Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lithium (Li+) chloride, 2 to 3 mEq. per kilogram of body weight, was administered intraperitoneally to normal Wistar rats daily for 4 to 66 days. This resulted in a marked reduction in urine osmolality (Uosm.) and increase in the excretion of water, Na+, K+, uric acid, and phosphate. The excretion of uric acid and potassium was a direct function of UNaV. The magnitude of depression in urine osmolality was significantly related to the rate of excretion of lithium in the urine, suggesting that the change in water reabsorption is dependent on the presence of the ion in the luminal side of the tubule. During 2 per cent saline diuresis, Li+-treated rats achieved less fractional free water reabsorption (TcH2O/GFR times 100) at any level of fractional osmolar clearance (Cosm./GFR times 100) than normal rats. On the other hand, during 0.225 per cent saline diuresis, fractional free water clearance (CH2O/GFR times 100) was normal over a wide range of fractional urine flow (V/GFR times 100), indicating intact function of the ascending limb of the loop of Henle. The intravenous infusion of vasopressin (VP) or dibutyryl cyclic-adenosine monophosphate (dcAMP) to Li+-treated rats resulted in a modest rise in Uosm. and a reduction in V/GFR times 100 and CH2O/GFR times 100. Although the response to VP appeared earlier than that to dibutyryl cyclic-AMP, the magnitude of the changes in Uosm., V/GFR times 100, and CH2O/GFR times 100 was eventually the same with both substances. Comparison between normal and Li+-treated rats revealed that the response to both VP and dibutyryl cyclic-AMP was blunted, albeit to a greater extent in the former. Inhibition by Li+ of adenylate cyclase will only partially explain the present data. Impairment in the release of endogenous VP or a block distal to the formation of cyclic-AMP must have played a role. In view of a normal diluting capacity and the increase in the excretion of phosphate and uric acid, it is suggested that Li+, when administered chronically in the present doses, inhibits proximal tubular reabsorption.
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PMID:Renal effects of lithium administration in rats: alterations in water and electrolyte metabolism and the response to vasopressin and cyclic-adenosine monophosphate during prolonged administration. 16 79

Although the pigment leakage method is one of the most conventional for determining vascular permeability, accuracy in macroscopic measurement of the diameter of the stained area with an arbitary scale leaves much to be desired. We developed a simple and beneficial method for quantitative assay using a densitometer (Chromatoscanner CS-900). Guinea pigs weighing 300 approximately 350 g were used. Formalin as a phlogistic, in a dose of 2.3 approximately 37 mg was injected intradermally in the shaved skin of the back, and 15 mg/kg of pontamine blue was then given into the femoral vein. One hour after the injection the animals were sacrificed and the skin of the back, which was stained by the leaked pigment, was stripped off and allowed to adhere to a wooden plate for 24 hours. Reflection and a zig-zag scanning technique were used to measure the volume of the leaked pigment. There was a liner relationship between the dose of formalin and the integrated values. A dose-dependent relationship was also obtained when histamine, serotonin, kallikrein and bradykinin were used as phlogistics. Representative anti-inflammatory drugs such as aspirin, hydrocortisone, oxyphenbutazone, benzydamine, diclofenac sodium, sodium salicylate and aminopyrine depressed the leakage due to formalin. Depression of leakage by aspirin in a dose of 400 mg/kg was the most remarkable. Pigment leakage elicited by histamine, serotonin, kallikrein and bradykinin was examined on the same individual animal. Aspirin more than the other agents depressed the leakages due to bradykinin and kallikrein. Hydrocortisone and oxyphenbutazone depressed the leakage due to bradykinin, serotonin and histamine, but enhanced that due to kallikrein. The results obtained were consistent with those of a previous study and as this method is simple and more reliable, it is applicable for assay of anti-inflammatory compounds.
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PMID:[A new method for assaying anti-inflammatory drugs. Quantitative analysis of pigment leakage into skin by Chromatoscanner CS-900 (author's transl)]. 56 14

16 dental students rinsed daily with a placebo solution, Taurolin 2% (formaldehyde releasing antimicrobial), Vantocil 0.1% (polybiguanide), and with amine fluoride 0.025%. Depression of plaque growth assess with the Sulcular Plaque Index was 50.6, 40.2 and 21.5%, respectively.
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PMID:Inhibition of plaque growth with taurolin, vantocil and amine fluoride. 77 7

