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PubMed1991

Effects of antihistaminics on locomotor activity in mice. Comparison with opiate and amphetamine-induced hyperactivity.

1. Three histamine H1-receptor antagonists (tripelennamine, diphenhydramine and cyclizine) and two H2-receptor antagonists (ranitidine and cimetidine)--1 and 10 mg/kg--were tested alone or in combination with the opioid partial agonist buprenorphine (1 mg/kg), the opioid antagonist naloxone (1 mg/kg) or dextroamphetamine (3 mg/kg) on locomotor activity in mice. 2. All three H1-antihistaminics tested and the H2-antihistaminic, cimetidine, enhance locomotor activity in a dose-dependent manner. 3. Furthermore, tripelennamine, diphenhydramine, cyclizine, ranitidine and cimetidine potentiate the buprenorphine-induced hyperactivity. 4. Previous administration of naloxone blocks the tripelennamine- and diphenhydramine-induced hyperactivity. 5. On the other hand, none of antihistaminics tested modifies the amphetamine-induced locomotor stimulation. 6. These results suggest that H1- and H2-receptor antagonists effects on locomotor behavior in mice may be related with opioid mechanisms, but not with amphetamine mechanisms.

Animals↗
PubMed1999

Evaluation of the histamine H1-antagonist-induced place preference in rats.

The place preferences by some histamine H1 antagonists, such as tripelennamine, optical isomers of chlorpheniramine (dl-, d- and l-forms) and pyrilamine, in rats were evaluated with the conditioned place preference paradigm. In the present study, tripelennamine and all of the optical isomers of chlorpheniramine, but not pyrilamine, produced a significant place preference. The degree of the place preference induced by optical isomers of chlorpheniramine (6.0 mg/kg) did not correlate with the H1-antagonistic potency of these drugs, suggesting that H1-antagonist-induced place preferences are not mediated by H1-receptor blockade. The tripelennamine (3.0 mg/kg)- and dl-chlorpheniramine (6.0 mg/kg)-induced place preferences were completely abolished by pretreatment with the dopamine D1-receptor antagonist SCH23390 (0.05 mg/kg). Furthermore, the doses of H1 antagonists that induced a place preference significantly reduced the levels of DOPAC, which may be mediated by inhibition of dopamine uptake, in the limbic forebrain (including the nucleus accumbens and olfactory tubercle). These results suggest that some H1 antagonists induce rewarding effects, which may be mediated by the activation of dopamine D1 receptors, followed by the inhibition of dopamine uptake.

Animals↗
PubMed1990

H1- and H2-histamine receptor blockers and opiate analgesia in mice.

In this paper, the interactions between opiates and antihistaminic compounds, both H1- and H2-blockers, were studied. CD1 mice were used, treated with saline, morphine CHl (5 mg/kg), and 1 or 10 mg/kg of the H1-antihistaminics tripelennamine, chlorpheniramine, diphenhydramine and cyclizine and the H2-antihistaminics ranitidine and cimetidine, all compounds by s.c. route. Using the hot-plate test, it was observed that the two doses of tripelennamine and the higher doses of chlorpheniramine and cimetidine had antinociceptive activity. This increase on analgesia was also observed after chronic treatment with all H1-antihistaminics (10 mg/kg, 3 times daily for 4 days). When antihistaminics were administered with morphine, it was observed that only ranitidine (10 mg/kg) blocked opiate analgesia. On the other hand, previous administration of the opiate antagonist naloxone (1 mg/kg) blocked the antinociceptive action of tripelennamine and chlorpheniramine (10 mg/kg) in control mice. In morphine-dependent mice (by s.c. implantation of a 75-mg morphine pellet), a single injection of diphenhydramine or ranitidine blocked the analgesic action of morphine. Chronic administration of all antihistaminics did not modify morphine analgesia. These data are discussed in relation to the possible binding to the opioid receptors by antihistaminics and their facility in crossing the blood-brain barrier.

Analgesics↗
PubMed1978

Sustained release from inert wax matrixes I: drug-wax combinations.

