different. The different patterns in changes of (K+)0 were classified into four types. Type 1. Both cortical and brain stem (K+)0 elevated significantly immediately after the trauma, and recovered to control level within 30 minutes. Type 2. Both (K+)0 elevated significantly as in type 1 but only brain stem (K+)0 recovered within 30 minutes. Type 3. With the exacerbation of vital signs, both (K+)0 elevated over 50 mM, resulting in the death of the animal. Type 4. Although cortical (K+)0 elevated significantly after the impact, the increase of brain stem (K+)0 was below 10 mM. In type 1,2 and 3, blood pressure always elevated and brady- or apnea appeared immediately after the impact. In type 4, blood pressure after the impact showed to become slightly lower transiently as compared to control blood pressure. In control study, spreading depression was elicited by application of KC1-solution on the cortex. Spreading depression caused the elevation of cortical (K+)0 only, and almost no changes of brain stem (K+)0 were observed. The present study suggested that during the acute phase of closed head injury, diffuse neuronal disturbances involving the brain stem existed. And the elevation of brain stem (K+)0 is an important finding of this study because it may affect the level of consciousness directly by the mechanisms as described above.

Animals↗
PubMed1985

Continuous measurement of fluid mobilization from ICF space following acute dehydration by dialyzation in dogs.

The changes of the distribution of body fluid following acute isotonic dialyzation were studied from the results of continuous monitoring of extracellular fluid volume and physiological parameters. An indicator of extracellular space, 51Cr-EDTA, was injected into splenonephrectomized dogs. After the equilibrium of tracer dilution was attained, 10 ml/kg of plasma water was isotonically withdrawn by means of a dialyzer of hollow fiber type. The volumes of extracellular fluid (ECF) and plasma (PV) were continuously monitored for 80 min and plasma osmolality was measured at 10 min intervals. At the 50-60th min after the fluid modification, the reduction of PV was only 3.8 ml/kg and that of ECF was 4.2 ml/kg. The continuous profile of ECF change showed a significant mobilization of water from intracellular fluid (ICF) soon after the dialyzation. It is concluded that, in the state of hypovolemia, plasma fluid is replenished with the transvascular fluid absorption from interstitial space and that, concomitantly, the reduction of ISF is restituted with the fluid mobilization from ICF into extracellular space within the early stage of 1 hr. Good linear correlation was found between the amount of mobilized water from ICF and the increment of plasma osmolality. An increase in osmotic force was considered the mechanism which caused the fluid shift. These findings suggest that the change in plasma osmolality is a good predictor of mobilized volume from ICF in hypovolemia. The effects of inverse fluid modification, i.e., isotonic infusion, were also compared.

Animals↗
PubMedDate not supplied

Light-dependent hydration of the space surrounding photoreceptors in the cat retina.

We have studied the effect of retinal illumination on the concentration of the extracellular space marker tetramethylammonium (TMA+) in the dark-adapted cat retina using double-barreled ion-selective microelectrodes. The retina was loaded with TMA+ by a single intravitreal injection. Retinal illumination produced a slow decrease in [TMA+]o, which was maximal in amplitude in the most distal portion of the space surrounding photoreceptors, the subretinal space. The light-evoked decrease in [TMA+]o was considerably slower and of a different overall time course than the light-evoked decrease in [K+]o, also recorded in the subretinal space. [TMA+]o decreased to a peak at 38 s after the onset of illumination, then slowly recovered towards the baseline, and transiently increased following the offset of illumination. It resembled the light-evoked [TMA+]o decreases previously recorded in the in vitro preparations of frog (Huang & Karwoski, 1990, 1992) and chick (Li et al., 1992, 1994) but was considerably larger in amplitude, 22% compared with 7%. As in frog, where it was first recorded, the light-evoked [TMA+]o decrease is considered to originate from a light-evoked increase in the volume of the subretinal space (or subretinal hydration). A mathematical model accounting for [TMA+]o diffusion predicted that the volume increase underlying the response was 63% on average and could be as large as 95% and last for minutes. The estimated volume increase was then used to examine its effect on K+ concentration in the subretinal space. We conclude that a light-dependent hydration of the subretinal space represents a significant physiological event in the intact cat eye, which should affect the organization of the interphotoreceptor matrix, and the concentrations of all ions and metabolites located in the subretinal space.

