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

The blood levels of stress mediators--catecholamines (adrenaline and noradrenaline), parameters characterizing the intensity of lipid peroxidation (hydroperoxides, blood antioxidant activity (from the levels of SH groups), and the content of prostaglandins F2 alpha and E (PGF2 alpha and PGE) were measured in patients with bronchial asthma and chronic asthmatic bronchitis before and after exercise. The studies have revealed that bronchial hyperreactivity to exercise is in accord with the high blood levels of catecholamines, hydroperoxides, PGF2 alpha and low content of thiol group reflecting the depression of the total antioxidant system in asthmatics. Increase of catecholamine, hydroperoxide, and PGF2 alpha levels and decrease of the total thiol group content after muscular exercise in the patients with bronchial asthma is in accord with the bronchial reactivity. Changes in the bronchoconstrictor PGF2 alpha are the most marked and measurements of its blood levels and computation of the PGF2 alpha/PGE coefficient may help assess the bronchial hyperreactivity without resorting to provocative tests.
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PMID:[Metabolic aspects of bronchial hyperreactivity to physical exertion in bronchial asthma]. 263 Dec 41

Imipramine is an established treatment for anxiety in adults. Some evidence also exists that it may be beneficial in children. Because of the frequent co-occurrence of anxiety and affective symptomatology in asthmatic children, a pilot study was undertaken to obtain clinical observations on the effects of imipramine on symptoms of asthma as well as those of separation anxiety and depression in children suffering from intractable asthma. The pilot trial was terminated because of medical complications after 6 patients participated.
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PMID:Use of imipramine in children with intractable asthma and psychiatric disorders: a warning. 264 63

The outcome of 49 asthmatics (20 men and 29 women) who had suffered a severe exacerbation of asthma requiring mechanical ventilation was investigated in a follow-up study ranging from 23 weeks to 10 years. Over this time, there were 6 fatalities, all female chronic asthmatics requiring treatment with bronchodilators, beclomethasone, and short courses of oral steroids. Three died at home as a consequence of a sudden attack. Another patient developed a cardiorespiratory arrest immediately after having received a sedative. In the remaining two cases, death occurred within hours or days of progressive deterioration. Four of the six women had required psychiatric treatment for an anxiety-depression syndrome. These findings support previous studies suggesting that psychological disturbances may be predisposing factors to death in bronchial asthma.
J Asthma 1989
PMID:Predisposing factors to death after recovery from a life-threatening asthmatic attack. 270 30

Many centrally acting drugs which are prescribed for hypertension, depression, epilepsy, insomnia and asthma may also affect fetal brain neurotransmission and behavioral states. Nearly all these drugs enter the fetal circulation following maternal administration. The immaturity of the blood-brain barrier and greater accumulation in the developing brain make the fetal brain a major target of its mother's medication. Adverse effects that are seen in the fetus are not necessarily evident in its mother. We have shown that drugs like clonidine (an antihypertensive) and clomipramine (an antidepressant), which act on noradrenaline and serotonin neurotransmission in the brain, suppress rapid eye movement sleep in the developing rat. In adulthood, the neonatally treated rats showed hyperactivity, hyperanxiety, reduced sexual behavior, disturbed sleep patterns and reduced cerebral cortical size. Furthermore, such treatment induced an increase in voluntary alcohol consumption and a decreased adaptability of responses to changes in water deprivation in a Y-maze. Little is known about long-lasting consequences of centrally acting drugs used during late gestation in humans. Minor neurological disturbances, such as delayed visual motor performance, smaller head circumference, increased anxiety and disturbed sleep-wake patterns, have been reported in children born to hypertensive mothers treated with clonidine or alpha-methyl-dopa.
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PMID:Neurochemical and electrophysiological disturbances mediate developmental behavioral alterations produced by medicines. 287 4

Transmission of information among neurons is of a chemical nature. The activity of the neurotransmitter in the brain is regulated by the spontaneous activity of neurotransmitter cell body and the sensitivity of both pre- and post-synaptic receptors. Neurotransmitters are present at very early stages of brain development; they do not only mediate the behavioral-physiological responses of the immature animal, but have trophic effects on the maturation of target neurons as well. Many centrally acting drugs which are frequently used also during pregnancy for the treatment of depression, hypertension, epilepsy, asthma, insomnia, hyperkinetism and other neurological and psychiatric disorders act directly on brain neurotransmitters (in particular monoamines) and behavioral states. Chronic administration of drugs acting on monoamines (such as clonidine, imipramine, alpha-methyl-Dopa, reserpine, monoamine oxidase inhibitors, diazepam) disturb the spontaneous activity and behavioral state dependency of the monoaminergic cells, influences neurotransmitter turnover and change the sensitivity of both pre- and post-synaptic receptors. Sensory deprivation during a critical period of development is known to produce permanent effect on the brain; e.g., monocular deprivation during a particular period of development in a kitten leads to a rewiring of the connectivity in the visual system in the adult cat. Disturbances in neurotransmitter activity during early life will induce a comparable reorganization of the chemical structure of the adult brain.
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PMID:Central neurotransmitter disturbances underlying developmental neurotoxicological effects. 287 1

Airway mucociliary dysfunction leading to a depression of mucus transport has been demonstrated in patients with acute and chronic bronchitis, cystic fibrosis, and bronchial asthma; use of bronchodilators that might further impair mucociliary function, therefore, generally has been discouraged. Atropine and ipratropium bromide are cholinergic antagonists that are effective bronchodilators in various clinical settings. Atropine has been shown to block the production of respiratory secretions in response to cholinergic stimulation, but to have no effect on baseline secretions. Atropine has also been clearly demonstrated to depress ciliary beat frequency and to slow airway mucociliary clearance, whereas the short-term and long-term administration of ipratropium bromide at higher than clinically recommended doses seems to lack these effects. No satisfactory explanation has thus far been offered for this difference between the two cholinergic antagonists. Nevertheless, with respect to airway mucociliary function, ipratropium bromide appears to be preferable to atropine in the treatment of obstructive airways disease.
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PMID:Effect of ipratropium bromide on airway mucociliary function. 294 58

