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

Histamine is released into the systemic circulation during anaphylaxis, by drugs and by surgical procedures. Studies in animal models have conclusively demonstrated that released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of histamine-releasing drugs. Several lines of evidence suggest a similar arrhythmogenic role for cardiac histamine in humans: (1) The human heart is rich in histamine; (2) cardiac histamine can be readily released from human heart in vitro by therapeutic concentrations of drugs; (3) histamine has potent arrhythmogenic effects on the human heart in vitro. Arrhythmogenic effects of histamine include enhancement of normal automaticity, induction of abnormal automaticity, induction of triggered tachyarrhythmias, depression of atrioventricular conduction, and increase in the vulnerability of the ventricles to fibrillation. A combination of H1 and H2 antihistamines is needed to block the arrhythmogenic effects of histamine. Certain arrhythmogenic effects of histamine (e.g. induction of slow responses and delayed afterdepolarizations) can also be blocked by drugs which inhibit the influx of cations through slow channels. In contrast, the commonly-used drug digitalis potentiates the arrhythmogenic effects of histamine. We propose that histamine release produced by drugs and surgical procedures may be an overlooked factor in fatal cardiac arrhythmias. Experimental studies suggest that selective pharmacological methods can be developed to block the arrhythmogenic effects of histamine.
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PMID:Dysrhythmias caused by histamine release in guinea pig and human hearts. 618 58

The accumulation of histamine into blood platelets of depressed patients, lithium-treated patients and controls was determined using radio-labelled histamine. All groups had significantly different mean accumulation rates: the depressives had the lowest, the controls had the highest while the lithium-treated patients had intermediate rates. No significant difference in histamine accumulation rates was detected between drug-free depressed patients or depressed patients receiving psychotropic medication apart from lithium. Histamine accumulation rates of depressed patients did not appear to have been influenced by their age or severity or endogenicity of their illness; no difference in histamine accumulation was detected between those patients who had an abnormal or normal dexamethasone suppression test response. We have concluded that while the biological significance of these results is unclear it would appear to be a very sensitive test for depression, especially in women. It would appear that prophylactic lithium treatment increased the rate of histamine accumulation: this result is discussed with reference to histamine's association with allergic disorders.
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PMID:Platelet accumulation of histamine in controls, depressed and lithium-treated patients. 623 70

1 RMI 12330A, a lactam-imine, at concentrations of 10(-4) M and higher, inhibited basal as well as isoprenaline and NaF-stimulated adenylate cyclase activity of guinea-pig heart homogenates. However, RMI 12330A was a more potent inhibitor of histamine-stimulated adenylate cyclase (IC50 of 1.5 X 10(-5) M). 2 In the isolated work-performing heart of the guinea-pig, RMI 12330A (IC50 of 1.1 X 10(-6) M) depressed all cardiac functions: pressures developed, dP/dt, contractile force, dF/dt, work performance and stroke work. Left atrial pressure rose and the positive inotropic response to increasing heart rate (staircase) became negative. Histamine, isoprenaline and ouabain no longer caused positive inotropic effects. 3 Increasing the perfusate calcium concentration from 2.5 mM to 4.5 and 6.5 mM completely restored cardiac function after its depression by RMI 12330A. 4 RMI 12330A uncoupled mitochondrial oxidative phosphorylation; the classical uncoupler, dinitrophenol, had the same effects on cardiac dynamics as RMI 12330A. 5 RMI in high doses inhibited hydrolytic activity of Na+, K+-ATPase of crude and purified heart preparations (IC50 of 1.7 X 10(-4) M) and inhibited ouabain binding to the same enzymes (IC50 of 1.5 X 10(-4) M). 6 A lactam-imine analogue of RMI 12330A that had no effect on adenylate cyclase, was also without effect on any of the systems examined.
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PMID:Effects of RMI 12330A, a new inhibitor of adenylate cyclase on myocardial function and subcellular activity. 625 99