The effect of bumetanide on renal function has been compared with that of furosemide and a placebo in a double-blind study of 9 healthy young men. The sequence for oral administration of the drug was subjected to a random assignation based upon the Latin-square methodology under three different conditions. (1) Normal hydration: The administration of bumetanide (2 mg) produced within the next 4 hr a diuresis comparable to that induced by 80 mg of furosemide. Urinary excretion of sodium, potassium, chloride, calcium, and uric acid also followed comparable patterns. Phosphaturia occurred only under bumetanide. The effect of bumetanide seemed longer lasting. (2) Water loading: The effects of bumetanide and furosemide were comparable with the exception of the phosphaturic effect induced by bumetanide. The action of both diuretics on the diluting segment of the nephron was well demonstrated by the marked depression of CH2O. (3) Water deprivation: The effects of the two diuretics were comparable, including depression tCH20. In none of these conditions did the placebo produce any significant effect.
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PMID:Bumetanide, a new loop diuretic. 78 89

The intravenous injection of horseradish peroxidase (HRP) into rats of the Sprague-Dawley strain caused vascular leakage as detectable by a 20-40% increase in the hematocrit and a 15-20% decrease in plasma protein concentration. These changes did not occur when the same amounts of HRP were injected into rats pretreated with antagonists to histamine and serotonin. After pretreatment with the antagonists, the reabsorption of HRP by the proximal tubule cells (the concentration of HRP in the total particulate fractions) showed a 77% decrease and the urinary excretion of sodium showed more than an 80% increase as compared to the values from rats treated with HRP alone. In addition, the blood clearance rate of HRP was decreased and the urinary excretion of HRP was increased after treatment with the antagonists to histamine and serotonin. Cytochemical observations of formaldehyde vapor-fixed tissue also showed the effects of vascular leakage. After the injection of HRP in physiologic or hypertonic saline, the basal infoldings of the proximal tubule cells were strongly peroxidase-positive. When the same amounts of HRP were injected after pretreatment with antagonists to histamine and serotonin, or with mannitol, the basal infoldings were not stained or were stained faintly. Rats of the Wistar/Furth strain did not show the effects of vascular leakage observed with rats of the Sprague-Dawley strains. The questions are discussed as to whether the marked depression of renal cortical HRP absorption by mannitol and hypertonic saline (J Histochem Cytochem 23:707, 1975) is related to the prevention of vascular leakage, and whether the reabsorption of both sodium and protein is increased during the leakage of serum proteins into the interstitial tissue.
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PMID:Altered renal cortical reabsorption of protein and urinary excretion of sodium in relation to vascular leakage induced by horseradish peroxidase. 83 63

Whether volume expansion influences NaC1 reabsorption by the diluting segment of the nephron remains a matter of controversy. In the present studies this question has been examined in normal unanesthetized dogs, undergoing maximal water diuresis. Free water clearance (CH2O/GFR) has been used as the index of NaC1 reabsorption in the diluting segment. Three expressions have been employed for "distal delivery" of NaC1: a) V/GFR, designated as the "volume term"; b) (CNa/GFR + CH2O/GFR), the "sodium term;" and c) (CC1/GFR + CH2O/GFR), the "chloride term". The validity of these terms is discussed. Three techniques were used to increase distal delivery: 1) the administration of acetazolamide to dogs in which extracellular fluid (ECF) volume was not expanded (grop 1); 2) "moderate" volume expansion (group 2); and 3) "marked" volume expansion (group 3). CH2O/GFR increased progressively with rising values for "distal delivery" regardless of which term was used to calculate the latter. With all three delivery terms, differences in distal NaC1 reabsorption emerged between the two volume-expanded groups, though only with the "chloride" term did substantial differences also emerge between the nonexpanded group 1 dogs and both volume-expanded groups. In group 1, values for CH2O/GFR increased in close to a linear fashion up to distal delivery values equal to 24% of the volume of glomerular filtrate. However, at high rates of distal delivery the rate of rise of CH2O/GFR was less in group 2 than in group 1 and the depression of values was even greater in group 3. Within the limits of the techniques used, the data suggest that volume expansion inhibits fractional NaC1 reabsorption in the diluting segment of the nephron in a dose-related fashion. The "chloride" term was found to be superior to the "volume" and "sodium" terms in revealing these changes.
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PMID:Influence of volume expansion on NaC1 reabsorption in the diluting segments of the nephron: a study using clearance methods. 97 43

