Histamine tele-methylhistamine ratios in rat blood as a function of time after i.v. injection of compound 48/80 or histamine

Irman-Florjanc, T.; Erjavec, F.

doi:10.1007/bf01997383

Cited by 8 publications

(5 citation statements)

References 6 publications

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“…However, one possible answer may lie in the fol lowing fact: fairly high histamine concentrations were de tected in the plasma of this species, suggesting that the peritoneal mast cells are always exposed to histamine at high concentrations in vivo. The levels of histamine in the rat plasma in this paper were approximately 5 times higher than those reported previously (17). Therefore, the assay of histamine in the respective plasmas from 3 groups consisting of 10 to 15 rats/group was further car ried out, but the histamine concentrations of each group were similar to the mean±S.E.…”

Section: Histamine Levels In Rat Plasmascontrasting

confidence: 45%

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

Kohno

Nakao

Ogawa

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 pM and enhanced by a 20 to 30-min treatment with thioperamide (H3-antagonist) at 3 pM with significance, but little affected by mepyramine (H,-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 106 mast cells/ml. At a low concentration of mast cells (104 mast cells/ml), (R)-a-methylhistamine (a-MH), an H3-agonist, at 0.9-90 pM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by a-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also a-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells. In the early 1980s, a third receptor of histamine was identified, which regulates the synthesis and release of histamine in the histaminergic nerve ends in the rat brain, and this was designated as the H3-receptor (1).Since then, the development of specific and selective agonists and antagonists of histamine receptor subtypes has revealed that H3-receptors exist in other tissues in cluding the ileum (2), airway (3, 4) and blood vessels (5); this was concluded from the observations that the neural stimulation-induced twitch responses of these tissues are inhibited by modulation of ACh, neuropeptides and other neurotransmitter release by H3-receptor stimula tion, in a similar manner to that of the rat cerebral cortex. Thus, the majority of the investigations on H3-receptors were initially focused on the modulation of neurotrans mitter release and/or histamine synthesis in the presynap tic ends of the brain or other tissues. In addition, there have recently been a number of reports on the roles of the receptor in effector organs: H3-receptor stimulation relaxed rabbit middle cerebral artery preconstricted with K+ by acceleration of nitric oxide and prostacyclin forma tion from the endothelium (6, 7); an H3-antagonist aggra vated experimental allergic asthma in the guinea pig (8); an H3-agonist and H3-antagonist inhibited and enhanced, respectively, the histamine release from isolated gastric glands (9), and H3-receptor stimulation specifically down regulated histamine synthesis in isolated fundic mucosal cells (10) in rabbits; an H3-receptor agonist reduced gas trin-induced vascular histamine release in the isolated rat stomach (11).In the present study, we obtained evidence indicating that isolated rat peritoneal mast cells have surface H3 re...

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Section: Histamine Levels In Rat Plasmascontrasting

confidence: 45%

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

Kohno

Nakao

Ogawa

et al. 1994

Japanese Journal of Pharmacology

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“…Blood was collected from the right carotid artery before histamine injection and 2 and 4 min afterwards. Plasma was prepared as described previously [7]. …”

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confidence: 99%

Amitriptyline and citalopram inhibit histamine-induced cardiovascular effects in rats