1 The role of histamine H1- and H2-receptors in mediating prejunctional inhibition of cardiac sympathetic neurotransmission and histamine-induced coronary vasodilatation were investigated in perfused dog hearts in situ. 2 Intra-arterial injections of histamine into the right coronary artery during the resting state caused slightly positive chronotropic responses in doses larger than 1 microgram. 3 Histamine in doses of 0.1 to 10 micrograms into the right coronary artery reduced the tachycardia resulting from electrical stimulation of the cardiac sympathetic nerves. 4 Intra-coronary infusions of chlorpheniramine (300 micrograms/min) significantly reduced the histamine-induced depression of cardiac nerve stimulation. The effects of cimetidine (300 micrograms/min) and metiamide (300 micrograms/min) were less pronounced. 5 Histamine (1 to 10 micrograms) further increased heart rate resulting from the continuous intra-coronary infusion of noradrenaline (1 or 3 micrograms/min). 6 Intra-arterial injections of histamine (0.1 to 10 micrograms) caused an increase in coronary blood flow in a dose-dependent manner. This was partially inhibited by intra-coronary infusion of chlorpheniramine (10 to 300 micrograms/min) and by cimetidine (10 to 300 micrograms/min). The combination of both drugs (10 to 100 micrograms/min of each) caused a larger inhibition. 7 The present results suggest that the histamine-induced depression of heart rate during cardiac sympathetic nerve stimulation is due to a prejunctional effect mediated mainly by H1-receptors. Histamine-induced coronary vasodilatation in the dog is mediated both by H1- and H2-receptors.
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PMID:Inhibition of cardiac sympathetic neurotransmission by histamine in the dog is mediated by H1-receptors. 630 86

Histamine is released from the heart during ischaemia-reperfusion injury. As histamine has cardiac effects, we investigated the role of histamine in ischaemia-reperfusion injury of isolated rat hearts. A Langendorff-model with 30 min global (37 degrees C) ischaemia followed by 60 min reperfusion was employed. The effects of ischaemia alone (n = 10, group 1.1 + n = 10, group 2.1, 2 different series), and ischaemia with H1- and H2-receptor blockade with cimetidine (10 microM, n = 10), chlorpheniramine (10 microM, n = 8), terfenadine (10 microM, n = 8), and promethazin (10 microM, n = 9), or both cimetidine and chlorpheniramine (n = 8), were studied. Histamine was measured in the coronary effluent and cardiac tissue of group 1.1. Release of histamine increased from 6.5 +/- 1 pmol min-1 before ischaemia to 19 +/- 3 pmol min-1 at the start of reperfusion. Ischaemia decreased left ventricular developed pressure to 18 +/- 11% (1.1) and 50 +/- 11% (2.1) of initial value (mean +/- SEM) at the start of reperfusion. Left ventricular end-diastolic pressure increased from 0 to 79 +/- 8 mmHg (1.1) and 39 +/- 9 (2.1) mmHg, while left ventricular systolic pressure was unchanged (101 +/- 12% in 1.1 and 101 +/- 10% in 2.1). Severe arrhythmias were induced in 90 (1.1) and 30 (2.1)% of the hearts, while coronary flow decreased during reperfusion. H2-blockade did not modify the changes in left ventricular pressures, coronary flow, or heart rate induced by ischaemia. Three different H1-blockers increased left ventricular systolic pressure, inhibited the decrease of developed pressure, attenuated the increase of end-diastolic pressure, and totally inhibited reperfusion arrhythmias. The effect of both blockers together was similar to that of H1-blockers alone. Coronary flow was increased during reperfusion in two of the groups with H1-blocker compared with ischaemic controls. Increased release of histamine from ischaemic-reperfused rat hearts concurred with depression of left ventricular function and arrhythmias during early reperfusion. Cardiac dysfunction during reperfusion was attenuated by three different H1-receptor blockers.
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PMID:Histamine release and its effects in ischaemia-reperfusion injury of the isolated rat heart. 751 35

