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Results for “Histamine Agents”

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At least 19 recordsLinked to original sources
PubMed1979

Effects of histamine, of histidine and of anti-histaminic agents on the release of glucagon and insulin from the rat pancreas.

We have studied the effect of histamine (HA) and histidine (HIS) on the release of immunoreactive glucagon (IRG) and insulin (IRI) by isolated rat islets and pieces of pancreas. In isolated islets, HA and HIS stimulated IRG release at a glucose concentration of 3.0 mg/ml and IRI release at a glucose concentration of 0.5 mg/ml. In pieces of pancreas incubated in the presence of glucose (3.0 mg/ml), HA at a 2mM concentration stimulated IRG release and had no effect on the release of IRI; however, when the concentration of HA was doubled (4 mM), an inhibition of IRI release could also be demonstrated. HIS was ineffective. Perphenazine and dexchlorpheniramine, two anti-histaminic agents, inhibited IRG and stimulated IRI release. These results indicate that histamine, whether endogenous or exogenous, directly stimulated IRG and inhibits IRI release and suggest that some of the in vivo effects of histamine, such as hyperglycemia and lipid mobilization, may be mediated, at least in part, by these endocrinologic effects.

Animals↗
PubMed1997

Effects of histamine agents on methamphetamine-induced stereotyped behavior and behavioral sensitization in rats.

In this study, effects of histamine (HA) agents on methamphetamine (METH)-induced stereotyped behavior and behavioral sensitization were examined in rats. Pretreatment with a precursor of HA, L-histidine (750mg/kg), significantly inhibited the METH (3 mg/kg)-induced stereotyped behavior, whereas pretreatment with an inhibitor of HA synthesis, alpha-fluoromethylhistidine (FMH) (100 mg/kg), an H1 antagonist pyrilamine (5 mg/kg) or an H2 antagonist zolantidine (5 mg/kg) enhanced it. The inhibitory effect of L-histidine on METH-induced stereotyped behavior was significantly blocked by coadministration of pyrilamine and zolantidine, indicating that the effect is mediated through H1 and H2 receptors. Moreover, chronic treatment with METH (3 mg/kg) significantly enhanced stereotyped behavior at the rechallenge with METH (1 mg/kg). Chronic treatment with L-histidine (750 mg/kg) plus METH inhibited the METH-induced argumentation of stereotyped behavior, while that with FMH (100 mg/kg), pyrilamine (5 mg/kg) or zolantidine (5 mg/kg) potentiated it. These findings suggest that the HA neuron system has an inhibitory role in METH-induced stereotyped behavior and behavioral sensitization.

Animals↗
PubMed1998

[Clinical trial of a new topical anti-histamine agent histimet in the treatment of seasonal allergic rhinoconjunctivitis].

21 patients with seasonal allergic rhinoconjunctivitis (SAC) entered the trial of a new topical antihistamine drug histimet (levocabastine). The drug is available as a nasal spray and eye drops. The relief of the main symptoms of SAC occurred 15-20 min after histimet introduction into the nose or eye. The effect of a single procedure lasted for 12 hours. Regression of SAC basic symptoms continued for 7 days after using histimet. A significant improvement of life quality was observed. Good effect achieved in 90% of the patients characterizes histimet as an effective new modality in SAC management.

Administration, Topical↗
PubMed2001

Pharmacokinetics of emedastine difumarate, a new anti-histaminic agent in patients with renal impairment.

OBJECTIVE: Emedastine difumarate is a new H1 receptor antagonist with well defined pharmacokinetic and pharmacodynamic profiles in healthy volunteers. However, to date it is not known whether impaired renal function in patients with chronic renal insufficiency affects its pharmacokinetics and probably also its tolerability. Therefore, we here set out to compare the pharmacokinetics of emedastine difumarate in patients suffering from different degrees of renal failure with a control group of healthy volunteers. METHODS AND RESULTS: For this purpose we conducted an open, single-centre, comparative parallel group study in patients and healthy volunteers. Emedastine difumarate 2 mg was administered orally to the study population in single and seven repetitive doses twice daily (b.i.d.). Pharmacokinetics differed markedly between volunteers (n = 6) and patients (n = 17). The maximum serum concentration of emedastine (Cmax), area under the serum concentration-time curve, mean residence time and terminal disposition half-life were significantly higher in patients (P < 0.05), while time to reach Cmax and apparent volume of disposition were not statistically different after single and repeated (steady-state) oral administrations. Blood pressure and heart rate were also not affected by the study medication. CONCLUSION: The present study shows that impaired renal function alters the pharmacokinetics of emedastine in plasma. Thus, dose adjustment of emedastine difumarate is advisable in patients with impaired renal function.