The melting and energy characteristics of several drug-wax combinations were investigated using differential scanning calorimetry. The phase diagrams of binary mixtures of tripelennamine hydrochloride and tolazoline hydrochloride with carnauba wax and castor wax showed no eutectic formation and gave no indication that a significant interaction was involved. However, in tripelennamine mixtures, a slight depression in the drug melting point was observed at around 50% concentration. For ternary systems, i.e., drug, carnauba wax, and stearyl alcohol, thermograms of samples prepared by a fusion method differed slightly from those obtained with mixtures formulated by dissolving all ingredients in chloroform and evaporating the solvent. However, the location of the peak of each component remained essentially the same. A plot of melting point versus concentration of each compound showed insignificant changes in melting point and indicated that no interaction was occurring. The phase diagrams suggested that the combinations are strictly physical and that it is the physical characteristics, such as the hardness and composition of the core and drug particle size, that influence the release or dissolution of drug from the waxy matrix.

Chemistry, Pharmaceutical↗
PubMed1999

Role of endogenous serotonin and histamine in the pathogenesis of gastric mucosal lesions in unanaesthetised rats with a single treatment of compound 48/80, a mast cell degranulator.

In unanaethetised rats with a single injection of compound 48/80, a mast cell degranulator (0.75 mg kg-1, i.p.), gastric lesions occurred with increased serum serotonin and histamine levels and reduced gastric mucosal blood flow at 0.5 h after the injection and developed at 3 h. Pretreatment with either cyproheptadine (a serotonin and histamine antagonist) or methysergide (a serotonin antagonist) prevented the formation of gastric mucosal lesions with attenuation of reduced gastric mucosal blood flow at 0.5 h after compound 48/80 injection, while pretreatment with either amitriptyline (a selective inhibitor of histamine release from mast cells), tripelennamine (a histamine H1-receptor antagonist), famotidine (a histamine H2-receptor antagonist) or cimetidine (a histamine H2-receptor antagonist) had no effect. Pretreatment with either cyproheptadine, methysergide, amitriptyline or tripelennamine prevented the development of gastric mucosal lesions at 3 h after compound 48/80 injection, while pretreatment with either famotidine or cimetidine had no effect. These results indicate that in unanaesthetised rats with a single compound 48/80 treatment, acutely released endogenous serotonin causes gastric mucosal lesions, while released endogenous histamine mainly contributes to the lesion development and that gastric acid plays little role in the pathogenesis of the compound 48/80-induced acute gastric lesions.

Adrenergic Uptake Inhibitors↗
PubMed1986

Pathogenesis of compound 48/80-induced gastric lesions in rats.

Intraperitoneal administration of 0.75 mg/kg of compound 48/80 (a mast cell degranulator) once daily for four days induced extensive gastric lesions in rats. Oral administration of tripelennamine (histamine H1-receptor antagonist) and cimetidine (histamine H2-receptor antagonist) twice daily for four days had little or no effect on the lesion formation. Oral administration of methysergide and cyproheptadine (serotonin antagonists) and FPL-52694 (a mast cell stabilizer) potently inhibited the compound 48/80-induced lesions. Intraperitoneal administration of histamine plus serotonin, or serotonin alone, induced gastric lesions which resembled those induced by compound 48/80. These lesions were potently inhibited by methysergide and cyproheptadine, but not by tripelennamine, cimetidine, and FPL-52694. Single or repeated administration of compound 48/80 significantly increased serum histamine and serotonin levels. After a single administration of compound 48/80, the increased histamine levels rapidly returned to normal levels, but serotonin levels remained high for 7 hr. Histamine and serotonin levels in the gastric mucosa were transiently increased after a single administration of compound 48/80, but remained normal after repeated administration. Single or repeated administration of compound 48/80 had little effect on arterial blood pressure. The compound 48/80-induced gastric lesions appear to be caused primarily by the release of serotonin, but not histamine, from extragastric sources.

Animals↗
PubMed1985

Relative activities of three calcium channel antagonists on histamine, acetylcholine and antigen-induced contractions of guinea pig ileum.

The molar concentrations of verapamil, diltiazem, nifedipine, tripelennamine and atropine necessary to block histamine, acetylcholine (ACH) and ovalbumin-induced contractions of the isolated guinea pig ileum were compared. The calcium blockers inhibited ovalbumin contractions in previously sensitized ilea at lower concentrations than those required to block the phasic component of histamine and ACH contractions. These compounds were, however, more active in blocking the tonic phase of histamine and ACH concentrations than ovalbumin contractions. Tripelennamine was almost as active against ovalbumin contractions as it was against histamine concentrations, while atropine was inactive against ovalbumin. The results are interpreted as being supportive of continued efforts to develop calcium channel antagonists which selectively block the smooth muscle effects of inflammatory mediators.