Although chronic lithium therapy has been associated with a defect in the urinary concentrating mechanism, short-term renal effects of lithium have received little attention in the intact animal. Solute-free water reabsorption (T-cH2O) and free water clearance (CH2O) were measured in primates of the genus Galago under control conditions and while animals were receiving either 0.5 mmol/kg-h or 1.0 mmol/kg-h lithium chloride (135 mM) intravenously. CH2O was unchanged by lithium infusion (P greater than 0.10), whereas T-cH2O was significantly depressed at all levels of osmolal clearance (P smaller than 0.01). Spontaneous recovery of near-normal T-cH2O was documented in two animals within 1 wk following acute lithium infusion. In addition it was observed that lithium-induced depression of T-cH2O could be partially prevented by pretreatment with intravenous amiloride. These results suggest that alterations in the renal concentrating mechanism can occur rapidly following the onset of lithium administration. They also imply that impairment of the renal concentrating mechanism by lithium is due at least in part to antagonism of the action of vasopressin on the collecting duct.
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PMID:Acute effects of lithium on the renal concentrating mechanism in a primate. 111 55

This study deals with the effects of chemical pollutants on the transmembrane potential difference for sodium (delta mu Na) in smooth muscle cells of Mytilus edulis. A method for indirect determination of extracellular space, intracellular ion concentrations and delta mu Na has been developed and is applied in the investigations. The determination is based on concentration data from haemolymph and muscle tissue samples. The precision of the method used was tested by direct measurements of the apparent intracellular concentration of sodium and the membrane potential. On the basis of these tests, the method was evaluated as reasonably good. The method was used to study the sensitivity of the transmembrane delta mu Na in Mytilus edulis to 96 h exposures to various sublethal concentrations of formaldehyde, methanol and mercury. Both formaldehyde and mercury induced a depression of delta mu Na. The observed depressions could be ascribed to a change in both the electrogenic and the chemical components of delta mu Na. A depression of delta mu Na was associated with subsequent clinical injury and death. Methanol did not cause death or any changes in delta mu Na. Because of the observed correlation between depression of delta mu Na and clinical injury, delta mu Na is suggested to have a potential as an indicator of toxicity.
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PMID:Pollutant-induced depression of the transmembrane sodium gradient in muscles of mussels. 132 57

1 Two cases of lethal poisoning following acute inhalation of extremely high concentrations of dichloromethane (DCM) are reported. The concentrations of the solvent found in the blood of the two subjects collected at autopsy and analysed by gas chromatography/mass spectrometry (572 and 601 mg l-1) were compatible with those measured in the air a few hours after the discovery of the bodies (up to 168,000 ppm). 2 Extensive brain and lung oedema and congestion, microhaemorrhagic changes of the stomach and congestion in other organs were observed on macroscopic and microscopic examination of both subjects. In addition, and in both cases, high but not lethal carboxyhaemoglobin (COHb) levels (30%) were found in the blood collected at autopsy. 3 Narcosis and respiratory depression due to the effect of DCM on the central nervous system (CNS) appear to have played a critical role in the death of the two men. However, biotransformation of the solvent to toxic metabolites, including carbon monoxide (via oxidative dehalogenation by the cytochrome P450-dependent mixed function oxidase system) or formaldehyde, formic acid, inorganic chloride and carbon dioxide (via the glutathione-S-transferase pathway) may have also contributed significantly to fatal toxicity.
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PMID:Double fatal inhalation of dichloromethane. 136 Nov 46

1. The rate of oxygen consumption has been monitored continuously in M. edulis during acute exposure to high sublethal concentrations of formaldehyde, phenol and benzene and subsequent recovery periods of 96 hr. 2. The results are discussed in relation to changes in the electrochemical potential difference of sodium, the content of ATP and the tissue concentration of strombine. 3. After exposure to benzene and phenol, an increase in the rate of oxygen consumption that could not be explained by oxygen debt from the exposure period was observed. 4. Depression of the rate of oxygen consumption after exposure to formaldehyde may be explained by a reduced ability to extract oxygen from the water. 5. The pattern of oxygen consumption and behavioural responses, as well as the combined changes in the biochemical markers, were distinctly different in the three cases.
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PMID:Measurements of oxygen consumption in Mytilus edulis during exposure to, and recovery from, high sublethal concentrations of formaldehyde, benzene and phenol. 167 79


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