Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344329 (collapse)
28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The preparation of patients for reintervention should aim at the correction of: - states of shock and collapse, found in one out of three patients; - hydroelectrolytic disturbances (sodium depletion, hypochloremia, dyskaliemia); - and finally, re-establishment of the acid-base balance.
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PMID:[Preparation of the patient for reoperation]. 0 40

We wish to determine what cellular and functional alterations are associated with the development of glomeruloscierosis when rats with one kidney are fed an excess of salt or protein. Rats with one kidney are more likely to develop pronteinuria and glomerulosclerosis than control animals. Blood pressure recordings indicate that proteinuria and glomerulosclerosis occur before hypertension is evident. Fluorescent antibody studies disclose that albumin accumulates in the epithelial cells of glomeruli and tubules. Ultrastructural examination shows that vacuolozation of epithelial cells and basement membrane thickening precede the sclerotic collapse of capillary loops. Increased concentrations of sodium or urea that are found in urines of these rats favor the point of view that an elevation of solute load when combined with a reduction of renal mass will on some unknown manner accelerate the deterioration of glomeruli.
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PMID:Protein overload nephropathy in rats with unilateral nephrectomy. A correlative light immunogluorescence and electron microscopical analysis. 4 49

BL-5255, 2-(2-n-propoxyphenyl)-5-(5-1 H-tetrazolyl)pyrimidin-4 (3H)-one, effectively inhibited allergic reactions in sensitized rats or guinea pigs when administered by oral or intravenous routes as the water-soluble sodium or ethanolamine monohydrate salts. In the IgE-mediated rat PCA, BL-5255 was 50 times more potent than disodium cromoglycate by intravenous administration. When administered orally in this model, BL-5255 inhibited the PCA reaction by 50% at 0.1 mg/kg. At less than 0.1 mg/kg p.o., the compound protected conscious actively sensitized guinea pigs from aerosolized antigen-induced collapse. In N. brasiliensis-sensitized rats, BL-5255 administered at 0.1--10 mg/kg p.o. inhibited antigen-induced airway constriction in a dose-related manner. BL-5255 is not a histamine or serotonin antagonist but appears to exert its antiallergic effect by inhibiting the release of mediators.
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PMID:BL-5255, a tetrazolylpyrimidinone with potent oral antiallergy activity in animals. 9 59

Colicins Ia and E1 are shown to inhibit the formation and bring about the collapse of a potassium diffusion potential imposed across the membrane of liposomes prepared from soybean or Escherichia coli phospholipids. Such depolarization results from a colicin-induced increase in membrane ion permeability. Colicins E2 and E3 do not depolarize such membranes. In addition to the colicin Ia-induced rapid efflux of preloaded rubidium, sodium, phosphate, or choline from liposomes, a slower efflux of preloaded sucrose or glucose 6-phosphate occurs. However, treated liposomes do not leak inulin or dextran, demonstrating that the effects of E1 and Ia are not due to a general disruption of membrane structure. The fact that colicin-induced ion efflux is observed in the complete absence of a membrane potential shows that the action of these colicins on liposomes is not voltage dependent. These results provide strong evidence that the depolarization of E. coli cells by colicins Ia and E1 results from a colicin-induced increase in membrane permeability to ions. It is proposed that this is brought about by the direct interaction of the colicin molecules with the bacterial cytoplasmic membrane.
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PMID:Effect of colicins Ia and E1 on ion permeability of liposomes. 9 88

The kallikrein-kinin system has been thought to participate in the pathogenesis of anaphylaxis. Kallikrein, released from lungs, has been postulated to contribute to cardiovascular collapse. Further to test the hypothesis, we examined for the occurrence of a kallikrein-like enzyme in guinea pig lungs and examined for release of such an enzyme by isolated, perfused lungs of guinea pig sensitized to and challenged with egg albumin. In addition, we treated guinea pigs with the bradykinin potentiating agents, BPP9a and SQ 14,225. In parallel experiments, we examined for effects of non-steroidal anti-inflammatory agents on the supposition that prostaglandin-related substances may mediate or modulate actions of kinins during anaphylaxis. A plasma kallikrein-like enzyme was found in lung homogenates and occurred in concentrations greater than that of plasma itself. Similarly, a store of kininogen occurs in lungs. However, using a sensitive radioassay for kallikrein-like enzymes, we were unable to confirm that antigenic challenge of sensitized lungs causes the release of enzyme into pulmonary venous effluent. Further, we were unable to modify the acute course of anaphylaxis by pretreatment of guinea pigs with bradykinin potentiating agents. However, indomethacin and aspirin at 20-40 mg/kg were found to greatly increase the severity of pulmonary anaphylaxis in terms of increased resistance to ventilation and increased numbers of lung hemorrhages. Paradoxically, aspirin or sodium salicylate at 80-100 mg/kg prevents the characteristic rise of insufflation pressure and the formation of lung hemorrhages.
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PMID:Pulmonary anaphylaxis and the kallikrein-kinin system. 22 44