Acetylcholine↗
PubMed1984

Gingiva as a site for xenobiotic metabolism in rats.

NADPH-dependent N-demethylation of aminopyrine and tripelennamine and hydroxylation of aniline, phenytoin and tripelennamine occurred in rat gingival homogenates. The metabolic profile in gingiva appeared to be similar to that in liver, the major organ in the body for the metabolism of these xenobiotics.

Aminopyrine↗
PubMed1985

Lethality of opioid and antihistaminic combinations in mice.

The lethality of morphine (37.5, 75, and 150 mg/kg) and tripelennamine (10,20,40 and 60 mg/kg), given alone and in combination, was evaluated in mice housed in groups of 16. When given alone, neither drug produced death at any dose. Combining the drugs produced supra-additive effects: some deaths occurred at all combination doses. The lethality of pentazocine (20, 40 and 80 mg/kg) and diphenhydramine (20, 40 and 80 mg/kg), given alone and in combination, also was evaluated. Neither drug alone produced death at any dose. Supra-additive effects were observed when the drugs were combined. These results are similar to earlier findings concerning the lethality of combinations of pentazocine and tripelennamine.

Animals↗
PubMed1998

Does histamine stimulate trigeminal nasal afferents?

The response to histamine of nasal afferents has been studied in guinea pigs by recording the electrical activity of the whole ethmoidal nerve (EN) or that of single units. Guinea pigs were anaesthetized with urethane and breathed through a tracheostomy. Prior to intranasal instillation of histamine (1 x 10(-4)-10(-1) M), the nasal mucosa was treated with 20 microl of saline (0.9% NaCl) or HCl (pH = 2), and in some cases, H2SO4 (pH = 2). In other experiments, following HCl instillation animals were pretreated by tripelennamine (1 x 10(-2) M) and/or cimetidine (1 x 10(-2) M) in order to determine the histamine receptor type of sensory nerve endings. Whole EN activity was not stimulated even by the highest dose (1 x 10(-1) M) of histamine when the nose was pretreated with saline, but was substantially stimulated by histamine in a dose-response fashion (1 x 10(-2) M) after pretreatment with HCI or H2SO4. Pretreatment with tripelennamine and HCl prevented the effect of histamine on the afferent EN activity; but after cimetidine and HCl pretreatment histamine still had a marked stimulant effect. In the case of single unit activities, histamine with HCl pretreatment had a long-lasting stimulatory effect (110.2 +/- 26.6 sec). It is concluded that the EN in guinea pigs include histamine-sensitive fibers whose sensitivity is mediated by H1 receptors and can respond to histamine only under abnormal conditions of the nasal mucosa.

Action Potentials↗
PubMed1998

The influence of an instruction on the stimulus effects of drugs in humans.

Participants discriminated between tripelennamine and placebo in experiments differing in instructional set. In 1 experiment (SED), participants were told that 1 of the 2 drugs was more sedative-like, and during the other (STIM), 1 was more stimulant-like. During generalization tests, participants received diazepam or d-amphetamine. Percent correct was the same in both experiments. Tripelennamine increased sedative and decreased stimulant effects. Amphetamine and diazepam produced typical subjective effects. Some subjective effects differed across experiments with more sedative and less stimulant effects during SED than STIM. In SED and STIM, capsules were labeled 80% of the time as a sedative and stimulant, respectively. Thus, instructions designed to give expectations had no effect on discrimination and only a few changes in subjective effects. When asked to name the drug that they believed they received, labels reflected instructional set.

Adult↗
PubMed1990

Effects of T's and blues abuse on pregnancy outcome and infant health status.

