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At least 433 records · Page 24Linked to original sources
PubMed1998

Improved detection of CD5 epitope in formalin-fixed paraffin-embedded sections of benign and neoplastic lymphoid tissues by using biotinylated tyramine enhancement after antigen retrieval.

To evaluate the effectiveness of the immunohistochemical staining of B- and T-cell lymphomas with Leu-1 (clone L17F12 CD5 antibody, Becton Dickinson, San Jose, Calif) in formalin-fixed paraffin-embedded sections, we stained 12 specimens reflecting cases of chronic lymphocytic leukemia/small lymphocytic lymphoma, 7 of mantle cell lymphoma, 13 of T-cell lymphomas, and 9 of various B-cell neoplasms that do not ordinarily express CD5, using a streptavidin-horseradish peroxidase method with biotinylated tyramine enhancement after antigen retrieval. We were able to detect CD5 reactivity of neoplastic cells in 9 (75%) of 12 cases of chronic lymphocytic leukemia, 6 (86%) of 7 cases of mantle cell lymphoma, and 13 (100%) of 13 of the T-cell lymphomas. B-cell neoplasms (9/9) not typically associated with CD5 expression showed no reactivity of tumor cells. We conclude that the Leu-1 (CD5) antibody, routinely used for cryopreserved tissues, is also effective in formalin-fixed paraffin-embedded sections using an antigen retrieval and streptavidin-horseradish peroxidase method with biotinylated tyramine.

Biotinylation↗
PubMed1987

Induction of oral cavity cancer by 3-diazotyramine, a nitrosated product of tyramine present in foods.

A mutagenic nitrosation product of tyramine, 4-(2-aminoethyl)-6-diazo-2,4-cyclohexadienone (3-diazotyramine, 3-DT) preferentially induced tumors of the oral cavity. Squamous-cell carcinomas of the mucosa of the oral cavity floor developed in 19 out of 28 male F344 rats administered 0.1% 3-DT in their drinking water. Tyramine and nitrite are found at fairly high concentrations in various foods. This demonstration of the carcinogenicity of 3-DT indicates that although the implications of 3-DT for human cancer are not clear, other nitrosable mutagen precursors need to be tested as possible risk factors in human cancer.

Animals↗
PubMed1975

The effect of noradrenaline, adrenergic blocking agents, and tyramine on the intrarenal distribution of blood flow in the baboon.

The intrarenal distribution of blood flow in the baboon was measured using the 133xenon clearance technique, and dose-response curves for the various components of renal blood flow were determined during intra-arterial infusions of noradrenaline; the alpha-adrenergic blocking agent, phenoxybenzamine; the beta-adrenergic blocking agent, propranolol; and tyramine which causes the release of endogenous NA. High doses of noradrenaline reduced flow in the outer cortex; this effect was attenuated by phenoxybenzamine, but not by propranolol. Tyramine had no effect. These r results suggest that there are alpha-adrenergic receptors in the resistance vessels of the kidney but are inconsistent with an important role for NA-mediated autonomic control of renal blood flow.

Animals↗
PubMed1991

Retinal blood flow following a tyramine-induced increase in blood pressure.

The effect of increasing systemic blood pressure on retinal blood flow was investigated in anaesthetised miniature pigs. Blood pressure was increased by the infusion of the sympathomimetic amine, tyramine. Volume flow was determined from axial erythrocyte velocity, measured by laser Doppler velocimetry, and vessel diameter, measured from monochromatic retinal photographs. Measurements were taken when mean arterial pressures were elevated by a mean of 22 +/- 3% and 50 +/- 8% above resting values, which represented increases of 31 +/- 2% and 74 +/- 16% in ocular perfusion pressures. Retinal blood flow increased by 8.5 +/- 8% at the lower infusion rate and by 57 +/- 19% at the higher infusion rate. We conclude that tyramine infusion is a suitable method for the study of retinal autoregulation and that the upper limit of retinal autoregulation in miniature pigs lies between 22-50% above resting mean arterial pressure.

Animals↗
PubMed1991

Altered responsiveness of saphenous vein grafts to norepinephrine and tyramine: relation to tissue catecholamine stores.

This study was designed to investigate early changes in reactivity in relation to the adrenergic innervation of venous grafts. Saphenous vein grafts were implanted into the carotid artery by the end-to-end technique in mongrel dogs. After 1 week, the grafts were harvested and dose-response curves to norepinephrine and tyramine were determined and compared with those of nongrafted saphenous veins and carotid arteries. Tissue norepinephrine levels of the blood vessels were measured by HPLC with electrochemical detection. Grafted vessels demonstrated an enhanced sensitivity to norepinephrine and a significant attenuation to tyramine. Additionally, grafted saphenous veins exhibited a significant depletion of norepinephrine content when compared to nongrafted veins. These differences suggest that denervation of the saphenous vein produces a supersensitivity to catecholamines that could account for enhanced vascular reactivity observed following implantation of saphenous vein grafts.