Administration, Oral↗
PubMed1989

Response localization of the pharmacological agents histamine and salbutamol along the respiratory system by forced oscillations in asthmatic subjects.

The bronchodilating effect of 1 mg and 0.4 mg salbutamol on the impedance of the respiratory system was studied in 25 asthmatic subjects after histamine-induced bronchoconstriction. Histamine caused an increase of respiratory resistance (Rrs) at lower frequencies and a frequency dependence of Rrs. Respiratory reactance (Xrs) decreased at all frequencies after histamine challenge. These changes can be explained by peripheral airway obstruction. Impedance measurements performed 5 min after inhalation of 1 mg and 0.4 mg salbutamol showed a decrease of Rrs values at lower frequencies, a disappearance of the frequency dependence of Rrs, and a significant increase of Xrs values. No significant differences in absolute changes of Rrs and Xrs are observed between the salbutamol regimens. These changes after inhalation of salbutamol can be explained by supposing a predominant action on the peripheral airways.

Adult↗
PubMed2006

Histamine, a vasoactive agent with vascular disrupting potential, improves tumour response by enhancing local drug delivery.

Tumour necrosis factor (TNF)-based isolated limb perfusion (ILP) is an approved and registered treatment for sarcomas confined to the limbs in Europe since 1998, with limb salvage indexes of 76%. TNF improves drug distribution in solid tumours and secondarily destroys the tumour-associated vasculature (TAV). Here we explore the synergistic antitumour effect of another vasoactive agent, histamine (Hi), in doxorubicin (DXR)-based ILP and evaluate its antivascular effects on TAV. We used our well-established rat ILP model for in vivo studies looking at tumour response, drug distribution and effects on tumour vessels. In vitro studies explored drug interactions at cellular level on tumour cells (BN-175) and Human umbilical vein endothelial cells (HUVEC). There was a 17% partial response and a 50% arrest in tumour growth when Hi was combined to DXR, without important side effects, against 100% progressive disease with DXR alone and 29% arrest in tumour growth for Hi alone. Histology documented an increased DXR leakage in tumour tissue combined to a destruction of the TAV, when Hi was added to the ILP. In vitro no synergy between the drugs was observed. In conclusion, Hi is a vasoactive drug, targeting primarily the TAV and synergises with different chemotherapeutic agents.

Animals↗
PubMed1981

Gastrointestinal ulceration in the guinea pig in response to dimaprit, histamine, and H1- and H2-blocking agents.

Histamine is known to induce gastric ulcers in guinea pigs after intraperitoneal administration and duodenal ulcers after repeated intramuscular administrations. This study was undertaken to clarify further the differential role of H1 and H2 receptor sites in respect to gastric and duodenal ulcer in the guinea pig. Groups of guinea pigs were treated with histamine, intraperitoneal (1.81 mg/kg intraperitoneal) or intramuscular (0.09 mg/kg intramuscular X 8 doses); the selective H2 agonist dimaprit (0.09-0.18 mg/kg X 8 doses intramuscular or 1.81-3.62 mg/kg intraperitoneal); NaCl, 154 mM (control); and the selective H1 and H2 antagonists, diphenhydramine (125 mg/kg X 2 doses, intramuscular) or cimetidine (50 mg/kg X 3 doses, intramuscular). Gastric and duodenal lesions were evaluated and residual gastric contents were analyzed. The selective induction of gastric or duodenal ulceration by histamine was confirmed, and the H2 agonist, dimaprit, has been shown to be ulcerogenic to the guinea pig duodenum by intraperitoneal or intramuscular administration. Diphenhydramine produced considerably more protection against histamine-induced gastric ulceration (62% decrease in incidence), while cimetidine was particularly effective in the prevention of histamine-induced duodenal ulcer (64% decrease in incidence). A differential role of histamine in the pathogenesis of gastric as opposed to duodenal ulcer is suggested by the present findings.