T's and blues (pentazocine and tripelennamine) abuse during pregnancy has been reported to be associated with adverse maternal and fetal effects. In this study, conducted at Parkland Memorial Hospital in Dallas, Texas, pregnancy outcome and health status of infants born to 23 T's and blues abusers were compared to a group of 100 unexposed women and their infants. Infants born to T's and blues abusers had significantly reduced birthweight, length, head circumference, and an increased frequency of major congenital anomalies (3 of 23), including two congenital cardiac anomalies. However, one of these cardiac anomalies occurred in the offspring of a woman who also reported moderate to heavy daily alcohol use during pregnancy. The other cardiac anomaly occurred in association with in utero anoxia. We therefore surmise that a known teratogen (alcohol) and perinatal complications caused two of the major anomalies, and not the pentazocine-tripelennamine combination per se.

Abnormalities, Drug-Induced↗
PubMed1994

Role of histamine in the intestinal flow response following mesenteric ischemia.

Sudden reperfusion of the gut following prolonged ischemia can itself have more deleterious consequences than the ischemia alone. Studies of vasodilator factors influencing the increased flow on reperfusion are therefore of importance. In the present study, a possible role of histamine in the postischemic flow response was examined after a period of total segmental ischemia. The artery supplying the terminal ileum was occluded in anesthetized dogs. Ischemia of 30 min duration was followed by a 30 min reperfusion period (control postischemic flow response), and the arterial blood flow to the segment was measured. After the control postischemic flow response, one of the following drugs was administered intravenously: histamine H1-or H2-blockers (tripelennamine, .5 mg/kg, cimetidine, 10 mg/kg, ranitidine, 2 mg/kg), cromolyn (a mast cell stabilizer, 25 mg/kg), and aminoguanidine (a diamine oxidase blocker, 50 mg/kg). The 30 min ischemia-30 min reperfusion cycle was then repeated (test postischemic flow response). A 30 min mesenteric ischemia-reperfusion period is reproducible once without a significant change in its hemodynamic parameters. The duration and volume of the postischemic flow response were significantly decreased by cimetidine, ranitidine, or cromolyn, and were increased by aminoguanidine. Tripelennamine did not affect the postischemic vasodilator response. At the onset of reperfusion, a release of endogenous histamine occurs from the gut, originating mainly from mast cells. It is proposed that histamine participates in the postischemic flow response through the H2-receptors.

Animals↗
PubMedDate not supplied

Effects of histamine receptor antagonism on adrenaline-induced changes in blood pressure in intact dogs.

This study was designed to test the hypothesis that histamine may contribute to the vasodepressor response which occurs in response to physiologic increments in adrenaline concentration in intact animals. Accordingly, following a control period of 30 min, adrenaline was infused intravenously for 45 min at a rate of 250 ng/kg per min in 14 anaesthetized dogs (Group I). A second group of eight dogs received an identical adrenaline infusion following complete H1- and H2-histamine receptor antagonism with tripelennamine plus cimetidine (Group II). A time control group of experiments, in which no drugs were infused, as well as groups receiving adrenaline plus either tripelennamine or cimetidine, were also performed. In Group I, adrenaline infusion increased heart rate and reduced mean arterial blood pressure by 10 mmHg (P less than 0.01). Following combined H1- and H2-histamine receptor antagonism (Group II), adrenaline infusion failed to reduce mean arterial blood pressure. However, mean arterial blood pressure was reduced significantly in the groups receiving adrenaline plus only one of the histamine receptor blocking agents. Since only the combined histamine receptor blockade completely eliminated the vasodepressor response to adrenaline, the data suggest that histamine may play a physiological role in the vasodepressor response to circulating adrenaline in the intact animal, and that both H1- and H2-histamine receptors may be involved.

Animals↗
PubMed1977

Histamine H1- and H2-receptor vasodilation of canine intestinal circulation.

Studies were conducted in anesthetized dogs to determine whether the mesenteric vasodilator response to histamine is mediated by H1 receptors alone or whether H2 receptors are also involved in the response. Evidence favoring a role for both receptors included: 1) the vasodilator response to histamine was inhibited by either the H1-receptor antagonist, tripelennamine, or the H2-receptor antagonist, metiamide; 2) both the H1 agonist, 2-methylhistamine, and the H2 agonist, 4-methylhistamine, induced dilator responses in the mesenteric circulation; and 3) two temporal patterns of vasodilation could be distinguished, namely a transient spike and subsequent fade of blood flow (seen with either the H1 agonist or with histamine after H2-receptor blockade) and a sustained and stable increase in flow (seen with either the H2 agonist or with histamine after H1 blockade). Metiamide appeared to be a potent inhibitor of the mesenteric vasodilator response to histamine at least equal to tripelennamine.

