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)

26 hypertensive patients groupded according to the severity-index and the WHO-index were treated with pindolol (monotherapy, 15 mg daily). The response of blood pressure depression was statistically significant, although not always sufficient when judged by clinical parameters. Plasma renin activity responded variably to the treatment in different patients and different groups. In 18 patients a statistically significant increase of serum potassium could be observed. No major side effects of therapy were encountered.
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PMID:[Pindolol as an antihypertensive agent]. 83 51

Extracellular potassium activity, [K+]0, was continuously measured using potassium specific microelectrodes in the cerebral cortex of cats before and after hypoxic or anoxic insults. Two patterns of [K+]0 increase were seen. A slow, linear rise occurred during hypoxia and hypothermia and was correlated with changes in mean blood pressure (B/P). A fast, complex, exponential rise resembling spreading depression occurred during anoxia and was unassociated with B/P changes. The fall of [K+]0 after reversal of the insult was described by a single exponential function with rate constants from 0.009 to 0.0194 sec-1. It is suggested that the linear rise is primarily a result of sodium pump inhibition and that the exponential rise is due to a superimposed sudden increase in cell membrane permeability perhaps secondary to transmitter release. The kinetics of the fall of [K+[0 is consistent with the normalization of the sodium and potassium gradients across the cell membranes secondary to Na+-K+ATPase activity.
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PMID:The kinetics of extracellular potassium changes during hypoxia and anoxia in the cat cerebral cortex. 84 9

Slices from rat hippocampus, striatum or cortex were incubated with l mum [3H] choline and following 75 min superfusion with Krebs solution the efflux of radioactivity was measured. The slices were stimulated either electrically (1 Hz) or with 25 mM potassium and the rate constant of the evoked release and the size of the releasable pool were estimated. The spontaneous efflux of radioactivity and the releasable pool but not the rate of evoked release correlated with the reported endogenous ACh content of the 3 areas. Raised potassium released radioactivity at a lower rate but from a larger pool than electrical stimulation from all 3 areas. In all 3 areas atropine alone potentiated while physostigmine, oxotremorine and carbamylcholine decreased the rate of evoked release. This depression was fully antagonized by atropine. The drugs had no effect on the size of the releasable pool. Findings suggest that muscarinic receptors located on cholinergic axons or terminals have a physiological role in the autoregulation of ACh release from these 3 areas.
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PMID:The effect of cholinergic drugs on [3H]acetylcholine release from slices of rat hippocampus, striatum and cortex. 84 27

A solid membrane electrode containing a highly selective ion-complexing agent immobilized in a polymer membrane is applied to measurements in vivo from the surface of an organ. For the measurements reported here, an ion-complexing agent selective for potassium is incorporated in a silicone rubber membrane and applied to measure ion changes in the brain. Comparison is made to the measurements recorded with an ion-selective microelectrode in the cortical tissue. The surface electrode compares favorably with the microelectrode in terms of amplitude of response and response time for the changes seen in the phenomenon of cortical spreading depression of Leao. The methods reported here are amenable to a selection of ion measurements by incorporation of a suitable ion exchanger in a polymer membrane. Extracellular ion activity is monitored in the anesthetized animal by holding the electrode in a balanced suspension which provides a light, flexible contact to the organ of interest. In the unanesthetized animal, when recording from the brain, the electrode is fixed in a skull-implanted cannula.
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PMID:Application of a solid membrane ion-selective electrode to in vivo measurements. 87 13

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Multiple serum chemical values were examined in 92 patients with chronic glaucoma who were treated with the carbonic anhydrase inhibitors (CAIs) acetazolamide or methazolamide, seeking relationships between serum composition and symptomatic side effects. Of the 92 patients, 44 complained of a symptom-complex of malaise, fatigue, weight loss, depression, anorexia, and loss of libido, which we have found most commonly to threaten continuation of therapy. Patients who had this symptom complex were significantly more acidotic than those without it. Ten of 24 patients who had chemical evidence of excessive acidosis reported a dramatic alleviation of symptoms when sodium bicarbonate was administered, although their serum CO2-combining power changed little. There was no correlation of the symptom complex with serum potassium concentration, except in a few patients who were simultaneously receiving chlorothiazide diuretics for systemic hypertension and who became frankly hypokalemic.
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PMID:Carbonic anhydrase inhibitor side effects. Serum chemical analysis. 88 13

The relationship between changes in EEG and the extracellular potassium concentration (K+e) in brain cortex was studied in rats during petylenetetrazol seizures and during respiratory arrest. During seizures an increase of K+e occurred subsequent to the electrical discharges, while during postictal depression of EEG normal levels of K+e were measured. During respiratory arrest K+e rose considerably one minute after flattering of EEG. These findings are against a concept of K+e determining the changes of the EEG pattern. It is hypothetized that during seizures the increased K+e may play an important role in the coupling of neuronal activity to cerebral blood flow and metabolism.
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PMID:EEG and extracelluar K+ in rat brain during pentylenetetrazol seizures and during respiratory arrest. 89 18

Cochlear microphonics (CM), action potentials (AP) and endochochlear potential (EP) were recorded on guinea pigs. The introduction of a small quantity of KCl solution (0.1 N) in the perilymph provoked a moderate decrease of CM and AP. During the period of depressed but stable amplitude, the presentation of intense sounds provoked an exaggerated susceptibility to fatigue and a delayed recovery. Similar changes were observed in the evolution of EP. However, the recovery was slower for EP than for CM. The results, as a whole, suggest that the fatigue which is manifested in the depression of cochlear potentials is related to a leakage of potassium ions from endolymph to fluids spaces within the organ of Corti.
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PMID:Increased fatigue of cochlear potentials after injection of KCl solution in the perilymph. 92 3

From 1971 to 1975, inclusive, 594 pronghorns (Antilocapra americana) were drive trapped in Alberta; subsequently, 74 of these animals were transported to enclosures. Deaths attributable to capture myopathy (CM) occurred in 20 of the trapped pronghorns and in 17 of the pronghorns that were trapped and subsequently transported. Two neonatal pronghorns that had been pursued died with signs and lesions similar to those seen in adult pronghorns affected with CM. The diagnosis of CM was based on history, clinical signs, clinico-pathologic findings, and gross and histologic lesions. Clinical signs of CM included depression, stiffness, weakness, incoordination, recumbency, and paralysis; myoglobinuria was observed in 1 neonatal animal. Of the pronghorns that died, fewer than one-half died acutely during processing, whereas the remainder died from 1 to 13 days following their release. Gross and histologic lesions were observed in the large muscles of the hindlimbs of most affected pronghorns. Values for serum enzymes, potassium, glucose, and creatinine, were higher for drive-trapped pronghorns than for tame, hand-reared pronghorns. These findings indicated extensive damage to muscle and to other organs as a result of the capture procedures.
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PMID:Capture myopathy in pronghorns in Alberta, Canada. 92 65

Defective potassium excretion with clinical acidosis, associated with fixed moderate sodium wasting, has been found to be a common abnormality in lead nephropathy. Lead poisoning has been shown by others to be associated with depression of the renin-aldosterone system and of sodium and potassium activated adenosinetriphosphatase (ATPase). Since these hormonal defects may contribute to the hyperkalemia and are reversible, lead poisoning should be treated aggressively. Management also requires proper regulation of dietary sodium, correction of acidosis, limitation of dietary potassium, and minimal use of antihypertensive agents, as well as the administration of allopurinal for urate control.
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PMID:Hyperkalemia and acidosis in lead nephropathy. 94 Oct 56


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