Irman-Florjanc

Jochem

Żwirska-Korczala

2004

Inflammation Research

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IntroductionExogenous histamine, acting peripherally via H 1 and H 2 receptors, produces a decrease in mean arterial pressure (MAP). Similarly, administration of compound 48/80, which increases a release of endogenous histamine from mast cells, leads to circulatory depression and occurrence of ventricular arrhythmias in rats [1]. Previous studies demonstrate that plasma histamine concentrations, after injection of compound 48/80, can be lowered by pre-treatment with tricyclic antidepressants in rats [2]. Moreover, amitriptyline (AMI) and mirtazapine treatment also reduces peak plasma histamine level, which follows an intravenous (i. v.) administration of histamine in rats [3] and cats [4], respectively. In this study we examined cardiovascular responses and changes in plasma histamine concentrations after i. v. histamine injection in rats pre-treated with AMI and citalopram (CIT) which are representatives of two different classes of antidepressants. Materials and methodsStudies were carried out in male Wistar rats anaesthetised with ethylurethane (1.25 g/kg intraperitoneally [i. p.]) weighing 230 -260 g in accordance with EU directives. Arterial pressure and heart rate (HR) were measured using the pressure transducer RMN-201 (Temed, Inflamm. res. 53, Supplement 1 (2004) S97-S98 Poland) and the electrocardiograph Diascope 2 (Unitra Biazet, Poland), respectively [5,6]. The animals (n = 6) were treated i. v. with histamine (10 mg/kg) 15 min or 1 h after i.p. pre-treatment with AMI (2.7 mg/kg), CIT (1 mg/kg) or saline (0.5 ml). In the control groups, the rats were treated with saline (0.5 ml i. v.). The animals were monitored continuously for 2 h. Body temperature was maintained at 36.5 -37.5°C using a heating lamp throughout the experiment. All the studies were performed between 8.00 and 12.00.In a parallel study rats (n = 5 to 10) were treated as described above, and plasma histamine concentrations were measured spectrofluorometrically. Blood was collected from the right carotid artery before histamine injection and 2 and 4 min afterwards. Plasma was prepared as described previously [7]. Results and discussionThere were no differences in initial (before pre-treatment) MAP, pulse pressure (PP) and HR between the groups, the values being 86.63 ± 4.61 mmHg, 35.67 ± 7.08 mmHg and 346 ± 12 beats/min, respectively. In the saline pre-treated group, bolus injection of histamine transiently decreased MAP and PP by 47.25 % and 59.23 %, respectively, with no influence on HR.Pre-treatment with AM and CIT (given 15 min or 1 h before histamine) reduced histamine-induced influence on MAP and PP, and this effect was greater in AMI-than in CITtreated group (Table 1). There were no differences between Table 1. Basal (before treatment) and minimal mean arterial pressure (MAP) and pulse pressure (PP) values after histamine (10 mg/kg i. v.) injection and pre-treatment with amitriptyline (AMI; 2.7 mg/kg) and citalopram (CIT; 1 mg/kg) in rats. Results are mean ± SD; six animals per group; * p < 0.05 vs. saline-pre-treated histamine-injec...

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“…In one control group of rats, both compound 48/80 and TCA were omitted and in the second one, only TCA was omitted. Blood samples for plasma preparation [6] were collected from carotid artery 5 and 15 min after the injection of compound 48/80. Experiments were performed according to the regulations for work with experimental animals.…”

Section: Methodsmentioning

confidence: 99%

“…This latter effect is due to gradual distribution of compound 48/80 in the tissues [6]. TCA probably do not affect histamine metabolism [8].…”

Section: Inflammation Researchmentioning

confidence: 99%

“…It is possible that at least part of their anti-inflammatory action is due to the inhibition of histamine release and/or to changing the rate of its elimination from the site of inflammation. After administration of compound 48/80 in the rat there is an increase of blood histamine levels [6]. A lowering of such increase may serve as an indirect measure for the inhibition of histamine secretion from mast cells.…”

Section: Introductionmentioning

confidence: 99%

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Tricyclic antidepressants change plasma histamine kinetics after its secretion induced by compound 48/80 in the rat

Irman-Florjanc

Stanovnik

1998

Inflammation Research

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Histamine tele-methylhistamine ratios in rat blood as a function of time after i.v. injection of compound 48/80 or histamine

Cited by 8 publications

References 6 publications

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

Amitriptyline and citalopram inhibit histamine-induced cardiovascular effects in rats

Tricyclic antidepressants change plasma histamine kinetics after its secretion induced by compound 48/80 in the rat

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