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At least 1,243 records · Page 69Linked to original sources
PubMed1991

Participation of H1-receptors in histamine-induced contraction and relaxation of horse coronary artery in vitro.

The mechanisms of histamine-induced contraction and relaxation were investigated in rings isolated from a middle part of the left descending coronary arteries of horses. Intact and endothelium-denuded preparations were compared. Rings of horse coronary arteries contracted in response to histamine in a concentration dependent manner, but some of them relaxed with lower concentrations and contracted with higher concentrations. Removal of the endothelium abolished the relaxation and potentiated the contraction. The pD2 values were 4.70 +/- 0.08 in the rings with intact endothelium and 4.95 +/- 0.08 in endothelium-denuded rings. Histamine-induced contractions in intact and denuded preparations were not affected by an H2-antagonist, cimetidine, but were inhibited by an H1-antagonist, diphenhydramine in non-competitive manner in the rings with endothelium and in competitive manner in denuded rings. After precontraction with PGF2 alpha or norepinephrine, histamine relaxed preparations with intact endothelium (pD2 value, 7.80 +/- 0.11), although histamine-induced relaxations were not observed in denuded preparations. The relaxation was competitively inhibited by diphenhydramine. Relaxing response was significantly attenuated by methylene blue, quinacrine, L-nitro-arginine, gossypol and AA861 but not by indomethacin. These results suggest that the histamine-induced contraction and relaxation in horse coronary arteries are mediated mainly by H1-receptors in the smooth muscle and endothelium, respectively, and H1-receptor activation of endothelial cells may liberate vasodilator substances.

Animals↗
PubMed1984

Cimetidine-drug interactions.

The use of cimetidine, the histamine H2 receptor antagonist, is associated with a relatively low incidence of adverse reactions. However, its liberal use has led to the identification of several clinically significant cimetidine-drug interactions that can lead to drug accumulation, toxicity, and life-threatening sequelae. A review of the literature and the clinical significance and physiologic basis of these interactions are presented. Recommended management of cimetidine-drug interactions is discussed.

Adrenergic beta-Antagonists↗
PubMed1994

L-carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities.

Carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) are natural imidazole-containing compounds found in the non-protein fraction of mammalian tissues. Carcinine was synthesized by an original procedure and characterized. Both carnosine and carcinine (10-25 mM) are capable of inhibiting the catalysis of linoleic acid and phosphatidylcholine liposomal peroxidation (LPO) by the O2(-.)-dependent iron-ascorbate and lipid-peroxyl-radical-generating linoleic acid 13-monohydroperoxide (LOOH)-activated haemoglobin systems, as measured by thiobarbituric-acid-reactive substance. Carcinine and carnosine are good scavengers of OH. radicals, as detected by iron-dependent radical damage to the sugar deoxyribose. This suggests that carnosine and carcinine are able to scavenge free radicals or donate hydrogen ions. The iodometric, conjugated diene and t.l.c. assessments of lipid hydroperoxides (13-monohydroperoxide linoleic acid and phosphatidylcholine hydroperoxide) showed their efficient reduction and deactivation by carnosine and carcinine (10-25 mM) in the liberated and bound-to-artificial-bilayer states. This suggests that the peroxidase activity exceeded that susceptible to direct reduction with glutathione peroxidase. Imidazole, solutions of beta-alanine, or their mixtures with peptide moieties did not show antioxidant potential. Free L-histidine and especially histamine stimulated iron (II) salt-dependent LPO. Due to the combination of weak metal chelating (abolished by EDTA), OH. and lipid peroxyl radicals scavenging, reducing activities to liberated fatty acid and phospholipid hydroperoxides, carnosine and carcinine appear to be physiological antioxidants able to efficiently protect the lipid phase of biological membranes and aqueous environments.

Antioxidants↗
PubMed1991

Eicosanoid generation from antigen-primed mast cells by extracellular mammalian 14-kDa group II phospholipase A2.

