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)

Urea and other small amides cross the toad urinary bladder by a vasopressinsensitive pathway which is independent of osmotic water flow. Amide transport has characteristics of facilitated transport: saturation, mutual inhibition between amides, and selective depression by agents such as phloretin. The present studies were designed to distinguish among several types of transport including (1) movement through a fixed selective membrane channel and (2) movement via a mobile carrier. The former would be characterized by co-transport (acceleration of labeled amide flow in the direction of net flow of unlabeled amide), the latter by counter-transport (acceleration of labeled amide flow in the opposite direction). Mucosal to serosal (M leads to S) and serosal to mucosal (S leads to M) permeabilities of labeled amides were determined in paired bladders. Unlabeled methylurea, a particularly potent inhibitor of amide movement, was added to either the M or S bath, while osmotic water flow was eliminated by addition of ethylene glycol and ethanol could not be demonstrated. Methylurea did not alter water permeability or transmembrane electrical resistance. The demonstration of co-transport is consistent with the presence of ADH-sensitive amide-selective channels rather than a mobile carrier.
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PMID:Amide transport channels across toad urinary bladder. 125 4

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

Stress can be defined as a "reaction by living beings to any relevant impairment". The effect of anaesthesia on endocrine function is closely related to the actual stress concept based on the works by Cannon and Selye. Cannon described the role of catecholamines in stress and characterised the fight-flight reaction. Selye emphasised the role of the adrenocortical reaction defining the "general adaptation syndrome", which evolves in three stages ("alarm reaction", "stage of resistance", "stage of exhaustion"). Later, Henry postulated the dual stress concept. The sympathetic-adrenomedullary system is activated during the fight-flight reaction, thus representing an active role of the organism. The pituitary-adrenocortical system is activated during loss of control, submission and depression, especially in a social context. Main valid parameters of this endocrine stress response are adrenaline, noradrenaline, ADH, ACTH and cortisol. In the perioperative period, both pathways are "stressed". The most important factors are patient, operation, and anaesthesia. Anaesthesia can influence the stress response by afferent blockade (local anaesthesia), central modulation (general anaesthesia) or peripheral interactions with the endocrine system (etomidate). Up to now, a total peripheral blockade of the nociceptive system is impossible, due to surgical technique (destruction of nerve fibres) and release of mediator substances. With regard to reduction of endocrine stress response, inhalation anaesthesia with volatile anaesthetics and nitrous oxide may be less effective than neuroleptic, spinal or epidural anaesthesia. Immediately after extubation, rapid increases of endocrine parameters are observed. In addition to central modulation of pain and stress, both halothane and enflurane inhibit catecholamine release from the adrenal medulla. Neuroleptic anaesthesia and total intravenous anaesthesia are very potent and sufficient to control the increases in endocrine parameters even during major surgery, due to their central effects. Spinal and epidural anaesthesia alone as well as in combination with general anaesthesia can reduce the endocrine stress response more than necessary. This is due to the sympathetic blockade, combined with an afferent blockade of central cord fibers which modulate the pituitary-adrenocortical system. Only few data are available concerning the stress response during infiltration anaesthesia or nerve block, but additional sedation seems to be beneficial. Peripheral interactions with the endocrine system like blockade of the adrenal cortex by etomidate is dangerous and has caused a high mortality in intensive-care patients if the substance was admitted for a longer period. Assessment of endocrine stress response in anaesthesia and surgery is controversial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The endocrine stress reaction in anesthesia and surgery--origin and significance]. 175 50

In order to demonstrate pharmacokinetic and pharmacodynamic interactions between fentanyl and buprenorphine, 3 groups of patients (n = 30) were compared, receiving either fentanyl (0.005 mg/kg b.w.) or buprenorphine (0.01 mg/kg b.w.) or both opioids as analgesic during surgery for disc protrusion. For a period of 4 h haemodynamic parameters were monitored and blood samples were taken for determination of the following concentrations: ADH, ACTH, cortisol, glucose, unbound glycerol, fentanyl and buprenorphine. Blood gas analyses were performed up to 2 h postoperatively. Although in all groups haemodynamic parameters were constant, there was an increase in factors related to operative stress (cortisol, glucose, unbound glycerol, postoperative acidosis) after the combination of both opioids, while postoperative ventilatory parameters in this group were not improved by the partial agonist buprenorphine. Plasma levels were not affected by combined application, except for a slight elevation of buprenorphine concentrations during additional use of fentanyl. Buprenorphine, at least in higher dosages, seems to antagonize analgesia induced by fentanyl, although respiratory depression is even more pronounced. It may be assumed, that with partial agonists the relation of agonistic and antagonistic activity may be different, depending on the dosage used and on the respective pharmacologic effect observed during investigation.
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PMID:[Intra- and postoperative interactions between the 2 opioids fentanyl and buprenorphine]. 301 44