The effects of histamine on baseline synaptic transmission and long-term potentiation (LTP) were investigated in the CA1 region of rat hippocampal slices. Bath applied histamine reversibly and dose-dependently increased the amplitude of extracellularly recorded population spikes in the concentration range 0.1-100 microM by a maximum of 40%. At higher concentrations (10-100 microM) histamine also caused a small depression of field excitatory postsynaptic potentials (fEPSPs) of approx 10%. The effect of histamine on population spikes was found to be mediated through histamine H2 receptors. Histamine (10-100 microM) was found to produce a statistically significant LTP of fEPSPs when combined with a weak tetanus (0.25 sec, 50 Hz). Histamine H1 (mepyramine, 1 microM) and H2 (cimetidine, 50 microM) receptor antagonists did not block this enhanced potentiation. In addition, histamine (10-100 microM) enhanced the late portion of the response produced by pressure ejection of glutamate receptor agonist N-methyl-D-aspartate into the slice, as recorded extracellularly or intracellularly. This effect of histamine was only apparent when large NMDA responses were obtained, using a high pipette concentration of NMDA (1 mM). In the presence of histamine H1 and H2 antagonists, potassium channel blockers or blockade of inhibition, this enhancement could still be observed. We conclude that histamine facilitated the induction of LTP, most likely by acting directly at the NMDA receptor.
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PMID:Histaminergic modulation of synaptic plasticity in area CA1 of rat hippocampal slices. 761 44

1. The effects of histamine on excitatory synaptic transmission in the dentate gyrus region of rat hippocampal slices were examined using extracellular and whole-cell patch-clamp recording techniques. The GABAA receptor antagonist picrotoxin (50 microM) was present in the bath in all experiments. 2. Histamine (0.7-70 microM) reversibly depressed field excitatory postsynaptic potentials (fEPSPs) or excitatory postsynaptic currents (EPSCs) recorded intracellularly by up to 30%. The presynaptic fibre volley and EPSC reversal potential were unaffected by histamine, as were responses following pressure ejection of the glutamate receptor agonist S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (S-AMPA) into the slice. 3. Histamine (7 microM) depressed equally the AMPA and N-methyl-D-aspartate (NMDA) components of the dual-component EPSC, recorded at -40 mV. 4. In addition to depressing synaptic transmission, histamine also reduced the magnitude of paired-pulse depression (PPD; 40 ms interpulse interval) of the medial perforant path EPSC. 5. Histamine depressed medial perforant path EPSCs more strongly than lateral perforant path EPSCs. Paired-pulse facilitation (PPF; 40 ms interpulse interval) in the lateral perforant path was enhanced by histamine. 6. The effects of histamine on synaptic transmission and PPD were mimicked by the selective H3 receptor agonist R-alpha-methylhistamine (0.1-10 microM) but not by the selective H2 receptor agonist dimaprit (10 microM). Similarly, the H3 receptor antagonist thioperamide (10 microM) blocked the effect of histamine whereas the H1 antagonist mepyramine (1 microM) and the H2 receptor antagonist cimetidine (50 microM) were ineffective. 7. Histamine actions on synaptic transmission and PPD were not occluded by application of the metabotropic glutamate agonist L-2-amino-4-phosphonobutyrate (AP4). 8. The results indicate that histamine depresses synaptic transmission in the dentate gyrus by binding to histamine H3 receptors located on perforant path terminals. The mechanism by which histamine depresses transmission is independent of that used by class III metabotropic glutamate receptors.
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PMID:Histamine H3 receptor-mediated depression of synaptic transmission in the dentate gyrus of the rat in vitro. 891 Feb 6

