UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical (psychometric), psychophysiological and biochemical (erythrocyte membrane transport) variables were studied in 44 patients with endogenous depression (unipolar/bipolar) during acute depressive episode and in remission. All parameters studied showed paralleled and unidirectional changes when depression was compared with remission period. During a depressive episode, unipolar patients had greater intensity of depression than bipolar patients. Ouabain-dependent sodium fluxes were significantly lower in female than in male patients during depression than in remission. In male bipolar patients, the indexes of active transport in erythrocytes showed significant correlations with clinical ratings and with results of psychophysiological tests. The results point to a possible relationship between various levels of physiological functioning in endogenous depression. This suggests a generalised "background" defect of energy-dependent membrane transport pertaining to both erythrocytes and nerve cells, which may be linked to disturbances of activational processes within the central nervous system.
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PMID:Erythrocyte cation transport in endogenous depression: clinical and psychophysiological correlates. 649 49

The effect of local infusion of ouabain into the forearm vascular bed has been examined in 15 normotensive male volunteers in an attempt to define the nature of the functional abnormalities of the resistance vessels in primary hypertension. Ouabain and other drugs were infused into the brachial artery and forearm blood flow was measured by venous occlusion plethysmography. Infusion of ouabain at 2 micrograms/min for 1 h caused a 26% reduction in forearm blood flow with a small rise in systemic arterial pressure; the increase in vascular resistance was unaffected by prior treatment with phentolamine. After infusion of ouabain the dilator response to potassium was reduced by 33% but the responses to verapamil and sodium nitroprusside were unchanged. The results show that acute depression of sodium pump activity by ouabain reproduces the increased resting resistance and impaired response to potassium that are seen in hypertension. It does not reproduce the relative enhancement of responsiveness to verapamil that is also observed in the resistance vessels of patients with hypertension and this abnormality must have some other cause.
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PMID:Effect of local infusion of ouabain on human forearm vascular resistance and on response to potassium, verapamil and sodium nitroprusside. 668 Oct 36

Ouabain-sensitive cation fluxes in red blood cells were measured in 23 patients with endogenous depressive syndromes during acute phase of the illness and during remission period as well as in 17 healthy subjects. The intensities of both sodium and potassium net fluxes during depressive phase were significantly lower than during remission both in patients with depression in the course of manic-depressive psychosis and in patients with unipolar depression. They were also lower than the intensities of fluxes found in control subjects. The values of female patients in remission did not differ from those of control females, while male patients had higher values in remission than control males. It is hypothesized that impaired activity of cation transport may be related to somatic and psychopathologic symptoms of depression and its stimulation may play a role in the mechanism of action of antidepressant drugs.
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PMID:Ouabain-sensitive sodium and potassium fluxes in red blood cells of patients with endogenous depressive syndromes. 725 80

1. A comparison has been made between the efflux of labelled phosphate from the non-myelinated fibres of the desheathed rabbit vagus nerve at 37 degrees C and the corresponding O2 consumption at rest and during activity, and during a variety of experimental interventions. 2. The resting rate constant of phosphate efflux was 2.61 X 10(-3) min-1: electrical stimulation (10 sec-1, 3 min) produced an extra fractional loss of 6.75 X 10(-6) impulse-1. 3. The corresponding resting O2 consumption was 0.484 m-mole x kg-1 impulse-1. 4. Ouabain (100 microM) produced a sustained depression (of about 40%) of the resting O2 consumption, accompanied by a transient fall (of about 14%) in the rate constant of phosphate efflux. 5. Na salicylate (10 mM) or Na arsenate (1 mM) produced a much larger increase in phosphate efflux than in resting O2 consumption. 6. Changing the external phosphate concentration (between 0.02 and 2 mM), addition of acetylcholine (1.7 mM), and addition of lanthanum (20 microM)--all of which are known to affect markedly the phosphate efflux in rabbit non-myelinated fibres--had little or no effect on the resting O2 consumption or, where tested, on the extra O2 consumption with electrical stimulation. 7. Changing the external Ca concentration (between 0.09 and 9 mM) had only minor effects on the O2 consumption (resting and stimulated) and on the rate constant of resting phosphate efflux. 8. It is concluded that although changes in metabolism of the nerve produce changes in the phosphate efflux expected on the basis of the concomitant changes in the internal concentration of inorganic phosphate, the converse is not true; and increases and decreases in the rate constant of phosphate efflux do not necessarily signal the corresponding metabolic changes.
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PMID:Oxygen consumption and phosphate efflux in mammalian non-myelinated nerve fibres. 744 28