1. The effects of theophylline and triaminopyrimidine on the passive permeability of Na+ and Cl- across sheets of rabbit ileum treated with 0.1 mM-ouabain were examined by determining the NaCl: mannitol dilution potentials, K+:Na+; choline: Na+ and SO24-:Cl- biionic potentials. The results indicate (a) that triaminopyrimidine reduces paracellular Na+ and K+ permeability without affecting Cl- permeability and (b) that theophylline increases Cl- permeability without affecting Na+ permeability and (c) that neither theophylline nor triaminopyrimidine interfere with each other's action. This is further evidence consistent with separate routes for paracellular Na+ and Cl- movement. 2. Electrical resistance changes across sheets of actively transporting rabbit ileum were measured as a function of time in various conditions. Theophylline has a biphasic effect on resistance. Initially it decreases resistance from 56 omega cm2 (control) to 40 omega cm2. In the ensuing 30 min, resistance rises to 50 omega cm2; whereas it falls to 30 omega cm2 in controls. When theophylline is present, with triaminopyrimidine, or with galactose, no secondary rise in tissue resistance occurs. The initial decrease in resistance is consistent with a theophylline-dependent increase in Cl- conductance and the secondary rise in resistance may be attributed to collapse of the lateral intercellular space following leakage of NaCl and fluid into the mucosal solution. 3. Electron microscopy of glutaraldehyde-fixed tissue confirms the above views, since, with theophylline present, the lateral intercellular spaces are collapsed and with both triaminopyrimidine and theophylline, or both theophylline and 20 mM-galactose present the spaces remain open. 4. It is shown in the Discussion that the theophylline- or choleragen induced increase in passive Cl- permeability of the mucosal border is the only requirement necessary to explain the increase in electrogenic Cl- secretion, the increase in short-circuit current, as well as neutral secretion of NaCl and net fluid secretion.
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PMID:Electrophysiological and electron-microscopical correlations with fluid and electrolyte secretion in rabbit ileum. 46 73

Sodium nitroprusside-induced cyanide intoxication has been demonstrated in the laboratory animal and has been experienced clinically during induced hypotensive anesthesia. This is a care report of a successful resuscitation of a severe cardiovascular collapse secondary to suspected sodium nitroprusside-induced cyanide intoxication.
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PMID:Suspected sodium nitroprusside-induced cyanide intoxication. 56 Jan 40

1. In goldfish intestine (perfused unstripped segments and mucosal strips) the serosal addition of ouabain (10(-4) M) resulted in a vanishment of the transepithelial potential difference and in a continuous increase in transepithelial resistance. 2. Incubation of mucosal strips with ouabain resulted in an increase in sodium content which was greater than the decrease in potassium content. The resulting increase in cation content was accompanied by an increase in chloride content and an increase in water content. 3. Histological examination showed that exposure to ouabain resulted in a swelling of the epithelial layer as compared to the control situation. 4. The ouabain induced resistance increase is greater in the presence of glucose, 3-OMG or fructose than in the presence of mannitol. Phlorizin (10(-4) M) inhibits the extra resistance increase induced by mucosal glucose but is without effect on the fructose induced extra resistance increase. The initial velocity and the magnitude of the glucose induced extra resistance increase depends on the glucose concentration. 5. The results suggest that in goldfish intestine ouabain induces cellular swelling with a concomitant collapse of the lateral intercellular spaces, which is the cause of the increased transepithelial resistance. The additional changes in resistance induced by sugars suggest that the cell membrane is more permeable to glucose, 3-OMG and fructose than to mannitol. The resulting changes in osmotically active material within the epithelial cell influence the cross-sectional area and consequently the conductivity of the paracellular shunt pathway. The hypothesis that these sugars do not induce a resistance change in the absence of ouabain is discussed.
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PMID:Effects of glucose and ouabain on transepithelial electrical resistance and cell volume in stripped and unstripped goldfish intestine. 57 48

