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)

Adrenal glands were collected from pigs of various ages under general anesthesia. Glutaraldehyde-fixed medullary tissue was postfixed with OsO4 for electron microscopy and with potassium dichromate or potassium iodate for light microscopy. Columnar epinephrine (E) cells formed cords between wide sinusoidal capillaries at the corticomedullary junction and were arranged in palisade fashion along the central vein and its major tributaries. The E cells usually were polarized, with the nuclei located away from the sinusoidal capillaries. Clusters of polygonal norepinephrine (NE) cells formed large central aggregates surrounded by E cells. Granulated vesicles were the predominant cytoplasmic feature of both E and NE cells. Round or oval E granules were bounded by a crenated membrane separated from the granule by a clear halo. The more electron-dense, elongate NE granules were bounded by a closely apposed, smooth membrane. The average longest granule axis was 270 nm for E granules and 305 nm for NE granules. Many cytoplasmic organelles were congregated in a granule-free paranuclear zone, which contained a prominent Golgi complex. Thin nonmyelinated nerve fibers (singly or in small groups) were interposed between the E and NE cells. Nerve fibers often were located close to the nucleus in a depression of the cell surface and often were wrapped by thin E or NE cell processes. The medulla of newborn pigs was composed predominantly or exclusively of NE cells. In both adults and pigs, E or NE cell cords radiated through the cortex toward the capsule, and isolated clusters of E or NE cells frequently were found in the capsule or zona glomerulosa.
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PMID:Certain cytologic features of the porcine adrenal medulla. 69 45

Previous studies have shown a significant linear relationship between the PTQ-index (a combination function of the PR-interval, corrected QT-time and T-wave depression in the ECG) and serum digoxin level in chronically treated patients. The relationship was confirmed in the present study and it was shown that it could be changed by concomitant administration of potassium chloride or furosemide, and that there was marked interindividual variation in response. An inverse linear relationship between PTQ-index and whole body potassium was found during chronic administration of a constant daily dose of digoxin, but no such relationship was found for serum potassium.
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PMID:Digoxin, whole body potassium and the electrocardiogram. 72 Mar 74

The renal and proximal tubule response to contralateral kidney exclusion was studied in a variety of circumstances. Recollection micropuncture studies were performed to assess the response to contralateral kidney clamping in the normal or a remnant kidney of the dog. Acute clamping of the contralateral kidney for a normal and unilateral remnant kidney resulted in marked reduction in proximal TF/P inulin ratios in the experimental kidney reflecting a 15 percent reduction in fluid reabsorption. Mean fractional excretion of sodium, potassium and water increased significantly in remnant kidney dogs but no significant change was observed in normal dogs except for potassium excretion. The marked reduction in proximal reabsorption occurred as soon as 5-15 minutes after contralateral kidney clamping and was compensated by distal reabsorption. Acute obstruction of the contralateral ureter results in a similar markedly reduced proximal tubular reabsorption. The reduction in proximal reabsorption induced by contralateral clamping occurred in the presence of reduced perfusion pressure and volume expansion and to some extent with renal denervation. When prostaglandin E(2) or acetycholine were infused prior to contralateral kidney clamping, proximal reabsorption remained at control levels and the contralateral clamping response was blocked. Similar blockade occurred after treatment with indomethacin. Acute reduction in nephron mass causes a marked depression of proximal tubular sodium and fluid absorption not obviously accounted for by hemodynamicphysical factors and humoral factors may be involved. The level of distal reabsorption to increased proximal delivery following contralateral clamping, determines the net urinary excretion.
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PMID:Acute functional adaptation to nephron loss: micropuncture studies. 73 48

Two mechanisms have been proposed to explain spreading depression (SD): one based on a release of glutamate (Van Harreveld, 1959), and the other on a release of potassium (Grafstein 1956) from neuronal elements. Both glutamate and KCl cause transparency changes in the retina, comparable to those occurring in this tissue during SD. The glutamate effect is inhibited by MgCl2 (10mM), in contrast to the transparency change due to KCl which is not affected by Mg++. Also SD is usually inhibited by MgCl2 which suggests that such SDs are based on a glutamate release. Impairment of the tissue metabolism promotes SDs which are insensitive to MgCl2. The resulting failure of the mechanisms that transport K+ and glutamate which leak out of the intracellular compartment back into the cells and fibers, seems to be involved in the generation of Mg++ insensitive SDs. This may facilitate either K-based SDs or glutamate-based SDs since the inhibitory effect of Mg++ is counteracted by an enhanced glutamate concentration. Both proposed mechanisms for SD seem to be possible under special circumstances.
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PMID:Two mechanisms for spreading depression in the chicken retina. 73 64

Decreasing the concentration of sodium in Meng's solution produced a non-parallel shift of the dose-response of acetylcholine on the intestine of the Giant African Snail Achatina fulica. This decrease in sodium decreases the sensitivity of the tissue to acetylcholine and sensitivity was not restored with several washings. The response to decrease calcium is very similar to that of sodium. In the case of potassium however 10% K+ produced less depression in sensitivity than 25% which even caused less depression of sensitivity compared with 50% potassium. The results show an abundance of spare receptors.
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PMID:Responses of the intestine of the giant African snail (Achatina fulica) to acetylcholine in Meng's solution with low sodium, potassium and calcium ions. 75 78