Animals↗
PubMed1984

Studies on cutaneous vascular permeability in the rat: increases caused by histamine and histamine-like agents.

The pharmacology of histamine-induced increases in microvascular permeability has been studied in rat skin. Histamine caused dose-dependent increases in microvascular permeability, assessed as increases in extravascular albumin accumulation. The responses to histamine were inhibited in a dose-dependent manner by pretreatment with mepyramine and were not changed by cimetidine. 2-(2-Aminoethyl)pyridine also increased microvascular permeability whereas impromidine did not. These results suggest that H1-receptors and not H2-receptors are involved in the permeability response to histamine in rat skin. In contrast, dimaprit increased microvascular permeability and responses to dimaprit exceeded the maximum response to histamine. The response to dimaprit proved to be independent of H2 receptors and was consistent with an indirect response due to mast cell degranulation.

Animals↗
PubMed2004

Dual acting antihistaminergic agents.

Histamine is a primary mediator in allergic response and acts in concert with other agents to impact disease progression. Respiratory disorders such as asthma, rhinitis and dermatological conditions such as urticaria involve histamine along with other mediators. An antihistamine that possesses an additional property of counteracting the effects mediated by these other mediators should offer some therapeutic benefit over a selective antihistaminergic agent.

Animals↗
PubMed1984

Auranofin, an oral chrysotherapeutic agent, inhibits histamine release from human basophils.

The effect of auranofin, an oral chrysotherapeutic agent, on histamine release from human basophils was studied. Auranofin inhibited IgE-mediated, anti-IgE-induced histamine release in a dose-dependent fashion with a concentration of drug required to produce 50% inhibition of 1.3 micrograms/ml. This compound also inhibited calcium ionophore A23187 and 12-0-tetradecanoyl-phorbol-13-acetate-induced histamine release with a concentration of drug required to produce 50% inhibition of 1.7 micrograms/ml and 0.9 micrograms/ml, respectively. Auranofin was less active for formyl-L-methionyl-L-leucyl-L-phenylalanine-induced release of histamine with 32 +/- 10% (mean +/- SEM) inhibition at 2 micrograms/ml. Auranofin effects were reversible when leukocytes preincubated with auranofin was washed with buffer. In contrast, gold sodium thiomalate enhanced IgE-mediated histamine release, suggesting that these two compounds exert their actions at different levels. These results suggest that auranofin may be beneficial to patients with allergic diseases such as bronchial asthma.

Asthma↗
PubMed1976

Influence of histamine releasing agents on gastric acid secretion of isolated bullfrog gastric mucosa.

The influence of histamine releasing agents on gastric acid secretion was studied in isolated bullfrog gastric mucosa preparations. Maximum acid secretory responses in our preparations were obtained by stimulation with tetragastrin (5 X 10(-7) g/ml), histamine (1 X 10(-5) g/ml) and bethanechol (1 X 10(-6) g/ml). Compound 48/80 (1 X 10(-4) g/ml) showed a transient stimulatory action which was followed by a gradual depression of basal acid secretion. The stimulatory phase of compound 48/80 was completely antagonized by burimamide (1 X 10(-5) g/ml), a histamine H2-receptor antagonist. In gastric mucosa preincubated with compound 48/80, the secretagogue action of tetragastrin or bethanechol was not exerted, although this preparation continued to respond to histamine. The effects of Triton X-100, decylamine and polymixin B were quite similar to those of compound 48/80. After pretreatment with compound 48/80, the gastric mucosa preparation became refractory to the stimulatory action of compound 48/80 or Triton X-100. It is thus suggested that endogenous histamine may play an important role in the secretagogue action of tetragastrin and bethanechol.

Animals↗