Effects Of Chlorpheniramine Research Articles

Effects of chlorpheniramine on emergence agitation after general anesthesia for ureteroscopic stone surgery: a retrospective cohort study.

BackgroundThe presence of a urinary catheter, postoperative pain, and postoperative nausea and vomiting are risk factors for emergence agitation (EA). Antimuscarinic agents are primary agents used in the prevention and treatment of urinary catheter-related bladder discomfort. Chlorpheniramine has antimuscarinic, antinociceptive, and antiemetic effects. This retrospective study investigated the role of chlorpheniramine in EA prevention following ureteroscopic stone surgery.MethodsOf 110 adult patients who underwent ureteroscopic stone surgery under general anesthesia between January and December 2019, the medical records of 93 patients were analyzed retrospectively. The patients were divided into control (n = 52) and chlorpheniramine (n = 41) groups according to the receipt of intravenous chlorpheniramine before the induction of anesthesia. The incidence and severity of EA were compared between the groups as primary and secondary endpoints, respectively. The effects of chlorpheniramine on the requirement for inhalation anesthetic (desflurane) during surgery, changes in mean blood pressure and heart rate during emergence, and adverse events were also compared.ResultsThe incidence (21.2% in the control group, 24.4% in the chlorpheniramine group) and severity of EA did not differ between groups. The intraoperative requirement for desflurane, changes in mean blood pressure and heart rate during emergence, and adverse events were also similar between groups.ConclusionsChlorpheniramine was not associated with a decrease in EA incidence or severity in patients who underwent ureteroscopic stone surgery.

Histamine H1 Receptor Antagonists Facilitate Electroacupuncture Analgesia.

This study investigated the influence of the histamine H1 receptor antagonists, chlorpheniramine (CHL) and pyrilamine, on the analgesic effects of acupuncture in mice. Nociceptive response was evaluated by the acetic acid-induced abdominal writhe test. Electroacupuncture (EA) at bilateral ST36 reduced the manifestations of acetic acid-induced abdominal writhing, whereas needle insertion without electrostimulation had no such effect. Notably, EA treatment was not associated with any analgesic effects in mice pretreated with naloxone. Low doses of CHL (0.6[Formula: see text]mg/kg; p.o.) or pyrilamine (2.5[Formula: see text]mg/kg; i.p.) as monotherapy did not affect acetic acid-induced abdominal writhing. However, when each agent was combined with EA, acetic acid-induced abdominal writhing was reduced by a greater extent when compared with EA alone. Interestingly, the effects of CHL on acupuncture analgesia were not completely reversed by naloxone treatment. Acetic acid induced increases of phospho-p38 expression in spinal cord, as determined by immunofluorescence staining and Western blot analysis. These effects were attenuated by EA at ST36 and by low doses of histamine H1 receptor antagonists, alone or in combination. Our findings show that relatively low doses of histamine H1 receptor antagonists facilitate EA analgesia via non-opioid receptors. These results suggest a useful strategy for increasing the efficacy of EA analgesia in a clinical situation.

Effects of selective histamine receptor antagonists on skin responses to intradermal bradykinin in healthy volunteers

The effects of chlorpheniramine and cimetidine on the cutaneous responses to intradermal injections of bradykinin were investigated in a randomized, double-blind, placebo-controlled, cross-over study. Chlorpheniramine significantly attenuated the increase in cutaneous blood flow and erythema induced by bradykinin but not the weal response. Cimetidine was without influence on these parameters and the effects of the combined therapy of chlorpheniramine and cimetidine were not significantly different from those due to chlorpheniramine alone. These results suggest that the cutaneous vasodilator effect of bradykinin is in part due to histamine release acting on histamine H1-receptors.

Chlorpheniramine exerts anxiolytic-like effects and activates prefrontal 5-HT systems in mice

The traditional antihistamine chlorpheniramine ameliorates panic attacks, phobias, and lowered mood, and this therapeutic effect is independent of the blockade of histamine H(1) receptors. Since chlorpheniramine inhibits the reuptake of serotonin (5-HT), the anxiolytic-like effect of chlorpheniramine may be produced by an increase in serotonergic function. To elucidate the mechanisms underlying the anxiolytic-like effects of chlorpheniramine in mice, we examined the involvement of 5-HT systems in the prefrontal cortex that is a crucial region in the regulation of emotional function. Chlorpheniramine (0.05-5 mg/kg, i.p.) dose-dependently and significantly decreased the duration of freezing behavior in both the elevated open-platform and conditioned fear tests. The anti-freezing effects of chlorpheniramine (5 mg/kg, i.p.) in these tests were inhibited by pretreatment with the non-selective antagonist at 5-HT receptors, methiothepin (0.01 mg/kg, s.c.). In addition, the local injection of chlorpheniramine (10-100 ng/mouse) and 5-HT (1-10 μg/mouse) into the medial part of the prefrontal cortex (mPFC) dose-dependently and significantly decreased the duration of freezing behavior in the elevated open-platform test. In a microdialysis study, chlorpheniramine (0.5 and 5 mg/kg, i.p.) dose-dependently and significantly increased the extracellular 5-HT level in the mPFC. In addition, the local perfusion of chlorpheniramine (10 and 30 μM), but not of the selective H1 receptor antagonist, cetirizine, into the mPFC markedly increased the extracellular 5-HT level in the mPFC. The anxiolytic-like effect of chlorpheniramine is produced, at least in part, by the facilitation of serotonergic neurotransmission in the PFC.