The effect of pretreatment with amantadine (AMN) on chlorpromazine (CPZ) and reserpine (RES)-produced behavioral depression was studied in the male mouse. The effect of this treatment on hepatic alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenase (L-ALDH), which catalyze the metabolism of biogenic amine aldehydes, was also investigated. Administration of AMN, 100 mg/kg, initially decreased spontaneous locomotor activity from saline control. Pretreatment with identical dose of AMN 15 min before small dose of CPZ or RES, 0.2 mg/kg, further suppressed motility compared to animals receiving the individual AMN, CPZ or RES treatment. Using a second dose regimen of these compounds, given 5 hr post the initial injection, altered L-ALDH as a function of its subcellular localization. This was demonstrated by AMN-produced induction of mitochondrial, but not cytoplasmic L-ALDH. Likewise, a moderate but not statistically significant increase in endogenous mitochondrial L-ALDH was determined subsequent to the CPZ treatment. Treatment with AMN prior to CPZ reduced the enhancement of L-ALDH to control levels. The RES dose used was devoid of action on remainder of hepatic enzymes measured. The results indicate that AMN possesses central depressant property which was potentiated by CPZ and RES. The enzymatic data suggest antagonism between AMN and CPZ on induction of mitochondrial L-ALDH.
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PMID:Effect of amantadine on chlorpromazine and reserpine-induced behavioral depression in the mouse. 322 46

As aged polyuria is often observed in the IVCS strain of mouse, biochemical and histological studies were undertaken in order to clarify its etiology. Polyuria was observed at 7-8 months of age, and significant increases in water intake and urine volume were noted at 10-11 months of age. IVCS strain mice over one year old showed water intakes and urine volumes about five to six times greater than those in DDI strain mice. The osmolarity of urine excreted from polyuric mice was low compared with DDI strain mice, and elevations of sodium and potassium excretion were observed at an early stage of polyuria. At a more advanced stage of the disease, proteins of low molecular weight were excreted in most animals. Furthermore, depression of kidney response to ADH was recognized soon after onset of polyuria compared with normal IVCS strain mice. Thus, polyuria observed in IVCS strain mice may result from a functional defect of the renal tubules. In addition, significant deposition of amorphous substances, especially in the liver, kidney and spleen, occurred almost in parallel with polyuria. From these findings, it is obvious that mice of the IVCS strain exhibit characteristic polyuria and storage disease as they age.
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PMID:Clinical and pathogenic studies on aged polyuria in the IVCS strain of mouse. 401 46

1. Neurones in the supraoptic nucleus were examined for their responsiveness to microiontophoretically applied monoamines and cholinomimetic agents. One hundred and sixty-one of the 749 neurones recorded were antidromically identified as neurosecretory cells.2. The monoamines, dopamine, noradrenaline and serotonin, reduced the activity of all cells which responded.3. Reduction in activity following noradrenaline administration was antagonized by the beta-adrenergic blocking agent MJ-1999 and potentiated by desmethylimipramine.4. Acetylcholine produced either a decrease or an increase in activity of responsive cells with depression the predominant result. Both the depressant and the excitatory response to acetylcholine were seen in individual neurosecretory cells which were depressed by noradrenaline.5. Application of acetyl-beta-methylcholine and carbaminoylcholine consistently resulted in depression of all responsive cells, while nicotine excited the majority of responsive cells. Both types of response were observed on the same neurosecretory cell.6. The depressant response was antagonized by the muscarinic blocking agent atropine while the excitatory response was antagonized by the nicotinic blocking agent dihydro-beta-erythroidine. Responses to acetylcholine were potentiated by the acetylcholinesterase inhibitor physostigmine.7. The data indicate that noradrenaline-containing terminals on these neurosecretory cells are likely to inhibit their discharge rate, while the presumed cholinergic terminals might function as either excitatory or inhibitory, depending on the receptor activated.8. These results support the hypothesis that ADH release is related to the neuronal activity of the supraoptic neurosecretory cell.
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PMID:Noradrenaline and acetylcholine responses of supraoptic neurosecretory cells. 439 77