Animals↗
PubMed1994

Extracellular brain glutamate during acute liver failure and during acute hyperammonemia simulating acute liver failure: an experimental study based on in vivo brain dialysis.

Hyperammonemia is thought to be important in the pathogenesis of hepatic encephalopathy. However, the mechanism leading to ammonia toxicity is still not known. Since the metabolism of the most important excitatory neurotransmitter, glutamate, is closely linked to that of ammonia, it has been postulated that hyperammonemia lowers the availability of the neurotransmitter glutamate. To study this hypothesis, we used brain dialysis to measure glutamate levels in extracellular cerebral fluid from rabbits with acute ischemic liver failure or acute hyperammonemia. The basal glutamate concentration was found to be increased during both acute liver failure (start of experiments 4.9 +/- 1.7 mumol/l; end of experiments 9.5 +/- 2.1 mumol/l, n = 6, difference p < 0.05) and acute hyperammonemia (start of experiments 4.4 +/- 1.2 mumol/l; end of experiments 7.3 +/- 1.8 mumol/l, n = 7, difference p > 0.05) (mean +/- SEM). Both the veratridine- and the potassium-evoked glutamate release were increased during acute liver failure but appeared normal during hyperammonemia. We conclude that during acute liver failure and acute hyperammonemia in the rabbit there is no decreased glutamate availability in the extracellular space of the cortical brain; on the contrary, we found evidence for increased extracellular glutamate concentrations in the cortical brain, which were more pronounced in acute liver failure. Experimental hepatic encephalopathy is thus not due to cerebral glutamate deficiency.

Ammonia↗
PubMed1978

[Circulatory insufficiency and edema in experimental constriction of the thoracic segment of the vena cava inferior].

A method for reproducing circulatory insufficiency in rats by constriction of the intra thoracic portion of vena cava inferior is described. A sham operation on the control animals was restricted to thoracotomy. Rats which had been subjected to constriction of the vena cava consumed 0.85% sodium chloride solution intensively under conditions of free choice. This lead to rapid increase in mass with the development of subcutaneous edema, hydrothorax, and ascites within two to three days after the operation. Thinned out muscle fibres with decreased SDH activity were found in the myocardium of the both ventricles. Study of THO, 22Na, 36Cl, and thiocyanate distribution spaces showed that the total body water increase was consequent upon growth of the extracellular space with a constant intracellular volume.

Animals↗
PubMed1993

Monitoring of segmental intra- and extracellular volume changes using electrical impedance spectroscopy.

Osmotically induced cellular volume changes in the perfused rat hindlimb were used to validate the use of bioelectrical impedance spectroscopy as a method for observing fluid shifts between the intracellular and extracellular spaces. Electrical impedance spectra were measured as cell volumes were manipulated by perfusion with Krebs-Henseleit solutions having different concentrations of NaCl. A simple equivalent circuit model of current conduction through the monitored tissue was fit to each measured spectrum to obtain segmental values of the equivalent intracellular resistance, membrane capacitance, and extracellular resistance. These parameters are theoretically governed by variations in the average cell volume fraction and ionic concentrations in the intra- and extracellular fluid spaces. In accord with this theoretical dependence, the parameters changed systematically and reversibly in conformance with both the magnitudes and directions of the perfusate concentration changes and the resultant cell volume changes. Results indicate that bioelectrical impedance spectroscopy, coupled with computer-aided equivalent circuit analysis, can be used to monitor segmental intercompartmental fluid shifts at minute-by-minute resolution.

Algorithms↗
PubMed1977

Calcium diffusion in transient and steady states in muscle.

