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)

The effects of various psychotropic drugs (benzodiazepines, antidepressants, neuroleptics and nootropic drugs, a family of cognition activator agents) on firing rates of septohippocampal neurons, identified by electrical antidromic stimulation, were studied in the medial septum-nucleus of the diagonal band of Broca of rats anaesthetized with urethan. Extracellular potentials from single septohippocampal neurons were recorded using glass pipettes. Drugs were applied by either microiontophoresis or intravenous injections (i.v.). Benzodiazepines produced a marked depression of spontaneous firing rates of septohippocampal neurons whether applied i.v. (diazepam) or iontophoretically (flurazepam, midazolam). In addition, diazepam had a potent depressant effect on the rhythmically bursting activity of the septohippocampal neurons. Baclofen also had an inhibitory effect. Antidepressant drugs (applied by iontophoresis) as well as amphetamine, had a depressant effect on spontaneous firing rates. Neuroleptics (i.v.) had less significant or consistent effects on septohippocampal neurons, although the effects of haloperidol were usually inhibitory. Nootropic drugs were generally ineffective. These data indicate that most psychotropic drugs tested (with the exception of nootropic drugs) have an inhibitory effect on the spontaneous activity of septohippocampal neurons. However, benzodiazepines seem to be more active than antidepressants or neuroleptics. Oxotremorine (i.v.) had a potent excitatory effect on septohippocampal neurons. Atropine (i.v.) increased the septohippocampal neurons' firing rate in some cases. These results are discussed in view of the possible implication of the involvement of septohippocampal neurons in the mediation of the effects of psychotropic drugs on the central nervous system and, more specifically, on the cholinergic systems.
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PMID:Effect of psychotropic drugs on identified septohippocampal neurons. 290 59

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

We have previously shown that delta-opioid agonists decrease ventilation and heart rate. Because of these results and the known interactions between opioid and acetylcholine metabolism, we hypothesized that opioids induce cardiorespiratory changes via the parasympathetic nervous system. To test this hypothesis, we administered atropine sulfate (systemically) at maximal effect of D-Ala-D-Leu-enkephalin (DADLE; a preferential delta-opioid agonist), injected intracisternally, and examined its effect on cardiorespiratory function. All experiments were performed on chronically instrumented and conscious adult dogs. Mean instantaneous minute ventilation or VT/TTOT decreased and PaCO2 increased after DADLE; atropine had little effect on these changes. Naloxone, even in small doses, reversed opioid effects on VT/TTOT and PaCO2. Atropine, however, reversed the DADLE-induced depression in cardiac rate. In doses that reversed this cardiac depression, atropine had no effect on cardiorespiratory function at rest, i.e., with no prior administration of DADLE. We conclude that DADLE decreases heart rate by increasing parasympathetic activity to the heart and induces hypoventilation by a different mechanism. We speculate that the opioid-induced ventilatory depression is due to either direct opioid action on central respiratory regulation or parasympathetic non-muscarinic or non-cholinergic mediating mechanisms.
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PMID:Effect of parasympathetic blockade on ventilatory and cardiac depression induced by opioids. 310 83

The effects of a novel piperazine derivative (INO 2628) on sinus node pacemaker activity and atrial contractile force were investigated in isolated, blood-perfused dog atrium. Injections of INO 2628 (0.03-100 mumol) into the sinus node artery of the isolated atrium induced a dose-dependent decrease in sinus rate and an increase in contractile force. The positive inotropic effects at more than 10 mumol were accompanied by a transient negative inotropism. Propranolol did not affect the positive inotropic response to INO 2628, but it significantly suppressed positive chronotropic and inotropic responses to norepinephrine. Atropine at a dose which completely blocked negative chronotropic and inotropic responses to carbachol, produced a slight but significant depression of INO 2628-induced negative chronotropic responses; inotropic responses were unaffected. These results suggest that INO 2628 induces noncholinergic negative chronotropic and nonadrenergic positive inotropic responses in isolated dog atria.
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PMID:Negative chronotropic and positive inotropic effects of a unique cardioactive agent, N,N'-dicyclopropyl methyl piperazine (bis) hydrochloride (INO 2628), in isolated, blood-perfused dog atria. 324 39

The verapamil analog falipamil is a new compound with specific bradycardic action on the sinus node. It differs from verapamil with respect to its electrophysiological and haemodynamic actions. Falipamil causes a slight prolongation of intraatrial and intraventricular conduction, whereas sinuatrial and AV-node conduction is enhanced. The refractory periods of atrial and ventricular myocardium and ventricular repolarization are significantly prolonged, whereas the refractory period of the AV-node is shortened. Falipamil fails to influence any haemodynamic parameter significantly at rest, if heart rate is kept constant. In exercise-induced myocardial ischaemia, changes in haemodynamics reflect changes in heart rate. Increased sinus rate at rest is significantly reduced by falipamil 15%-25%. Around 150 mg falipamil prove aequieffective to about 40 micrograms pindolol. Atropine-induced and catecholamine-induced sinus tachycardia is also significantly diminished. Increased sinus rate during exercise is lowered by about 10%. Through reduction of heart rate, falipamil proves capable of significantly diminishing or even preventing ischaemic ST-segment depression and ischaemia induced increase in pulmonary capillary pressure. Thus falipamil can be used to normalize sinus rate in patients with sinus tachycardia of various origin, particularly in intensive care, in acute ischaemic heart disease, in anaesthesia and in surgery cases.
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PMID:A summary of the acute effects of falipamil in man. 333 May 25