A total of 132 urine specimens were obtained from 17 depressed patients and 18 controls under conditions of mild water deprivation. Mean values of milliosmoles of solute and millilitres of urine excreted per hour were obtained for each subject. The depressed patients excreted significantly less solute than the control group per unit volume of urine. There was no significant difference between the solute excretion rates of depressed patients and those who had recently recovered from depression-though the trend was towards normality. The significance of these results is discussed in relation to studies on body fluids and electrolytes and the role of ADH and aldosterone in affective disorders.
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PMID:Urine concentration in depressive illness. 555 92

Fentanyl, a synthetic opiate with a (clinical) potency of 50 to 100 times that of morphine, was introduced into clinical practice in the early 1960s. Usually administered by single intravenous doses, it developed a reputation for having a short duration of action and it was assumed that this was a consequence of rapid removal from the body. However, as clinical experience increased, it was realised that administration of multiple doses or large doses during narcotic-based anaesthesia sometimes led to delayed recovery and prolonged respiratory depression, suggesting that the duration of action was limited by redistribution within the body rather than removal from the body. Recent developments in analytical techniques have allowed pharmacokinetic studies and these have confirmed this opinion; fentanyl is rightly regarded as having a redistribution-limited duration of action after single or infrequent doses (analogous to thiopentone). However, the magnitude of the pharmacokinetic constants reported for fentanyl are remarkably inconsistent even in healthy volunteers, for reasons apparently only explainable by assay differences. Hence, estimates of apparent volume of distribution (area) range from around 60L to over 300L, estimates of terminal half-life range from about 1.5 to 6 hours (15 hours in geriatric patients) and total body clearance ranges from 0.4 to over 1.5 L/min. Renal excretion accounts for up to 10% of the dose; the remainder of the clearance would appear to be predominantly hepatic, but with contributions from other tissues. Continued clinical developments of narcotic-based anaesthetic techniques have resulted in high doses of narcotic being used, with oxygen, as the sole anaesthetic agents. At present these techniques are usually based on fentanyl, and the technique is frequently called 'stress-free anaesthesia' because of the effects in obtunding the 'stress response' caused by surgery (elevation of plasma concentrations of cortisol, glucose, ADH, etc. in the intra- and post-operative period) and the lack of deleterious effects on the cardiovascular system.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical pharmacokinetics of fentanyl and its newer derivatives. 622 71

Congestive heart failure is associated with ventricular hypertrophy and dilatation, increased circulating catecholamines, and peripheral vasoconstriction. The extent to which these changes occur, whether they are a favorable "compensatory mechanism" or contribute to cardiocirculatory dysfunction, depends on the cause and severity of the heart failure. The addition of new sarcomeres through ventricular hypertrophy distributes the excess workload of the failing ventricle over more contractile units. In ventricular pressure overload, hypertrophy primarily increases wall thickness and ventricular volume is not usually increased; the converse is true with ventricular volume overload. Hypertrophy can result in enhanced or depressed contractile performance, depending on the stimulus for hypertrophy and method by which contractility is evaluated. The "ventricular function curve," which relates stroke volume to ventricular filling pressure or volume, overestimates the role played by the "Starling principle" as a compensatory mechanism and underestimates how well contractile performance is preserved. The evaluation of end systolic pressure-volume relationships under conditions of variable afterload closely reflects the isometric length-tension relationship and is therefore a more accurate way to quantitate cardiac muscle performance. Pressure overload hypertrophy usually leads to a depression in contractility whereas volume overload may not. An exaggerated sympathoadrenal response is another hallmark of severe heart failure that enhances contractility, helps initiate hypertrophy, and maintains arterial perfusion pressure. A generalized increase in peripheral vascular resistance occurs and is most prominent in those circulations most susceptible to neurohumoral control (renal, splanchnic, cutaneous). This favors perfusion of the cerebral and coronary circulations. Vasoconstriction is further enhanced by the activation of the renin-angiotensin-aldosterone system and secretion of ADH. This results in sodium retention and plasma volume expansion. In early mild heart failure, vasomotor tone may be normal at rest; however, the sympathoadrenal response to exercise may be intense. Moderate alpha receptor stimulation reduces skeletal muscle blood supply and favors the intramuscular redistribution of blood flow from inactive to active muscle fibers, thereby maintaining a normal oxygen consumption. During the later stages of heart failure, increased vascular stiffness due to increased sodium content and excessive norepinephrine appears to restrict nutritional blood flow to exercising muscle at the conductance-vessel level. Vasodilator drugs may reduce aortic impedance and improve cardiac output, may lower ventricular filling pressure, and relieve congestive symptoms, and may result in complex but favorable changes in the distribution of blood flow to the regional circulations.
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PMID:Cardiocirculatory dynamics in the normal and failing heart. 645 90


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