The extracellular form of 14-kDa group II phospholipase A2 has been found to accumulate at various types of inflammatory sites. In the present paper, we have studied the possible role of the extracellular 14-kDa group II phospholipase A2 in the process of prostaglandin production in activated rat mast cells. When mast cells obtained from the peritoneal cavity of rats were sensitized with IgE, challenged with antigen and then exposed to extracellular 14-kDa group II phospholipase A2, appreciable release of prostaglandin D2 was observed. Generation of prostaglandin D2 was dependent on the concentration of the phospholipase A2 as well as that of the antigen, while no appreciable prostaglandin D2 generation was observed with cells in the absence of the antigen. No histamine release was observed under the same conditions. Phosphatidylcholine in mast cell membranes was appreciably hydrolyzed to liberate free arachidonic acid when mast cells were incubated with 14-kDa group II phospholipase A2 added exogenously in the presence of the antigen. Both the generation of prostaglandin D2 and the release of arachidonic acid were retarded by inhibitors specific to 14-kDa group II phospholipase A2. Thus, 14-kDa group II phospholipase A2 may function in the process of inflammation by acting on IgE-antigen-primed mast cells, which are not fully activated, to generate eicosanoids.

Animals↗
PubMed1985

Arachidonic acid release in rat peritoneal mast cells stimulated with antigen, ionophore A23187, and compound 48/80.

Rat peritoneal mast cells respond to various types of secretagogues, such as antigen (receptor-mediated), A23187 (calcium mobilizing), and compound 48/80 (membrane perturbing), and release arachidonic acid from membrane phospholipids prelabeled with [3H]arachidonate. The rate of arachidonic acid liberation varied from one stimulant to the other. Ionophore A23187 (0.1 micrograms/ml) appeared to be most potent in releasing arachidonate among the three stimulants at which doses each secretagogue caused almost equivalent histamine secretion. However, upon stimulation with these three secretagogues, the radioactivity of phosphatidylcholine (PC) was markedly reduced with a concomitant increase of arachidonate radioactivity. Hydrolysis of PC by phospholipase A2 is likely to be the major route of arachidonic acid liberation in either IgE-mediated or non-IgE activation in mast cells.

Animals↗
PubMed1980

[Neurotransmitters, neurohormones and prolactin].

After pointing out the reasons for undertaking the study of the regulation of prolactin secretion, the neuroendocrine mechanisms implicated in such secretion are discussed. Special attention is dedicated to the participation of chemical agents. Thus, the principal effects dealt with are: the net inhibition produced by dopamine and the less generalized inhibition effects of nicotine and somatostatin; the facilitatory action of serotoninergic pathways, TRH, histamine and endorphins. The dual effect described for GABA and noradrenaline, as well as some paradoxical actions, e.g., the antiserotoninergic and antihistaminergic H2 drugs which liberate prolactin in basal conditions but abolish the prolactin releasing effect of the respective agonist, or the immediate blocking effect of muscarinic agonists and antagonists are discussed. Finally, the possibility of a new mechanism of control at anterior pituitary receptors level is postulated.

Catecholamines↗
PubMed1981

Oxatomide protects against degranulation of rat peritoneal mast cells during in vitro challenge with antigen or compound 48/80. Ultrastructural aspects.

The ultrastructure of isolated rat peritoneal mast cells was evaluated after in vitro degranulation and treatment with oxatomide, a new anti-allergic compound. In a first series of experiments, mast cells of rats infected with Trichinella spiralis larvae were incubated with Trichinella larvae somatic antigen to produce histamine release. The release was visualized in the electron microscope by exocytosis of the peripheral amine-containing granules, which resulted from fusion between several perigranular membranes and fusion of these membranes with the plasma membrane. A more drastic degranulation was provoked in a second series by incubation of unsensitized mast cells in the presence of the amine liberator compound 48/80. This treatment led to a complete extrusion of the granules in most of the cells, while in a smaller number of cells, only large vacuoles containing remnants of several granules were seen. The plasma membrane of these cells however was intact and there were no signs of exocytosis. The effect of oxatomide against mast cell degranulation was dose-dependent and comparable for the two types of histamine release. After incubation with high doses (10(-4) M, 5.10(-5) M) granule liberation was rarely observed in antigen-challenged and compound 48/80-challenged cells. Protection was apparently situated at the level of the plasma membrane which seemed to be unable to fuse with the perigranular membranes while fusion of perigranular membranes of individual granules was still possible. None of the tested concentrations of oxatomide induced spontaneous degranulation. High doses, however, led in a number of cells to some ultrastructural alterations such as partial disappearance of plasmalemmal folds, slight cytoplasmic oedema and the appearance of intranuclear microtubules. The latter were also seen in oxatomide-treated challenged mast cells.