Animals↗
PubMed1985

A placebo controlled comparison of the effects of pirenzepine and amitriptyline on the tyramine pressor test in healthy volunteers.

The possibility of an interaction between pirenzepine, an antimuscarinic drug structurally similar to the tricyclic antidepressants, and sympathomimetic agents was investigated in a group of healthy volunteers. The effect of pirenzepine on response to intravenous tyramine was compared with that of placebo and amitriptyline. The mean dose of tyramine required to elevate systolic blood pressure by 30 mm Hg was 5.0 mg (+/- s.d. 0.8) after placebo, 5.1 mg (+/- 1.0) after pirenzepine and 11.3 mg (+/- 1.8) after amitriptyline. These results suggest that pirenzepine will not potentiate the effects of concurrently administered sympathomimetic drugs.

Adult↗
PubMed2004

An investigation of components of variance and tachyphylaxis in a placebo-controlled intravenous tyramine study.

AIMS: To explore inter- and intra-volunteer variability for the dose of intravenous tyramine eliciting a 20 mmHg increase in systolic blood pressure from baseline (TYR20) and to evaluate potential tachyphylaxis. METHODS: Twelve healthy volunteers received blinded placebo-controlled ascending and descending sequences of intravenous tyramine injections on two separate occasions. The TYR20 was derived by linear interpolation, using three interventions to deal with missing data. RESULTS: Analysis of covariance (ancova) demonstrated no significant difference in TYR20 between sequences, regardless of the missing data methodology applied. Inter-volunteer variability was 2.4-3.4 times larger than within-volunteer variability. No evidence of tachyphylaxis was seen using either the sign test or generalized additive models. CONCLUSIONS: Since inter-volunteer variability was greater than intra-volunteer variability, a crossover study design would be a more efficient study design, and the descending sequence of injections could be omitted since tachyphylaxis was not demonstrated.

Adult↗
PubMed1988

Identification and function of octopamine and tyramine conjugates in the Limulus visual system.

Major metabolites of octopamine and tyramine in the Limulus nervous system are identified here as gamma-glutamyl octopamine and gamma-glutamyl tyramine. We show that these conjugates are normal products of amine metabolism in Limulus, and that they are normally present in octopamine-rich Limulus tissues. The synthesis of these conjugates is not restricted to nervous tissue, but the highest activity of gamma-glutamyl amine synthetase was measured in the CNS. Our interest in these molecules stems from our previous observations which showed that they were synthesized and stored in, and released from, the efferent fibers to Limulus eyes which modulate the sensitivity of the eyes to light. Here we provide direct evidence for the release of the conjugates from Limulus eyes in response to depolarization, and that gamma-glutamyl octopamine can increase the sensitivity of the lateral eye to light. Our observations lend support to the hypothesis that gamma-glutamyl octopamine may serve as an intercellular messenger in the Limulus visual system.

Animals↗
PubMed1991

No influence of prejunctional alpha 2-adrenoceptors on the effects of nicotine and tyramine in guinea-pig atria.

1. Guinea-pig left atria were stimulated at a rate of 0.5 Hz and preloaded with 10 microCi 7-[3H]noradrenaline. In the presence of cocaine, 3 x 10(-6) mol l-1, and atropine, 10(-7) mol l-1, noradrenaline release was stimulated twice in each atrium, either by electrical field stimulation (one pulse, 0.2 ms 30 V, during each refractory period for 5 min) or by addition of either nicotine, 3 x 10(-5) mol l-1, or tyramine 10(-5) mol l-1. 2. The release of radioactivity caused by field stimulation and the associated positive inotropic effect were almost abolished by 3 x 10(-8) mol l-1 tetrodotoxin. Pretreatment with 3 x 10(-7) mol l-1 idazoxan increased the effects of field stimulation, while they were attenuated in the presence of clonidine, 3 x 10(-7) mol l-1. 3. The inotropic effect and the release of radioactivity caused by nicotine were greatly attenuated by tetrodotoxin, but were not significantly influenced by idazoxan or clonidine. 4. The release of radioactivity caused by tyramine and the inotropic effect of this drug were resistant to tetrodotoxin pretreatment and were not modified by idazoxan or clonidine. 5. It is concluded that nicotine releases noradrenaline by initiating a propagated action potential. But activation of prejunctional alpha 2-adrenoceptors does not seem to attenuate the transmitter release by limiting the spread of the action potential in the prejunctional sympathetic neuronal network.