The development of potassium specific ion exchanger microelectrodes has enabled investigators to measure directly brain extracellular potassium ion activity. Although serum potassium in various species ranges between 3.5 and 6 mEq/l, brain extracellular potassium is maintained at a level close to 3 mEq/l independent of fluctuations in serum values. Despite this buffering of the internal brain environment by extracerebral changes, local variations in extracellular potassium occur in response to evoked neuronal activity, seizures, and spreading depression. Mechanisms involved in the maintenance of this ionic homeostasis in the brain include mediated transport at the level of the cerebral capillary and the choroid plexus epithelium. In addition, there are ouabain-sensitive clearance mechanisms presumably involving Na,K-ATPase that participate in the removal of excess potassium. The relative roles of simple diffusion, high glial cell conductance of potassium, and active ionic pumps in restoring basal potassium levels after activity are still controversial.
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PMID:Maintenance of a constant brain extracellular potassium. 77 Jan 98

Previously accumulated GABA was released from isolated forebrain synaptosomes with repeated calcium stimulation in elevated-potassium medium. Fractional release (calcium-dependent) in response to a second calcium pulse (90-120 sec later) was depressed to approximately 60% of initial release. Neither initial GABA release nor the subsequent depression of release was affected by variations in the labelling duration. Stimulation-dependent depression of labelled GABA and norepinephrine release was demonstrated from both cerebral cortex and cerebellum synaptosomal preparations. In addition, depression resulted from prior stimulation in the presence of veratridine, A23187 or elevated-potassium. Although release of previously accumulated GABA was depressed by calcium stimulation, the release of GABA accumulated between stimulations was not. Release of this recently accumulated GABA was indistinguishable from the initial release of previously accumulated GABA and larger than the subsequently depressed release from the previously accumulated pools. These data imply (1) that the depressed release resulted from a decrease of available transmitter in pools that support secretion processes, (2) that depressed release did not result from a depression of stimulus-secretion coupling processes, and (3) that transmitter accumulated subsequent to release events is released preferentially to transmitter accumulated prior to the intervening stimulation.
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PMID:Stimulation-dependent depression of readily releasable neurotransmitter pools in brain. 78 58

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 present study was designed to develop an animal model applicable to the clinical patient in the investigation of the pathogenesis of septic shock. The model currently described is a lightly anesthetized, unrestrained monkey, carefully monitored during a 24 hour observation period. Varying doses of live Excherichia coli organisms were infused intravenously during a 30 minute period, and a variety of hemodynamic, respiratory and metabolic parameters were monitored. Doses of organisms varied between 7.6X10(9) and 3.0X10(11) organisms per kilogram of body weight, and there was no obvious correlation between size of dose and survival time. Two of nine experimental monkeys survived the Excherichia coli, while times of death of the remaining monkeys varied between three and 27 hours. Two control monkeys, not administered organisms, survived the 24 hour period with minimal changes in all measured parameters. Results reveal two patterns in response to organism administration. These were early acute death, after three to four hours, and prolonged life, death after 20 to 27 hours. The acute response was characterized by marked systemic hypotension, hypoglycemia, hypoinsulinemia, increased lactate level, decreased pH or respiratory depression. The other type of response involved profound sustained hypotension with hypoglycemia and hypoinsulinemia in most monkeys and elevations in lactate, blood urea nitrogen potassium creatinine, serum glutamicoxalacetic, lactic dehydrogenase and fractionatedlactic dehydrogenase levels. Depressions in respiration were not evident in the group which survived a longer period of time. Renal fibrin thrombi, prominent in baboons administered Escherichia coli, were absent in the rhesus monkey regardless of the size of the dose of organisms. The results of this study suggest the operation of a multifactiorial mechanism in septic shock with interactions between hemodynamic and metabolic factors varying within the species.
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PMID:Physiopathologic responses of the rhesus monkey to live Escherichia coli. 82 5

Two groups of depressed subjects, one with a history of recurrent depression, the other with a history of persistent apathy, were given lithium carbonate 1,200 mg q.i.d. and supplementart potassium 1,200 mg t.d.s. for 1 week. Measurements were made before and after the lithium treatment of total body water (tritium space), extracellular fluid (sulphate space), total exchangeable sodium (Nae) and total exchangeable potassium (Ke) using sodium-24 and potassium-42 multiple isotope dilution techniques. Prior to treatment when compared with a group of normal subjects, both depressed groups showed changes in body fluid volumes and electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while electrolyte levels. Total body water, intracellular fluid and intracellular potassium were lowered, while intracellular sodium was raised. After treatment with lithium the values in the apathetic group showed little change but the group with recurrent depression showed a significant increase in intracellular fluid (p less than 0.025), Ke (p less than 0.001), intracellular potassium (p less than 0.025) and a significant decrease in Nae (p less than 0.05). There was a marked increase in mood in the group with recurrent depression but not in the apathetic group following lithium treatment. These findings suggest that recurrent depression, both in clinical improvement, mood and also correction of water and also correction of water and electrolyte disturbances arise, but not in patients with long-standing apathy.
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PMID:Lithium in depression: a biochemical study. 83 Feb 57


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