Rates of diffusion through the extracellular space of thin sheets of myocardium from the right ventricular outflow tract of kittens were estimated at 23 degrees C for 45Ca2+ and an inert reference tracer, [14C]sucrose. The myocardial sheets were mounted in an Ussing chamber and equilibrated with Tyrode solution with varied calcium concentrations, Cao. The tracers were added to one side and their concentrations on the other side measured at 5-15-min intervals for 6 h. The apparent tracer diffusion coefficient for sucrose was 1.11 +/- 0.06 X 10(-6) cm2s-1 (mean +/- SEM, n = 74), 22% of the free diffusion coefficient; the lag time before reaching a steady state provided estimates of the intratissue volume of distribution or diffusion space of 0.41 +/- 0.15 ml/ml tissue (n = 74), a value compatible with expectations for extracellular fluid space. Over the range of Cao from 0.02 to 9.0 mM, the intratissue apparent diffusion coefficient for Ca, DCa, averaged 1.65 +/- 0.10 X 10(-6) cm2s-1, n = 74, which is 21% of the free DoCa, and was not influenced by Cao. Because transsarcolemmal Ca permeation is slow, DCa is the diffusion coefficient in the extracellular region. The paired ratios DCa/Ds averaged 1.32 +/- 0.05 (n = 67) for all levels of Cao but at physiologic or higher Cao averaged 1.45 +/- 0.07 (n = 39), close to the ratio of free diffusion coefficients, 1.53. Equations distinguishing transient from steady state diffusion were fitted to the data, showing that the apparent distribution volume of "binding sites" external to the diffusion pathway diminished at higher Cao in a fashion suggesting that a least two different Ca2+ binding sites were present.

Animals↗
PubMed1981

Morphological evidence of gap junctions between bone cells.

Cell membrane specializations occur at contact sites between adjacent osteoblasts and osteoblasts and osteocytes. These junctions have been described by other investigators as being important in preventing the extracellular movement of material around bone cells. Previously we described how certain small proteins circumvented the osteoblast population and rapidly penetrated the canalicular-osteocyte system. In the present study we used lanthanum colloid as an extracellular marker, the lanthanum readily penetrated the bone cell junctions and the extracellular space of bone. Morphologically, these junctions were not "tight" or "occluding" structures, but resembled "gap" junctions. These gap junctions contained elements which formed intercellular bridges between adjacent cells but also maintained a 2 nm space between cells that contained extracellular fluid. These gap junctions may have an important function in the control or coordination of bone cell activity throughout a given volume of bone.

Aging↗
PubMed1999

Extracellular matrix degradation by metalloproteinases and central nervous system diseases.

Matrix metalloproteinases (MMPs) are a gene family of neutral proteases involved in normal and pathological processes in the central nervous system (CNS). Normally released into the extracellular space, MMPs break down the extracellular matrix (ECM) to allow cell growth and to facilitate remodeling. Proteolysis becomes pathological when the normal balance between the proteases and their inhibitors, tissue inhibitors to metalloproteinases (TIMPs), is lost. Cancer cells secrete neutral proteases to facilitate spread through the ECM. MMPs increase capillary permeability, and they have been implicated in demyelination. Neurological diseases, such as brain tumors, multiple sclerosis, Guillain-Barré, ischemia, Alzheimer's disease, and infections, lead to an increase in the matrix-degrading proteases. Two classes of neutral proteases have been extensively studied, namely the MMPs and the plasminogen activators (PAs), which act in concert to attack the ECM. After proteolytic injury occurs, the process of ECM remodeling begins, which can lead to fibrosis of blood vessels and gliosis. TIMPs are increased after the acute injury and may add to the fibrotic buildup of ECM components. Thus, an imbalance in proteolytic activity either during the acute injury or in recovery may aggravate the underlying disease process. Agents that affect the proteolytic process at any of the regulating sites are potentially useful in therapy.

Animals↗
PubMed1987

Simultaneous microdialysis and amphetamine infusion in the nucleus accumbens and striatum of freely moving rats: increase in extracellular dopamine and serotonin.