Lowering myocardial temperature increases contractile force, presumably by increasing intracellular calcium content. To study the mechanisms behind this, we compared the effects of some known inotropic interventions with hypothermia on mechanical restitution and post-rest contractile force in isolated guinea-pig papillary muscles. In four groups (n = 6 per group), the effects of: (1) reducing the ability for Na/Ca exchange to extrude Ca2+ (a) by increasing [Na+]i with ouabain or (b) by increasing [Ca2+]o; and (2) activation of calcium channels with Bay-K 8644, were compared with lowering temperature from 37 to 27 degrees C. Normally (at 37 degrees C and 2 mM CaCl2), mechanical restitution could be described by a rapid recovery phase with a time constant between 180 and 220 ms, followed by a slowly decaying phase with a time constant between 5000 and 8000 ms and post-rest contractions (1-10 min rest) were markedly depressed compared to steady-state contractions. Steady-state developed force was markedly increased at 27 degrees C, after 1 microM ouabain, 6 mM CaCl2 or 0.1 microM Bay-K 8644. At 27 degrees C the rapid recovery phase of restitution was delayed while the slowly decaying phase was not affected. Ouabain and increased [Ca2+]o caused elevation of the slowly decaying phase of restitution and markedly attenuated the post-rest depression of developed force, which may be attributed to a reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger. Hypothermia and Bay-K 8644 on the other hand, augmented this post-rest depression. Hence, this study suggests that increased Ca2+ influx due to delayed inactivation of calcium channels may account for the increased developed force during hypothermia rather than reduced diastolic extrusion of Ca2+ via the Na/Ca exchanger.
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PMID:Mechanisms for hypothermia-induced increase in contractile force studied by mechanical restitution and post-rest contractions in guinea-pig papillary muscle. 769 97

The effects of a bufadienolide isolated from toad venom, arenobufagin, a potent Na+/K+ pump inhibitor, were studied in single guinea-pig ventricular cells in the whole-cell patch-clamp configuration. Arenobufagin (50 microM) applied extracellularly decreased the amplitude of the delayed rectifier K+ current (IdK) by 30% without affecting the gating kinetics. The L-type Ca2+ current was also depressed, but to a lesser extent. The inward rectifier K+ current was hardly affected. Ouabain and the internal dialysis of cells with the solution containing 20 mM Na+ depressed IdK in a similar way as arenobufagin. On the other hand, arenobufagin also depressed IdK when the Na+/K+ pump was already inhibited in the K(+)-free Tyrode solution. Therefore, both a direct effect on the channel and an indirect effect through the inhibition of the Na+/K+ pump may be involved in the depression of IdK by arenobufagin.
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PMID:Depressive effects of arenobufagin on the delayed rectifier K+ current of guinea-pig cardiac myocytes. 817 14

The effect of pretreatment with phenytoin (diphenylhydantoin), lidocaine, and, for comparison, quinidine, on the doses of ouabain which produce a maximal inotropic effect, onset of arrhythmias and cardiac arrest, was explored in the cat heart-lung preparation. Ouabain was administered as an infusion (0.5 micrograms/min) either alone or after treatment with phenytoin (0.095 +/- 0.012 mM), lidocaine (0.090 +/- 0.004 mM) or quinidine (0.028 +/- 0.006 mM) and the cardiodynamic and electrophysiological changes monitored. Phenytoin, lidocaine and quinidine were administered in doses which were maximally tolerated by the preparations to ensure full effect, as evidenced by early cardiac depression. Ouabain alone produced a maximal increase in contractility prior to the development of arrhythmias at a blood concentration of 0.212 +/- 0.014 microM, onset of arrythmias at 0.227 +/- 0.015 microM, stable ventricular tachycardia at 0.269 +/- 0.010 microM and cardiac arrest at 0.342 +/- 0.014 microM. Pretreatment with phenytoin or lidocaine did neither modify these values nor change the pattern of the arrhythmias or the terminal cardiac event. Pretreatment with quinidine prevented the development of ventricular extrasystoles and aberrant ventricular conduction, which were the earliest arrhythmias in all other series. It also made the preparations develop stable ventricular tachycardia at an ouabain blood concentration of 0.246 +/- 0.007 microM, which was not significantly different from the concentration at which early arrhythmias were noted in the other series. In addition, quinidine decreased the dose of ouabain producing cardiac arrest by 13% but did not modify the terminal event. Pretreatment with phenytoin, lidocaine and quinidine did not affect the electrocardiographic pattern, but at the maximal increase in contractility with ouabain prior to the development of arrhythmias, the PR interval increased to comparable limits with ouabain alone and ouabain after quinidine and lidocaine. However, with ouabain after phenytoin, this increase was 61% less than that with ouabain alone and 31% less than that with ouabain after quinidine. Ouabain given alone or after phenytoin, lidocaine or quinidine produced comparable maximal effects on dp/dt, -dp/dt and left atrial pressure. It may be concluded that pretreatment with phenytoin and lidocaine does not modify the maximal inotropic dose of ouabain prior to the development of arrhythmias, the arrhythmogenic dose or the dose producing cardiac arrest, and that phenytoin partly counters the ouabain-induced depression of AV conduction. Quinidine has an additive effect on the ouabain-induced depression of AV conduction, prevents the ouabain-induced increase in idioventricular rhythm responsible for extrasystoles but not that responsible for ventricular tachycardia, and reduces the dose of ouabain producing cardiac arrest.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Influence of pretreatment with phenytoin, lidocaine and quinidine on the cardiodynamic and electrophysiological effects of ouabain in the cat heart-lung preparation. 829 85