Action Potentials↗
PubMed1980

Role of histamine H1- and H2-receptors in myoelectric activity of small bowel in the dog.

Studies were conducted in conscious dogs implanted with monopolar silver electrodes along the small intestine to determine whether the intestinal motility response to histamine is mediated by H1-receptors alone or whether H2-receptors are also involved in the response. Histamine infusion alone induced a marked increase in the appearance rate and the propagation velocity of the interdigestive myoelectric complexes (IMC). This effect was reproduced by the administration of the selective H1-receptor agonist, 2-methylhistamine, and abolished by the H1-receptor antagonist, tripelennamine. Tripelennamine alone decreased the frequency of occurrence of the IMC in fasted animals and reduced significantly the spike potential activity of the small bowel in fed dogs. Neither the H2-receptor agonist, dimaprit, nor the H2-receptor antagonist, metiamide, had any influence on the motility patterns in fasted or fed animals. We conclude that histamine influences the patterns of small bowel motility via stimulation of H1-receptors but its physiological role in modulating intestinal motility remains to be determined.

Animals↗
PubMed1968

Mechanisms of reflex vasodilation: assessment of the role of neural reuptake of norepinephrine and release of histamine.

The mechanisms of reflex vasodilation were studied in an innervated canine hindlimb preparation which was perfused at a constant rate. Reflex vasodilation was produced by suddenly increasing the pressure in the trunk by the intravenous injection of norepinephrine, with consequent stimulation of the baroreceptors. When the basal vasoconstrictor tone exerted by the sympathetic nervous system on the systemic arterial bed was minimized, either by pretreatment with the alpha adrenergic blocking agent phenoxybenzamine or with reserpine, which depletes endogenous catecholamine stores, reflex vasodilation was virtually abolished. Administration of cocaine, a drug which blocks reuptake of norepinephrine by the nerve terminals, significantly reduced reflex vasodilation, the response after cocaine averaging 47% of the vasodilator response in the control period. Cocaine also potentiated the vasoconstriction caused by intra-arterially administered norepinephrine but attenuated the vasoconstriction induced by tyramine. The antihistamine, tripelennamine, had effects similar to those of cocaine. It is suggested, therefore, that reflex vasodilation results from a sudden decrease in the level of norepinephrine at the neuroeffector junction, which is a consequence of the cessation of norepinephrine secretion, together with continued and possibly augmented uptake. When the uptake mechanism is impaired, either by the administration of cocaine or tripelennamine, the magnitude of reflex vasodilation is diminished. It does not appear necessary to postulate active secretion of a vasodilator substance to account for reflex vasodilation.

Animals↗
PubMed1989

Stimulation of gastric alkaline secretion by histamine in rats: possible involvement of histamine H2-receptors and endogenous prostaglandins.

The mechanism of stimulatory action of histamine on gastric alkaline secretion was investigated in anesthetized rats. Intravenous infusion of histamine (2-8 mg/kg/hr) dose-dependently stimulated acid secretion and in the presence of omeprazole (60 mg/kg), an H+/K+-adenosine triphosphatase inhibitor, produced an increase of gastric but not duodenal alkaline secretion; the degree of gastric alkalinization was also dependent on the dose of histamine, reaching the maximal values of approximately 1.0 microEq/10 min. Cimetidine (100 mg/kg s.c.) significantly inhibited both acid and alkaline secretory responses caused by histamine, whereas indomethacin (5 mg/kg s.c.) significantly prevented the increased alkaline secretion caused by histamine as well as mucosal acidification (100 mM HCl for 10 min). Tripelennamine (10 mg/kg s.c.) had no effect on either acid or alkaline secretion. Histamine (8 mg/kg/hr) reduced the arterial blood pressure (25.3%) and increased the mucosal vascular permeability in the stomach as determined by Evans blue (160%), but these vascular responses were significantly prevented only by tripelennamine, excluding the possible contribution of the vascular effects to the increased gastric alkaline secretion. These results suggest that histamine may stimulate gastric alkaline secretion as well as acid secretion, and the mechanism of histamine-induced alkaline secretion may involve both endogenous prostaglandins and stimulation of H2-receptors.

Animals↗