Heartworm (Dirofilaria immitis) infection alters the behavior of vascular endothelial cells in vivo and in vitro, with the potential, therefore, to influence vascular function. Histamine, an autocoid implicated in the pathogenesis of parasitic and inflammatory diseases, is vasoactive, and causes endothelium-dependent relaxation in some vascular beds. Experiments were designed to determine if histamine is an endothelium-dependent vasodilator in in vitro rings of canine pulmonary artery from heartworm and control dogs; to elucidate the mechanisms involved in histamine vasoactivity; and to measure circulating levels of histamine. Dose-response relationships to histamine were done in rings of canine pulmonary artery from heartworm and control dogs, in the presence and absence of endothelial cells, the H1 receptor blocker tripelennamine, or the H2 receptor blocker cimetidine. Histamine caused a dose-dependent constriction in control, that was not influenced by endothelial cell removal. However, histamine caused an endothelium-dependent relaxation in heartworm pulmonary artery that was converted to constriction by endothelial cell removal. In heartworm, histamine relaxation was mediated by H2 receptors, but did not appear to involve nitric oxide or cyclooxygenase products. While diseases cause depression of endothelium-dependent relaxation, this is the first report of a disease that changes a constriction response to an endothelium-dependent relaxation.
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PMID:Dirofilaria immitis: heartworm infection converts histamine-induced constriction to endothelium-dependent relaxation in canine pulmonary artery. 953 69

The role of mast cells and their main secretory products in the effects of oestradiol on the uterus was investigated. Ovariectomized rats were treated with a single injection of oestradiol (10 micrograms per rat, i.m.) or vehicle together with drugs affecting the activity of mast cells, cromoglycate (10 mg per rat, i.m.), which diminishes the degranulation of mast cells, or compound 48/80 (0.5 mg per rat, i.m.), which enhances this process. Oestradiol or vehicle was also administered with two important secretory products of mast cells, heparin (0.4 mg per rat, i.m.) or histamine (2 mg per rat, i.m.). All drugs were injected simultaneously with oestradiol (first injection) and then every 6 h until the animals were killed. Observations were performed at 24, 36 and 48 h after oestradiol or vehicle injection. The condition of mast cells was determined by the percentage of degranulated mast cells in sections stained with toluidine blue. Oestradiol-induced effects in the uterus were estimated by the mitotic index, proliferating cell nuclear antigen-labelling index, DNA content, volumes of cells, nuclei and nucleoli in the luminal epithelium, glandular epithelium and stroma cells of the endometrium. Cromoglycate treatment resulted in a decrease in both mast cell degranulation and all examined oestradiol effects in the uterus at all periods of observation. Compound 48/80 increased mast cell degranulation and expression of one aspect of oestradiol effects on the volumes of cell compartments. Histamine or heparin led to a marked increase in the cell, nucleus and nucleolus volumes in all uterine structures. However, heparin produced a depression in proliferation, whereas histamine had a weak transient stimulating action on this process. No effects of the protocols were found in the absence of oestradiol treatment. These results suggest that mast cells are involved in the realization of oestrogen action, including the stimulation of cell growth and proliferation in the uterus, and that the effect of mast cells is mediated by both histamine and heparin.
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PMID:Role of mast cells in oestradiol effects on the uterus of ovariectomized rats. 971 77

Itch sensation is reduced by cooling the skin. We tested whether lowering skin temperature attenuates responses of spinal dorsal horn neurons elicited by intracutaneous (i.c.) microinjection of histamine in anesthetized rats. Cooling the skin to 3 degrees C significantly and reproducibly reduced (to a mean of 48%) i.c. histamine-evoked responses in 20 of 24 wide dynamic range-type dorsal horn neurons. Histamine-evoked responses recovered to control levels after rewarming the skin. Assuming that such neurons play a role in signaling itch, depression of their responses during skin cooling may account for the psychophysical observation that skin cooling relieves itch in humans.
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PMID:Skin cooling attenuates rat dorsal horn neuronal responses to intracutaneous histamine. 992 64


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