To test the effects of systemic and local amphetamine on dopamine and serotonin release in freely moving rats, guide cannulas were implanted in the nucleus accumbens and ventral striatum for removable 200 mu microdialysis probes. Comparing 45 min samples before and after IP amphetamine (2 mg/kg), dopamine (DA) in dialysate from the accumbens increased from a baseline of 3 pg/20 microliters to 11 pg/20 microliters whereas dopamine metabolites, DOPAC and HVA decreased. This was probably due to block of DA reuptake and inhibition of monoamine oxidase, MAO. Accumbens serotonin increased from a baseline of 8 to 11 pg/20 microliters. Changes in the ventral striatum were similar. In the second experiment, microdialysis was performed before and after local injection of amphetamine (4 micrograms) to reveal effects of amphetamine in the terminal area only instead of the whole brain. DA in the accumbens increased from 11 to 147 pg per sample; serotonin, from 11 to 107. The effect was even larger in the ventral striatum. DA increased from 12 to 409 pg/20 microliters; serotonin, 3 to 139. To avoid handling the rat or disturbing brain tissue in experiment three, amphetamine was infused via the microdialysis probe during ongoing dialysis sampling. Perfusate containing amphetamine was switched into the flow line which allowed roughly 10% or 4 micrograms to diffuse out into the extracellular space. During this 20 min, extracellular DA in the accumbens increased from a baseline of 10 pg/20 microliters to 300 pg/20 microliters sample. Serotonin increased from barely detectable to 60 pg/20 microliters. DOPAC decreased significantly; HVA and 5HIAA drifted lower.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Carboxypeptidase Z is present in the regulated secretory pathway and extracellular matrix in cultured cells and in human tissues.

Carboxypeptidase Z (CPZ) is a newly reported member of the metallocarboxypeptidase gene family, but unlike other members of this family, CPZ contains an N-terminal domain that has amino acid sequence similarity to Wnt-binding proteins. In order to gain insights as to the potential function of CPZ, the intracellular localization of this protein was determined in cell culture and in human tissues. When expressed in the AtT-20 mouse pituitary cell line, CPZ protein is routed to the regulated secretory pathway and secreted upon stimulation. A fraction of the secreted CPZ remains associated with the extracellular matrix. Endogenous CPZ in the PC12 rat pheochromocytoma cell line is also associated with the extracellular matrix. In human placenta, CPZ is present within invasive trophoblasts and in the surrounding extracellular space, indicating an association with extracellular matrix. CPZ is also present in amnion cells, but is not readily apparent in the extracellular matrix of this cell type. A human adenocarcinoma of the colon shows expression of CPZ in the extracellular matrix adjacent to malignant cells. Taken together, CPZ appears to be a component of the extracellular matrix in some cell types, where it may function in the binding of Wnt.

Animals↗
PubMed2003

Biochemical and molecular characterization of galectins from zebrafish (Danio rerio): notochord-specific expression of a prototype galectin during early embryogenesis.

Galectins are a family of beta-galactoside-binding lectins that on synthesis are either translocated into the nucleus or released to the extracellular space. Their developmentally regulated expression, extracellular location, and affinity for extracellular components (such as laminin and fibronectin) suggest a role in embryonic development, but so far this has not been unequivocally established. Zebrafish constitute an ideal model for developmental studies because of their external fertilization, transparent embryos, rapid growth, and availability of a large collection of mutants. As a first step in addressing the biological roles in zebrafish embryogenesis, we identified and characterized members of the three galectin types: three protogalectins (Drgal1-L1, Drgal1-L2, Drgal1-L3), one chimera galectin (Drgal3), and one tandem-repeat galectin (Drgal9-L1). Like mammalian prototype galectin-1, Drgal1-L2 preferentially binds to N-acetyllactosamine. Genomic structure of Drgal1-L2 revealed four exons, with the exon-intron boundaries conserved with the mammalian galectin-1. Interestingly, this gene also encodes an alternatively spliced form of Drgal1-L2 that lacks eight amino acids near the carbohydrate-binding domain. Zebrafish galectins exhibited distinct patterns of temporal expression during embryo development. Drgal1-L2 is expressed postbud stage, and its expression is strikingly specific to the notochord. In contrast, Drgal1-L1 is expressed maternally in the oocytes. Drgal1-L3, Drgal3, and Drgal9-L1 are expressed both maternally and zygotically, ubiquitously in the adult tissues. The distinct temporal and spatial patterns of expression of members of the zebrafish galectin repertoire suggest that each may play distinct biological roles during early embryogenesis.