Action Potentials↗
PubMed1971

Bretylium potentiation of the contractor responses of isolated rabbit aortic strips to potassium and tyramine.

1. Pretreatment of rabbit aortic strips with bretylium potentiated the contractor response to potassium and tyramine but not to noradrenaline. On the other hand, such pretreatment inhibited the response to nicotine.2. Even in reserpinized or cold stored aortic strips, pretreatment with bretylium enhanced the contractor response to potassium and tyramine.3. Pretreatment of fresh, reserpinized, or cold stored aortic strips with pheniprazine potentiated the contractor response to potassium and tyramine.4. Pretreatment of aortic strips with bretylium or pheniprazine did not potentiate the response to 5-hydroxytryptamine (5-HT).5. The results indicate that both bretylium and pheniprazine potentiate the action of tyramine and potassium, not by presynaptic mechanisms, but by postsynaptic action, causing an increase in the sensitivity of the effector cells to the stimulants.

Animals↗
PubMed1973

Interaction between tyramine and iproniazid on guinea-pig atria.

The inhibition of monoamine oxidase (MAO) by iproniazid may be antagonized by large doses of tyramine as shown by the restoration, or otherwise, of inotropic responses to tyramine in isolated atria from guinea-pigs that had been treated with reserpine.

Animals↗
PubMed1983

Tyramine-induced noradrenaline release from rat brain slices: prevention by (-)-deprenyl.

Clorgyline (1 and 10 microM) and (+)-deprenyl (10 microM) both significantly potentiated the tyramine (100 microM)-induced release of [3H]-noradrenaline from rat cerebral cortex slices. (-)-Deprenyl (50 microM) significantly reduced it, while lower concentrations had no effect on noradrenaline release. However, in combination, 1 microM (-)-deprenyl blocked the release-facilitating action of 1 microM clorgyline, and 10 microM (-)-deprenyl that of 10 microM (+)-deprenyl. Low concentrations of (+)- and (-)-deprenyl (1 and 10 microM), both selectively inhibited phenylethylamine oxidation by monoamine oxidase B. Higher concentrations of (-)-deprenyl (20 and 50 microM) also inhibited 5-hydroxytryptamine oxidation by monoamine oxidase A. Clorgyline (1 and 10 microM) inhibited both enzymes. Thus, the effects of these drugs on noradrenaline-release cannot be explained solely in terms of irreversible inhibition of monoamine oxidase A and B, and other possible mechanisms are discussed. If the brain-slice model faithfully mirrors the sequence of events manifesting peripherally as the tyramine hypertensive response ('cheese effect'), then it is possible that low doses of (-)-deprenyl, administered with antidepressant monoamine oxidase inhibitors, can prevent this adverse reaction.

Animals↗
PubMed1982

Tyramine sensitivity in dietary migraine: a critical review.

The hypothesis that oral tyramine causes migraine headache in certain patients was proposed by Hanington in 1967. In all, there are 11 published reports that experimentally test the hypothesis. Six of these studies provide support for the hypothesis whereas the results of four studies are clearly not supportive. All of the supporting evidence was generated in one laboratory (Hanington). In an attempt to evaluate this conflicting evidence, a comparison was made of outcome measures, subject selection procedures, and various methodological differences. There were some anomalous findings, most notably that there were marked differences in "placebo" headaches elicited by lactose capsules from study to study. Further, methodological differences among the studies preclude direct comparisons of the results. Taking these differences into account, the tyramine hypothesis appears to have some validity. The implications of these findings were discussed.

Food Hypersensitivity↗
PubMed1981

The effects of cadmium ions on blood pressure, dopamine-beta-hydroxylase activity and on the responsiveness of in vivo preparations to sympathetic nerve stimulation, noradrenaline and tyramine.

Changes in sympathetic nervous function of the rat caused by acute and chronic treatment with cadmium ((Cd2+) have been studied in vivo by measurement of changes in blood pressure and plasma dopamine-beta-hydroxylase (DBH) activity. In anaesthetized animals, acute injection of Cd2+ (0.1-1 microM) caused an initial fall followed by a rise in both diastolic and systolic blood pressure, plasma DBH activity increased in a dose-dependent manner. Animals subjected to repeated treatment with Cd2+ (0.5, 1 microM) daily for 12 days became markedly hypertensive, the increases in the systolic pressure being greater than those seen in the diastolic pressure. In pithed animals the blood pressure responses of the treated animals to electrical stimulation of the lower sympathetic outflow (T10-L1) and tyramine injection (35, 70, 140 nmol kg-1) were markedly decreased, whilst responses to low doses of noradrenaline (NA) (7, 15, 30 nmol kg-1) were potentiated compared with untreated animals. In addition, plasma DBH activities following sympathetic outflow stimulation and tyramine administration were markedly increased and decreased respectively compared with untreated controls. The data suggest that a correlation exists between changes in sympathetic nervous function and the induction of hypertension caused by Cd2+.