The surface properties of fatty acid and fatty acid-alcohol mixtures were examined at 22-24 degrees C. At pH 12, sodium stearate forms a rigid surface film that generates an equilibrium spreading pressure of 16.5 dynes/cm. At pH 12, stearate-alkaline earth cation films collapse at the air-water interface and do not generate significant equilibrium spreading pressures. The rate of film collapse depends on the counterion decreasing in the sequence Ba2+ greater than Sr2+ greater than Ca2+. Stearate-stearyl alcohol mixtures form solid (condensed) films that are relatively stable and behave initially as homogeneous surfaces in their selectivities for counterions. Stearate-oleyl alcohol mixtures form fluid (expanded) films that are unstable. Lateral phase separations occur rapidly in fluid films and the stearate-alkaline earth cation phase collapses. The rate of film collapse in the fluid mixtures also depends on the counterion decreasing in the sequence Ba2+ greater than Ca2+. These surface properties suggest how a lipid anion may function as an ionophore in the translocation of alkaline earth cations.
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PMID:Surface phase separation and collapse of the stearate anion--alkaline earth cation complex. 83 1

1. It has been confirmed that the agent 2,3,6-triaminopyrimidine decreases Na+ conductance in the paracellular pathway of rabbit ileum. 2. Triaminopyrimidine has been used as a means of measuring transcellular bidirectional Na+ flux, and also, of assessing the contribution of the paracellular pathway to transepithlial Na+ flux. 3. Reduction of Ringer [Na+] to 25 mM or incubation with 0.1 mM ouabain reduces paracellular Na+ permeability. This effect may be due to lateral space collapse. Ringer galactose increases serosa to mucosa Na+ flux by a stimulating reflux through the tight junctions. A proportion of net Na+ flux in control tissues is due to asymmetry generated in the paracellular pathway. It is likely that this passive asymmetry results from an osmotic pressure gradient across the tight-junction. 4. Measurement of the tissue isotope specific activity ratio together with bidirectional transcellular Na+ fluxes allows calculation of the four unidirectional fluxes across the mucosal and serosal boundaries. Values obtained for Na+ entry (J12) and exit (J21) across the mucosal boundary are 7.97 alnd 7.13 mumol-cm(-2)-h(-1) respectively. Entry flux (J12) is a saturable function of Ringer [Na+]. The calculated Km is 295 mM and the V is 17.6 mumul-cm(-2)-h(-1). Na+ entry flux is insensitive to ouabain (0.1 mM). Ouabain results in elevation of exit (J21) flux of Na+ across the brush border. D-Galactose causes a saturable increase in Na+ flux (J12) across the mucosal boundary; the Km for this relationship is 1.2 mM and the V 2.17 mumol-cm(-2)-h(-1). The stoichiometry between sugar and Na+ entry is applixmately 1:1. In contrast to the effect of galactose on entry flux, no change in Na+ efflux across the mucosal boundary is observed when Ringer [galactose] is raised. This finding is dissonant with the prediction of the Na+ -gradient hypothesis. The calculated values of exit (J23) and entry (J32) Na+ fluxes across the serosal border are 16.74 and 15.90 mumol-cm(-2)-h(-1). 0.1 mM ouabain markedly reduces both these unidirectional fluxes. This result is consistent with a serosal location of the Na+-pump. Serosal Na+ exit flux J23 increases as a hyperbolic function of Ringer [galactose]. A small galactose-dependent decrease in entry (J32) is also observed. 0.1 mM ouabain abolishes these galactose-dependent changes. 5. The present findings together with those in the previous paper are discussed in relation to the convective-diffusion model for sugar transport.
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PMID:Bidirectional sodium ion movements via the paracellular and transcellular routes across short-circuited rabbit ileum. 97 42


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