Amino Acid Sequence↗
PubMed1979

The physiopathogenetic basis for the angiographic diagnosis of bacterial infections of the brain and its coverings in children. I. Leptomeningitis.

This is a descriptive analysis of the angiographic characteristics of leptomeningeal infections in 36 children and a correlation of these angiographic observations with anatomopathologic changes. Vascular, meningeal and parenchymal changes are described and discussed. In the normal situation, tracer protein particles injected into the subarachnoid space perfuse easily through the extracellular spaces but stop at the outer continuous arachnoidal layer. The parenchymal layer, pia-arachnoid, on the other hand, consists of a uni or pluricellular layer which is regularly crossed by tracer particles. Though the internal carotid, vertebral and basilar arteries have some anatomical characteristics: thinner tunica media and adventitia, the absence of vasa vasorum and the presence of a fluid cushion (CSF) in which they are bathed. The most striking angiographic observation in leptomeningitis is the transmural extravasation of the contrast meding 'halo' formation. Long after the cerebral circulation time, one may identify contrast media 'pooling' within the cisterns and sulci.

Acute Disease↗
PubMed1992

Freeze-fracture and lanthanum studies of the retinal microvasculature in diabetic rats.

To see whether or not blood-retinal barrier breakdown during diabetes was associated with breakdown of the endothelial cell tight junctions or with other membrane alterations in the cells comprising the wall of the retinal microvasculature, streptozotocin-induced diabetic rat retinas were studied using lanthanum tracer and freeze-fracture electron microscopic morphometry. This study showed that endothelial cell tight junction permeability to lanthanum and luminal surface area were normal in these diabetic rats. However, freeze-fracture morphometry showed several alterations in the diabetic retinal microvessels. First, the endothelial cell membranes had abnormally large (80-120 nm) plasmalemmal vesicles not evident in the control retinas, suggesting that membrane turnover was abnormal. Second, endothelial cell P-face membranes at the blood front contained more larger particles than those in the control rats (P less than 0.05), implying an alteration in endothelial cell luminal membrane composition. Third, endothelial cell P-face membranes in areas of close apposition with pericyte membranes showed abnormal areas of particle clearing not seen in the control animals, suggesting a change in pericyte-endothelial cell interactions. Finally, pericyte membranes facing the neural retina contained increased numbers of plasmalemmal vesicles compared with control membranes (P less than 0.05). Moreover, the association of these vesicles with collagen fibrils in the extracellular space suggested an alteration in extracellular matrix turnover.

Animals↗
PubMed1989

Activation of calcium entry by the tumor promoter thapsigargin in parotid acinar cells. Evidence that an intracellular calcium pool and not an inositol phosphate regulates calcium fluxes at the plasma membrane.

The depletion of an inositol 1, 4,5-trisphosphate-sensitive intracellular Ca2+ pool has been proposed to be the signal for Ca2+ entry in agonist-activated cells. Consistent with this idea, thapsigargin, which releases intracellular Ca2+ without inositol phosphate formation, has been reported to activate Ca2+ entry in certain cells. We now report the effects of thapsigargin on Ca2+ entry in parotid acinar cells. In fura-2-loaded parotid acinar cells, thapsigargin caused a sustained elevation of [Ca2+], but did not increase inositol phosphate formation. In the absence of extracellular Ca2+, the increase in [Ca2+], was transient, suggesting that thapsigargin activates both the release of Ca2+ from intracellular stores and the entry of Ca2+ from the extracellular space. In the absence of extracellular Ca2+, pretreatment with methacholine, an agonist believed to mobilize Ca2+ through the production of inositol 1,4,5-trisphosphate, inhibited but did not completely block the response to thapsigargin; likewise, pretreatment with thapsigargin inhibited the response to methacholine. In permeabilized cells, thapsigargin gradually released Ca2+, whereas inositol 1,4,5-trisphosphate caused a rapid and transient discharge of Ca2+. The simultaneous addition of thapsigargin with inositol 1,4,5-trisphosphate evoked a maximum Ca2+ release similar to that for inositol 1,4,5-trisphosphate alone, but the reuptake seen with inositol 1,4,5-trisphosphate alone was abolished. In intact cells, methacholine and thapsigargin together produced a greater initial release of Ca2+ than either alone, but they were not additive in the sustained phase of Ca2+ mobilization. These results demonstrate that the mechanisms for activation of Ca2+ entry by thapsigargin and methacholine are the same and are consistent with the idea that entry is initiated by the depletion of the intracellular inositol 1,4,5-trisphosphate-sensitive Ca2+ pool. The results also indicate that, in contrast to previously proposed models, Ca2+ entry into agonist-activated cells occurs directly across the plasma membrane to the cytoplasm rather than through a cycle of uptake and release by the intracellular Ca2+ pool.