An 8-month-old female infant was brought in after ingesting cigarette butts. Upon presentation to the ED approximately 2.5 hr post-ingestion, the child was very lethargic and respirations were depressed. She was intubated and a NG tube was placed. Gastric lavage was performed, after which activated charcoal and sorbitol were given. Atropine was administered to treat excessive secretions. The patient became progressively more obtunded throughout the emergency department stay. Upon admission to the PICU she was minimally responsive. The urine tox screen was positive only for nicotine. The patient gradually improved with supportive care and was sent home on the third hospital day. Although the effects of Nicotine are well documented, few cases have been reported of severe toxicity in pediatric patients. We believe this to be the only reported case of severe CNS depression secondary to the ingestion of cigarette butts in a pediatric patient.
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PMID:CNS depression in an infant after the ingestion of tobacco: a case report. 335 77

Clinical and pulmonary function changes induced by intravenous dichlorvos (2,2-dichlorvinyldimethyl phosphate) (DDVP) toxicosis, and reversibility of these changes after atropine treatment were investigated in six Friesian calves one to three months old. From one minute after dosage, all animals showed severe respiratory distress, excitation, weakness, muscle fasciculation and cholinesterase inhibition. Decrease in dynamic lung compliance and arterial oxygen tension and increase in total pulmonary resistance, viscous work of breathing and alveolar arterial oxygen gradient were highly significant (P less than 0.01). On the other hand, body secretions, heart rate, respiratory rate, tidal volume and arterial carbon dioxide tension were not significantly affected by DDVP injection. Atropine promptly and completely reversed these changes, except for muscle fasciculations, central depression and cholinesterase inhibition which disappeared progressively within 24 hours.
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PMID:Pulmonary function changes induced by experimental dichlorvos toxicosis in calves. 373 27

In addition to depolarizing the ventral horn cells including antidromically identified motoneurons in thin transverse neonatal rat spinal cord slice preparations, exogenously applied acetylcholine (ACh) suppressed the amplitude of excitatory postsynaptic potentials (EPSPs) either occurring spontaneously or elicited by stimulation of dorsal rootlets. A reduction of EPSPs could still be detected when the ACh-induced depolarization was nullified by hyperpolarizing current. Atropine but not D-tubocurarine effectively antagonized the depolarization and synaptic depression caused by ACh. While depressing the EPSPs, ACh had no appreciable effect on membrane depolarizations elicited by glutamate. Methacholine mimicked the depolarizing and synaptic depressant effects of ACh. The results suggest that muscarinic agonists inhibit synaptic transmission of ventral horn neurons including motoneurons by a presynaptic mechanism in reducing the output of excitatory transmitters.
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PMID:Presynaptic suppression of excitatory postsynaptic potentials in rat ventral horn neurons by muscarinic agonists. 375 97

The possibilities of participation of adenosine in the peristaltic reflex of guinea pig ileum was studied pharmacologically and histologically. Adenosine apparently depressed the peristaltic activity induced by elevation of intraluminal pressure from zero to 1-8 cm H2O, and the extent of the depression somewhat decreased in proportion to the elevation in intraluminal pressure. Also, dipyridamole depressed the peristaltic activity by itself; however, the extent of the depression significantly increased in proportion to the elevation in intraluminal pressure. On the other hand, in the presence of dipyridamole, the elevation of the intraluminal pressure from zero to 1-8 cm H2O elicited an 3H-output increase from 3H-adenosine preloaded guinea pig isolated ileum, with the effect being more pronounced as the pressure was increased. In contrast, the peristaltic activity was more pronounced at lower pressurization. Atropine greatly depressed the peristaltic response but did not affect 3H-output induced by 4 cm H2O pressurization. Tetrodotoxin depressed both markedly. Fluorescence histochemical localization of quinacrine, which binds to adenosin triphosphate (ATP), revealed dense nerve cell bodies and fine interconnecting strands in the ileal myenteric plexus of Auerbach. Also, in microradioautographs of ileal longitudinal muscle incubated with 3H-adenosine, the concentration of developed silver grains was localized in the ganglion cells and in the musculature as varicose fibre. From these results, evidence is provided that the peristalsis of guinea pig ileum may be physiologically modulated by endogenous adenosine, which may be released from neuronal elements of the myenteric plexus in response to the applied intraluminal pressure.
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PMID:Possibilities for adenosine modulation of peristaltic reflex in guinea pig isolated ileum. 409 42

Cardiac slowing occurring during diagnostic coronary arteriography was studied in 78 patients. Comparable degrees of slowing occurred with injections into the right and into the left coronary arteries into the contralateral artery, and with injections into the coronary artery giving rise to the sinus node artery and into the contralateral artery. Rapid intracoronary injections of isosmotic dextrose solution produced significantly less slowing than comparable injections of contrast medium. Slow injections of contrast medium produced cardiac slowing comparable to that caused by rapid injections of contrast medium. However, the cardiac slowing was significantly greater than that produced by rapid injections of dextrose solution. Inhalation of 100% oxygen did not alter the heart rate response to injections of contrast medium. Atropine produced dose-related attenuation of cardiac slowing. Bradycardia persisting after cholinergic blockade was significantly greater after injections into the coronary artery supplying the sinus node than it was after injections into the contralateral artery. Coronary arteriography produced transient, occasionally profound, arterial hypotension in 38 of 41 patients in whom arterial pressures were recorded. Arterial pressure did not change in three patients. This study suggests that the cardiac slowing which occurs during coronary arteriography in man is due primarily to a cholinergic reflex which may be a human counterpart of the Bezold-Jarisch reflex, observed heretofore only in experimental animals. This slowing appears to be mediated primarily by receptors sensitive to contrast medium, rather than by changes of coronary artery pressure, and secondarily, by direct depression of sinus node function by contrast medium.
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PMID:Mechanisms mediating bradycardia during coronary arteriography. 443 42


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