Numerous studies have been, and are being devoted to the nature of adrenergic and purinergic receptors in the bronchopulmonary system. Studies of beta-adrenoceptors performed with ligands (table I) have demonstrated the presence of two types of receptors, beta 1 and beta 2 in proportions of about 15 : 100 respectively; this proportion is approximately the same at all levels of the tracheobronchial tree. Beta-adrenoceptors (beta 1 + beta 2) are globally more numerous in peripheral organs which contain heterogeneous tissues. Their number can be modified in certain circumstances, notably in asthma, infection and after prolonged treatment with sympathomimetic amines. Functional studies using specific beta 1-adrenoceptor agonists (RO-363 or prenalterol) or determining the relative activities of beta 1 and/or beta 2 stimulants and their inhibition by selective beta-blockers have shown that stimulation of beta 1-adrenoceptors may produce partial relaxation of the isolated trachea but not of lung parenchyma, the latter being supposed to represent distal airways. Studies on isolated small bronchi, about 0.1 mm in diameter (fig. 1 and 2A) have confirmed that stimulation of beta 1-adrenoceptors has not effect on distal airways. They have also demonstrated that beta 2-stimulants have different intrinsic activities (fig. 2B). Studies of alpha-adrenergic receptors using ligands (table II) have shown that these receptors are in small number in the tracheobronchial tree of numerous animal species. Functional studies on the conscious guinea-pig have shown that clonidine can potentiate the bronchoconstrictor effects of acetylcholine, histamine and serotonin (fig. 3) and that this potentiating effect is specifically inhibited by yohimbine and piperoxan (fig. 4). This action of clonidine has been attributed to depression of the reflex sympathetic activity associated with bronchospasm. Alpha 1-adrenoceptor agonists (phenylephrine, methoxamine) induce contracture of the isolated bronchial smooth muscle (fig. 5) but may partially reduce the bronchoconstrictor effects of acetylcholine, histamine or serotonin (fig. 6). This last effect is partially inhibited by alpha 1-blockers (fig. 7) and seems to be due to shrinkage of the bronchial mucosa. Finally, studies of purinergic receptors in the bronchopulmonary system have shown that they probably are of the A2-P1 type (tables III and IV) and that they do not seem to be involved in the bronchodilator activity of theophylline.
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PMID:[Adrenergic and purinergic receptors and bronchial motoricity]. 299 53

Oral angiotensin converting enzyme inhibition was introduced eight years ago and is becoming increasingly popular for the treatment of hypertension and congestive heart failure. This treatment causes blood pressure lowering associated with suppression of angiotensin and aldosterone, lack of orthostatic hypotension or metabolic disturbances, redistribution of regional blood flows in favor of vital organs and, in the long term, decreased sympathetic drive and regression of left ventricular hypertrophy. It is effective as monotherapy in more than 50 percent of unselected patients; addition of a diuretic increases the percentage of responders to more than 80 percent. It is the treatment of choice for patients with concurrent diabetes, asthma, gout, depression, or very active life-style. Side effects, observed originally in patients with severe hypertension and renal failure treated with very high doses of captopril, are rare in otherwise healthy hypertensive patients receiving smaller doses of this drug and virtually absent with second-generation angiotensin converting enzyme inhibitors like enalapril.
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PMID:Clinical utility of angiotensin converting enzyme inhibitors in hypertension. 302 82

Transmission of information in the brain is of a chemical nature. Neurotransmitters are present at very early stages of brain development, having trophic effects on maturation of target neurons as well as mediating the behavioral repertoire of the immature brain. Many centrally acting psychoactive drugs which are commonly used (also during pregnancy) for treatment of depression, asthma, hypertension, epilepsy, parkinsonism, hyperkinetism and other neurological and psychiatric disorders act directly on brain neurotransmitters (in particular monoamines) and behavioral states. Disturbances observed later in life in animals and man, as a result of early interference with brain neurotransmitters, using these drugs, are not gross physical malformations but are in fact subtle behavioral and neurological symptoms such as hyperactivity, emotional lability, attentional distractability and sleep disturbances, similar to symptoms observed in the minimal brain dysfunction syndrome.
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PMID:The role of the central monoaminergic system and rapid eye movement sleep in development. 309 90

We studied the effects of urapidil on bronchospasm, myocardial hypoxia and postural hypotension in experimental animals. Urapidil dose-dependently inhibited bronchospasm induced by histamine in anaesthetized guinea pigs and the contraction of isolated trachea induced by noradrenaline or phenylephrine. Urapidil markedly delayed the appearance of severe dyspnoea induced by histamine aerosol in guinea pigs. Further, urapidil inhibited isoproterenol-induced ST depression in rats and inhibited histamine-induced ST depression in rabbits. The postural hypotension induced by prazosin was greater than that induced by urapidil in equihypotensive doses in conscious rabbits. Urapidil induced a lesser alpha-blockade in the vein than in the artery compared with prazosin. These combined properties of urapidil suggest that the drug is worth investigation in hypertensive patients with bronchial asthma or ischaemic heart disease.
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PMID:Pharmacological effects of urapidil on bronchospasm, myocardial hypoxia and postural hypotension in experimental animals. 323 Apr 72


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