The cellular mechanisms underlying rhythmic bursts induced in the isolated neonatal rat spinal cord by bath application of strychnine and bicuculline (which block glycine- and gamma-aminobutyric acid-A-receptor-mediated inhibition, respectively) were probed with pharmacological tools. Such spontaneous bursts were recorded either intracellularly from lumbar motoneurons or extracellularly from ventral roots. As previously described, these network-driven events consisted of large-amplitude depolarizations arising abruptly from baseline with a highly regular period (on average 28 s). Burst episodes (lasting on average 7 s) comprised several oscillations and appeared synchronously on flexor and extensor motoneuron pools of both sides of the spinal cord. Their diffuse location made convenient to use bath-applied substances in the attempt to selectively block distinct membrane processes operating through the network. Application of apamin (0.4 microM) shortened both cycle period and burst duration without changing their regular rhythmicity. Similar results were obtained with carbachol (10 microM). Cs+ (4 mM) reversibly hyperpolarized the motoneuron membrane potential and largely increased burst duration, which was characterized by a long series of repetitive oscillatory waves. Cycle period and rhythmicity remained unaltered. Ouabain (10 microM), strophanthidin (4 microM), or K(+)-free solutions disrupted rhythmic bursting, which was fragmented into irregularly occurring paroxysmal activity mixed with short depolarizing events, still developing simultaneously on both sides of the spinal cord. Bursting activity eventually ceased after approximately 30-40 min of application of ouabain or strophanthidin. Prolonged washout of strophanthidin or K(+)-free solutions reestablished regular bursting patterns, whereas no recovery from ouabain was observed. At the time of strong depression of bursting, it was still possible to evoke bursts by single electrical pulses applied to the segmental dorsal root. Antidromic spikes of motoneurons could still be evoked by ventral root stimulation. These results demonstrate that, in a spinal bursting network mainly made up by excitatory processes, blockers of slow Ca(2+)-dependent K+ currents, such as apamin or carbachol, or of the slow inward rectifier, such as Cs+, did not suppress rhythmicity, suggesting that these conductances simply contributed to control cycle period and/or burst duration. Conversely, pharmacological blockers of the electrogenic Na+ pump such as ouabain, strophanthidin, or K(+)-free solutions severely disrupted all characteristics of rhythmic bursting. It is proposed that the operation of the electrogenic Na+ pump of premotoneurons was a crucial element for rhythmic bursting.
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PMID:Pharmacological block of the electrogenic sodium pump disrupts rhythmic bursting induced by strychnine and bicuculline in the neonatal rat spinal cord. 912 May 58

We used ouabain (100 microM) to block Na+,K(+)ATPase of in vitro rat hippocampal slices. This treatment was sufficient to cause the sudden depolarization that is the hallmark of both spreading depression (SD) and of the SD-like anoxic depolarization (AD). This depolarization was accompanied by a large and sudden increase in [K](o), also reminiscent of that observed during both SD and AD. Ouabain-induced SD did not require a complete inactivation of Na+,K(+)ATPase, as it occurred when the enzyme was still capable of providing recovery of both V(o) and [K](o). The data indicate that functional inactivation of Na+,K(+)ATPase per se initiates events that lead to an SD-like AD. This ouabain-induced depolarization was not affected by block of synaptic transmission, instead it was abolished by hyperosmolarity of the extracellular space. The possible relevance of these findings to the pathophysiology of AD is discussed.
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PMID:Block of (Na+,K+)ATPase with ouabain induces spreading depression-like depolarization in hippocampal slices. 1044 14

The nature of the platelet response to osmotic shock and its relationship to platelet viability were studied. Light absorbancy changes of human platelet concentrates exposed to hypotonic shock were measured in a spectrophotometer: a sudden drop of light absorbancy was followed by a reversal of light absorbancy towards normal (reversal reaction). It was confirmed that the reversal reaction is a complex phenomenon dependent on the integrity of biochemical and enzymatic functions of the platelets. It was suppressed by glycolytic inhibitors and by SH-blocking agents. Ouabain had no immediate effect, but with prolonged incubation it depressed the reaction. Suspension of the platelets in a protein-free medium caused a rapid loss of the reversal reaction. Disappearance of the marginal bundle of microtubules by exposure to colchicine did not change the reaction leading to the hypothesis that microfibrils rather than the microtubules may have been responsible for the reversal reaction. The conclusion was derived that the reversal reaction is due to cell volume contraction for which integrity of the platelet contractile protein and energy availability are essential. Platelet storage at 4 degrees C or at 22 degrees C caused a progressive depression of the reversal reaction which was more severe in platelets preserved at 4 C than in those preserved at 22 degrees C, and paralleled the loss of the platelet capacity to survive in vivo. Cryoprotective agents (DMSO, DMAC and glycerol) partially inhibited the reversal reaction. Freezing with these agents caused a more severe depression of the reaction. The least depression was observed with 5 per cent DMSO. The results demonstrated that the reversal reaction is a valid and accurate in vitro indicator of in vivo platelet viability when the results to be compared are limited to a single method of storage. Usefulness of the reversal reaction is reduced when results obtained with different methods of storage are compared.
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PMID:The platelet response to hypotonic shock. Its value as an indicator of platelet viability after storage. 1273 85

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