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 effect of dopamine on the acute ventilatory response to hypoxia was investigated in four newborn lambs studied on the 1st day of postnatal life and eight lambs studied between 7 and 12 days of age. Studies were accomplished during nonrapid-eye-movement sleep in unanesthetized tracheotomized animals. Changes in minute ventilation (VE/kg), tidal volume, and frequency induced by intravenous bolus injection of dopamine (10 micrograms/kg) or saline control were assessed while animals were breathing room air or N2, before and after carotid body denervation (CBD). Dopamine depressed resting ventilation at both postnatal ages. This effect was greater in the older animals. Dopamine blunted the hypoxia-induced increase in VE/kg at both ages. The magnitude of this depression did not vary with postnatal age. Dopamine induced cessation of respiratory effort at end expiration (apnea) during room air and N2 breathing significantly more often in the older animals. The effect of dopamine was mediated at the carotid body. CBD decreased ventilation by an increase in breath-to-breath interval in older animals, suggesting carotid sinus nerve afferent activity is more important during eucapnic respiration in older animals than in the immediate newborn period.
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PMID:Dopamine and carotid body function in the newborn lamb. 684 Dec 28

Dopamine produces dilation predominantly in renal and mesenteric vascular beds. An action on a specific receptor has been confirmed in vitro using a perfused canine mesenteric vessel preparation. Reductions in resistance produced by dopamine are selectively inhibited by methylergometrine (pA2 = 8.3) and sulpiride (pA2 = 5.6). Evidence is accumulating which suggests that vascular dopamine receptors are innervated. Periaterial nerve stimulation in anesthetized dogs produces increases in blood flow in the superior mesenteric artery which are not influenced by atropine and propranolol but are inhibited by haloperidol. Dopamine receptors are also present at sympathetic ganglia and sympathetic nerve terminals. Inhibition of noradrenaline release resulting from stimulation of these receptors may make an important contribution to the depressor effects of dopamine receptor agonists in anesthetized animals and in man. Reductions in blood pressure induced by bromocriptine and other long-acting dopamine receptor stimulants are frequently associated with reductions in heart rate, but not always with a corresponding depression of myocardial contractile force. This phenomenon may be explained by a selective distribution of prejunctional receptors in sympathetic neurons innervating the sinus node.
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PMID:Peripheral dopamine receptors. 699 Nov 52

Factors that contribute to the lethality of amitriptyline overdosage were studied in cats. Amitriptyline (50 mg/kg) given i.p. to unanesthetized cats produced convulsions in all of the animals and death in five of six animals; pretreatment with diazepam (5 mg/kg) protected against the convulsions and death. Respiratory depression contributed to the mortality when amitriptyline was given i.v. in cats anesthetized with pentobarbital as indicated by the finding that artificial respiration delayed the time of death induced by a continuous i.v. infusion of the drug. The i.v. infusion of amitriptyline in pentobarbitalized cats under artificial respiration produced death due to cardiovascular collapse. The latter was characterized by hypotension, bradycardia, depression of myocardial contractile force, atrioventricular block, intraventricular conduction delay and cardiac arrhythmias. These effects appear to be due to a direct membrane (quindine-like) cardiotoxic action of amitriptyline. Dopamine and dobutamine were effective in protecting the animals against the acute cardiovascular collapse induced by amitriptyline. The protection was associated with a diminution of the hypotension, the negative inotropic and chronotropic actions and the incidence of atrioventricular block produced by the tricyclic antidepressant drug. The results suggest that the positive chronotropic, inotropic and dromotropic actions of the amines may all be contributory factors in their protection action. Isoproterenol and norepinephrine were less effective than the other two amines.
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PMID:Protective action of diazepam and of sympathomimetic amines against amitryptyline-induced toxicity. 709 63