Animals↗
PubMed1995

Preliminary studies on the inflammatory actions of the venoms of some Australian spiders.

Experiments were performed using an anaesthetised rat model to investigate the local inflammatory responses produced by intradermal injections of crude venom gland extracts from a number of Australian spiders, namely, Phonognatha graeffei, Delena cancerides, Isopeda montana, Badumna insignis, Lampona cylindrata, Steatoda grossa, S. capensis Hann. All of the venom gland extracts tested, with the exception of that from S. capensis, produced increases in vascular permeability consistent with acute inflammatory responses. The responses primarily involved the activation of 5-HT receptors, since they were markedly reduced by the nonselective 5-HT1/5-HT2-receptor antagonist methiothepin. Some of the venoms caused liberation of endogenous mediators of inflammation, and some had components that acted directly on the vasculature to increase vascular permeability. Histamine appeared to have little if any role in the observed increases in vascular permeability following intradermal injection of the spider venoms.

Anesthesia↗
PubMed1981

Release of platelet-activating factor (PAF) and histamine. II. The cellular origin of human PAF: monocytes, polymorphonuclear neutrophils and basophils.

The origin of platelet activating factor (PAF) from human leucocytes was investigated. Purified monocytes release PAF passively at pH 10.6, when challenged with Ionophore A 23187 or under phagocytic stimuli. Pure preparations of polymorphonuclear neutrophils liberate PAF passively, when challenged with C5a, neutrophil cationic proteins (CP), their carboxypeptidase B derived products (C5a des Arg, CP des Arg) or under phagocytic stimuli. Basophil rich buffy coat cells release PAF when challenged with C5a, CP, anti-IgE (in low amount) or Synacthen concomitantly with basophil degranulation and histamine release. Electron microscopy studies, carried out on Synacthen-stimulated basophil rich buffy coat, provide morphological evidence for platelet-basophil interaction. In conclusion our data demonstrate that PAF can be released from different leucocyte populations. However, the stimuli able to trigger such release appear to have some specificity for the cell target.

Antigen-Antibody Complex↗
PubMed1977

Liberation of endogenous compounds by tolazoline.

The anomalous cardiac stimulation by tolazoline (2-benzyl-2-imidazoline), and alpha-adrenergic blocking agent, appears to result from the release of histamine and catecholamines. These responses can be blocked by metiamide and propranolol, respectively. It is probably that tolazoline also releases acetylcholine from the guinea pig atria. The direct effect of tolazoline on chronotropic activity of atrial pairs after blockade appears to be depressant at high concentrations, and this decrease in rate, below control levels, is not blocked by atropine.

Animals↗
PubMed1996

[Importance of the leukotriene C4 liberation test for the diagnosis of drug allergy (preliminary results)].

Pharmacological or immunological activation of human basophil induces the expression of membrane markers such as CD63 and the release of histamine and leukotriene C4 (LTC4). LTC4 release test has the advantages of a cellular test which is obviously closer to the physio-pathological reaction than the direct determination of circulating antibodies. Moreover, the determination of a newly formed mediator eliminates the spontaneous release of mediator by simple cellular damage. We present here, after having controlled the reliability of the method for aero-allergens, preliminary results of LTC4 release obtained for haptens (ampicillin, methylprednisolone and acetylsalicylic acid) which are in favour of the use of this method in the complex field of drug allergy diagnosis.

Adult↗