Animals↗
PubMed1975

Identification and distribution of m-tyramine in the rat.

A procedure for the quantitative evaluation of m-tyramine in mammalian tissues is described. It involves isolation of the amine by ion-exchange chromatography, followed by conversion to the dansyl derivative, chromatographic separation, and quantitation by the mass spectrometric integrated ion current technique using an isotopically labelled internal standard. The concentrations of m-tyramine in some tissues of male Wistar rats were (mean plus or minus S.D., nanograms per gram): brain 0.32 plus or minus 0.03, heart 0.44 plus or minus 0.13, kidney 12.6 plus or minus 3.4, liver 0.27 plus or minus 0.04, lung 0.33 plus or minus 0.11, spleen 0.25 plus or minus 0.07, and blood 0.15 plus or minus 0.04.

Animals↗
PubMed1975

Contractile responses of canine isolated pulmonary lobar arteries and veins to norepinephrine, serotonin, and tyramine.

Isolated helical strips of canine intrapulmonary lobar arteries and veins (about 4 mm in diameter) undergo dose-related tension development when exposed to increasing concentrations (10(-8) - 10(-3) M) of norepinephrine (NE), serotonin or 5-hydroxytryptamine (5-HT) and tyramine (Tyr). Venous segments were generally more sensitive while the maximum tension development was greater in the arterial strips, probably owing to their greater thickness. Both strips were more sensitive to 5-HT than NE and only responded to Tyr at high concentrations. Norepinephrine and 5-HT were nearly equally efficacious, whereas Tyr was less so. Responses to the latter were slow to develop, exhibited tachyphylaxis, and were greatly inhibited by phentolamine (10(-8) M), an alpha-adrenergic blocker. Exposure to cocaine (10(-5) M) enhanced submaximal NE responses, inhibited Tyr contractions and had no consistent effect on 5-HT responses. Phentolamine (10(-8) M) was also found to inhibit NE responses without altering 5-HT probably acts on other receptors. Tyramine may, in part, act directly on alpha-adrenergic receptors but may also release NE from surviving adrenergic nerve terminals in the preparation. Cocaine inhibits this effect and potentiates responses to lower levels of NE, presumably by blocking NE uptake into nerve terminals although a post-junctional action cannot be excluded.

Animals↗
PubMed1987

Potentiating effect of tyramine on acetaldehyde-induced vasoconstriction in isolated dog mesenteric arteries.

The stainless steel cannula inserting method was used to investigate the effects of acetaldehyde on isolated and perfused dog mesenteric arteries. Acetaldehyde when intraluminally administered induced a marked vasoconstriction, but repetitive injections of acetaldehyde caused tachyphylaxis. Acetaldehyde-induced vasoconstrictions were blocked by bunazosin, an alpha-1 adrenoceptor antagonist. After tyramine treatment, the acetaldehyde-induced constriction was consistently restored temporarily. It is suggested that tyramine may induce a release of norepinephrine mostly from the vesicle to the neuronal cytosol, and acetaldehyde may cause a release of norepinephrine from the cytosol to the extracellular space in the isolated canine mesenteric artery.

Acetaldehyde↗
PubMed2000

Induction of N-hydroxycinnamoyltyramine synthesis and tyramine N-hydroxycinnamoyltransferase (THT) activity by wounding in maize leaves.

Both N-p-coumaroyl- and N-feruloyltyramine accumulated in response to wounding in leaf segments of maize. The amount of N-hydroxycinnamoyltyramines started to increase 3-6 h after wounding and peaked at 12 h. Thereafter, the amount of N-p-coumaroyltyramine decreased rapidly, while the N-feruloyltyramine content remained at a high level. The accumulation of N-hydroxycinnamoyltyramines was accompanied by an increase in the tyramine N-hydroxycinnamoyltransferase (THT) activity. This increase was initially detected 3 h after wounding and reached a maximum at 36 h, the level of activity being 40 and 11 times that in the leaves before wounding and in the control leaves, respectively. Partial purification of THT from wounded leaves by (NH4)2SO4 precipitation and subsequent two steps of anion-exchange chromatography resulted in a 12.5-fold increase in specific activity. Kinetic studies with this partially purified enzyme revealed that the best substrates were tyramine and feruloyl-CoA, although tryptamine and sinapoyl-CoA also efficiently served as substrates. The apparent native molecular weight of the enzyme was determined by gel filtration as 40 kDa.

Acyltransferases↗