Our purpose was to study the effects of three related vasoactive drugs on gastric epithelial oxygenation and metabolism. By means of an ultramicroelectrode technique, oxygen tension and transmembrane potential difference of surface epithelium were determined in an in vivo canine gastric chamber model. Intra-arterial papaverine (30 micrograms kg-1 min-1) caused a significant depression of epithelial PO2 and potential difference (PD), a transient inhibition of total gastric oxygen consumption, and a 70% increase in total gastric blood flow. Following cessation of the papaverine infusion, epithelial PO2 and PD continued to decline, whereas gastric blood flow and oxygen consumption return to baseline. Isoproterenol (0.0125 microgram kg-1 min-1), on the other hand, had no significant effect on epithelial PO2 and PD although it increased total gastric blood flow 33%. Dopamine (0.1 microgram kg-1 min-1) had no significant hemodynamic effects. To test the importance of papaverine-induced epithelial hypoxia, hydrochloric acid (160 mM) and sodium taurocholate (3 mM) were added to the epithelial bathing solution during intra-arterial infusion of either papaverine or isoproterenol. Necrosis and ulceration of the gastric mucosa were seen with the infusion of papaverine but not with the infusion of isoproterenol. Our results indicate that papaverine increases total gastric blood flow at the expense of nutrient blood flow to surface epithelium. We conclude that nutrient blood flow to surface epithelium is critical to the ability of the gastric mucosa to resist injury by luminal acid and bile. Furthermore, papaverine should not be used clinically to enhanced gastric blood flow because it is potentially injurious to the mucosa.
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PMID:Contrasting effects of vasodilators on oxygen tension and membrane potential of canine gastric surface epithelium. 724 49

The catecholamine response of injured tissue after severe spinal cord injury (SPI) remains a puzzling controversy. This study was undertaken in an attempt to resolve that controversy. The influence of the biochemical assay method, the magnitude of injury, and the spinal cord region injured on catecholamine levels was determined in the cat spinal cord. It was found that the concentration of norepinephrine (NE) in the traumatized spinal cord is dependent on both the magnitude and the region of injury. The relatively large tissue samples necessitated by the older, less sensitive assay methodology show little or no change in NE levels after a 500-g/cm injury in the cat. When regional samples are analyzed with more sensitive methods, a net depression in the NE level of local tissue is observed. The results of earlier studies from this laboratory indicating an increase in tissue NE after trauma were apparently artifactual, presumably due to the nonselective nature of the biochemical assay used at that time. Dopamine levels were not elevated after SCI, and previous reports from other laboratories indicating an increase in dopamine levels were probably also errant due to methodology-related problems.
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PMID:Catecholamine alterations attending spinal cord injury: a reanalysis. 739 23

Dopamine (DA) given IV by bolus injection (5, 10, 20 micrograms/kg) and by slow IV infusion (20 micrograms . kg . min) depressed VE significantly in awake normoxic goats. These responses were attenuated but not eliminated during hypoxia (FIO2 = 0.14) and hyperoxia (FIO2 = 1.0). After administering haloperidol (0.3 mg/kg) or removing the carotid bodies (CBE) there was greater attenuation of the response to DA. In normal goats haloperidol also caused a significant increase in ventilatory response to acute hypoxia and exaggerated depression of VE after 3--5 breaths O2 during steady-state hypoxia. After CBE haloperidol caused mild hypoventilation (delta PaCO2 = +2.5 Torr). CBE induced hypoventilation in goats (delta PaCO2 = +7.8 Torr) and reduced, but did not totally eliminate, peripheral chemoreceptor responses to acute stimuli (NaCN injection, transient N2 and transient O2 breathing). Attempted aortic body denervation did not eliminate these residual responses. We conclude: (1) DA may function as a modulator of carotid body (CB) function in the goat, (2) there may be central excitatory DA receptors in the goat, (3) the CB is important in regulating resting ventilation in the goat.
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PMID:Depression of ventilation by dopamine in goats--effects of carotid body excision. 744 22