Animals↗
PubMed1978

Fine structure and radioautography of rabbit photoreceptor cells.

The retina of the adult rabbit contains two types of photoreceptors. Type I predominates and is a typical rod. The identity of the type II cell has been uncertain until now. This study demonstrates that the type II cell has certain conelike morphologic features including a pale nucleus, complex synaptic pedicel, and multiple wrappings of the outer segment by microvilli of the pigment epithelium. The type II outer segment is also conelike in that some intradisc spaces are patent to the extracellular space, that the pattern of renewal is diffuse as demonstrated radioautographically with sugar and amino acids as precursors, and that the few examples of distal tip shedding found in this study occur mainly in the early part of the dark cycle. The interior of the type II outer segment is labeled selectively with 3H-fucose, whereas the interior of the type I outer segment remains unlabeled with this sugar at all time intervals examined. The label probably reflects the presence of a fucose-containing glycoprotein in the conelike outer segment which is lacking in the rod outer segment and may represent a visual pigment or other intrinsic molecule(s). An amorphous material which forms a symmetric sleeve around the photoreceptor connecting cilium has been demonstrated after intravitreal injections of horeseradish peroxidase. This cilium-associated material is labeled specifically by 4 hr following intravitreal injection of 3H-fucose, before the interphotoreceptor matrix shows significant labeling, suggesting that it is composed of a sugar-containing material. Possible functions of the cilium-associated material, including structural support and ionic regulation, are discussed.

Animals↗
PubMed1995

Inhibition of parathyroid hormone-related protein release by extracellular calcium in dispersed cells from human parathyroid hyperplasia secondary to chronic renal failure and adenoma.

The relationship between parathyroid hormone-related protein (PTHrP) release from parathyroid cells and extracellular calcium ion concentration was investigated in three cases of parathyroid hyperplasia secondary to chronic renal failure and in four cases of parathyroid adenoma. Amounts of PTHrP released from individual parathyroid cells dispersed from surgical specimens were estimated by cell immunoblot assay. Parathyroid cells from both hyperplasias and adenomas showed significant suppression in the release of PTHrP with increase in extracellular calcium ions, but the amounts of PTHrP released from adenoma cells were significantly larger than from hyperplasia cells. The maximal value for PTHrP released within 120 minutes from adenoma cells was 2.91 +/- 2.11 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 1.32 +/- 0.35 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). On the other hand, the maximal value for PTHrP released from hyperplasia cells was 1.79 +/- 1.56 x 10(-2) fmol/cell ([Ca2+], 0.4 mmol/L), and the minimal value was 0.32 +/- 0.19 x 10(-2) fmol/cell ([Ca2+], 2.0 mmol/L). These results demonstrate actual release of PTHrP from abnormal parathyroid tissues into the extracellular space with the response to extracellular calcium ions depending on the cell status. Given the lack of definite histological criteria to differentiate between hyperplasias and adenomas in the parathyroid gland, the presently demonstrated significant difference in the ability to release PTHrP is important in pointing to parathyroid hyperplasia secondary to chronic renal failure as a distinct pathological entity separate from parathyroid adenoma.

Adenoma↗