The contribution of sympathetic and vagal inputs to ventilatory depression induced by dopamine was studied in eighteen anaesthetized, spontaneously breathing, normoxic cats. Breathing was via a tracheostomy. Dopamine (20 micrograms (kg body wt)-1) was injected intravenously in the intact animal, then after section of the cervical sympathetic trunks, and finally after midcervical vagotomy. Dopamine, injected as a bolus, induced depression of ventilation, affecting predominantly the volume component of the breathing pattern at all experimental stages. The extent of volume reduction was larger and different from that in intact animals following section of sympathetic (P < 0.05) and vagal trunks (P < 0.01). The respiratory cycle was significantly prolonged (P < 0.01) prior to vagotomy, due entirely to the increase in the expiratory time (TE). Bilateral section of the carotid sinus nerves performed in six cats virtually abolished postdopamine ventilatory depression.
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PMID:Depression of ventilation by dopamine in cats: effects of bilateral cervical sympathetic and vagal trunk section. 778 16

d-Amphetamine (DEX) and phencyclidine (PCP) increased motor activity in rats as measured in automated activity cages. Analysis of the stimulation indicated that both drugs increased horizontal activity (total activity), locomotion, and peripheral activity. However, DEX increased while PCP decreased the incidence of rearing. The ability of different drugs to antagonise DEX- and PCP-induced increases in total activity (called stimulation) was measured. Dopamine (DA) D1 receptor antagonists (SCH23390, NNC-01-0112) were 7-8 times more potent in blocking DEX than PCP. DA D2 receptor antagonists (raclopride, remoxipride, haloperidol) were only 1-2 times more potent against DEX-induced stimulation. Nonselective DA receptor antagonists were also tested. Chlorpromazine was more potent against DEX than against PCP. Buspirone and sertindole were slightly more potent in blocking PCP than DEX. Ritanserin (5-HT2 receptor antagonist) was inactive against both stimulants. 8-OH-DPAT (5-HT1A receptor agonist) potentiated the stimulant effects of DEX and PCP. Prazosin (alpha 1-adrenergic receptor antagonist) partially blocked both DEX and PCP. Most drugs tested depressed spontaneous motor activity. Remoxipride and sertindole, however, caused very little depression even at doses several times higher than those needed to block DEX or PCP. The data show clear pharmacological differences between DEX- and PCP-induced stimulation.
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PMID:Dopamine receptor antagonists block amphetamine and phencyclidine-induced motor stimulation in rats. 809 Aug 16

The effects of dopamine on non-adrenergic, non-cholinergic (NANC) neurotransmission have been investigated using rat bladder strips in-vitro. Dopamine administered alone did not produce any effect on the bladder but it depressed responses to NANC nerve stimulation in a dose-related fashion. All doses of dopamine employed depressed KCl-evoked contractions of the bladder to similar extents. The depressant action of dopamine on NANC transmission was not mediated by blockade of purinergic receptors, but was partially reversed by haloperidol. It is suggested that depression of NANC neurotransmission induced by dopamine in the rat bladder is partly mediated by dopaminergic receptors.
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PMID:Dopamine depresses non-adrenergic, non-cholinergic neurotransmission in the rat bladder. 810 8

Dopamine infusion test (DIT) was compared with treadmill exercise test (TMT) in 20 patients of chronic stable angina (TMT +ve) for inducing reversible myocardial ischaemia so as to assess its efficacy as an alternative to TMT in patients who cannot perform exercise test due to certain non-cardiac diseases. DIT was positive in 15 of the 20 patients studied; five patients in whom DIT was negative had late onset, early offset changes in TMT. Haemodynamically the increase in heart rate (HR) was less but rise in systolic blood pressure (SBP) was more with dopamine infusion in comparison to the corresponding stage of TMT. However, evidence of myocardial ischaemia (ST segment depression) appeared at a lower rate pressure product (RPP) with dopamine infusion compared to exercise test. The test was tolerated well, in higher doses (stages III & IV) side effects like ventricular ectopic beats, palpitation and angina not warranting stoppage of test, were seen in some patients. Dopamine infusion is a good chemical stress test, and can be used as an alternative to TMT especially in situations where the latter cannot be performed. The test is simple, cost effective, non-invasive and well tolerated.
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PMID:Comparative evaluation of dopamine infusion & treadmill exercise tests in the diagnosis of coronary artery disease. 811 54


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