Effects of Chlorpheniramine and Ranitidine on the Visceral Nociception Induced by Acetic Acid in Rats: Role of Opioid System

In this study, effects of chlorpheniramine (H1-receptor blocker), ranitidine (H2-receptor blocker), morphine (an opioid agonist) and naloxone (an opioid antagonist) in separate and combined treatments were investigated on the visceral nociception in rats. Visceral nociception was induced by intraperitoneal injection of acetic acid (1 mL, 1%). The latency time to the beginning of the first abdominal wall contraction (first writhe) was measured and the numbers of writhes were counted for 1 h after acetic acid injection. Intraperitoneal injections of chlorpheniramine and ranitidine significantly (p < 0.05) increased the latency time to the beginning of the first writhe and also significantly (p < 0.05) decreased the numbers of writhes. The same results were obtained after subcutaneous injection of morphine. Subcutaneous injection of naloxone did not change the intensity of visceral nociception, but significantly (p < 0.05) prevented the morphine-induced antinociception. Intraperitoneal injection of chlorpheniramine significantly (p < 0.05) enhanced the morphine-induced analgesia, but did not reverse the effect of naloxone on nociceptive responses. Intraperitoneal injection of ranitidine, with no effect on the morphine-induced antinociception, significantly (p < 0.05) reversed the effect of naloxone on pain responses. These results suggest that both chlorpheniramine and ranitidine exert antinociceptive effect in the visceral nociception. In addition, morphine through a naloxone-dependent mechanism produces visceral antinociception. Moreover, the endogenous opioid system may participate in the chlorpheniramine- but not in the ranitidine-induced antinociception.

Effects of Chlorpheniramine and l-histidine on vestibular compensation in goldfish, Carassius auratus

Histamine is thought to be involved in the recovery of vestibular function after damage to the vestibular receptors of the inner ear. This study evaluated the effects of post-operative treatment using Chlorpheniramine (H 1 histamine antagonist) and l-histidine, (a histaminergic precursor), after hemilabyrinthectomy in goldfish. In this lesion model, the unilateral removal of the labyrinth induces a transient postural imbalance in response to light. After the lesion, the animals were injected intraperitoneally, during 12 consecutive days, with Chlorpheniramine, l-histidine and saline. All the substances were administered in a volume of 1 ml/kg body weight. Another group, which served as a non-lesion control, did not receive hemilabyrinthectomy or systemic injections. Chlorpheniramine accelerated the functional recovery when compared with that of the saline group. These data suggest that the inhibition of the histaminergic system facilitates the functional recovery in goldfish.

The H1-receptor antagonist dextro-chlorpheniramine impairs selective auditory attention in the absence of subjective awareness of this impairment.

Although previous studies have shown that the human attention system is partially affected by chlorpheniramine, the effects of chlorpheniramine on human auditory selective attention have not yet been explored. This study examines the effects of a single dose of 4 mg of dextro-chlorpheniramine on human auditory selective attention by means of the evaluation of the event-related brain potential (ERP) processing negativity (PN). The study sample consisted of 20 healthy male humans, who received either a single 4-mg dose of dextro-chlorpheniramine or a placebo in a double-blind design. The subjects were given a dichotic listening task, in which they were instructed to press a response button upon detecting deviant tones (target) while their ERPs were recorded. In parallel, subjective tests evaluated the daytime sleepiness, overall vigor, and affect of the subjects. Results showed that the auditory selective attention is impaired under the effects of chlorpheniramine, as reflected by an attenuation of PN amplitude and by a decrease of performance in the group of subjects who took a single 4-mg dose of dextro-chlorpheniramine. No subjective change in the daytime sleepiness, overall vigor, or affect of the subjects was observed. This lack of conscious awareness of the side effects may lead to situations of risk in tasks for which auditory information is important, because no subjective indicators of attention impairment are available to the subjects.

Effects of antihistamines on 3, 4-methylenedioxymethamphetamine-induced depletion of serotonin in rats.

This study investigated the effects of chlorpheniramine (CPA, 10-25 mg/kg), diphenhydramine (DIPH, 20 mg/kg), tripelennamine (TRIP, 20 mg/kg), and pyrilamine (PYRI, 20 mg/kg) on 3, 4-methylenedioxymethamphetamine (MDMA, 20 mg/kg x 2)-induced hyperthermia and depletion of indoles in rat brains, on the uptake of serotonin and dopamine into rat synaptosomes, on the binding affinity of CPA for biogenic amine transporters in the synaptosomes of rat brain, and on the scavenging hydroxyl free radicals activity. Rats were treated with two injections of MDMA, CPA, DIPH, TRIP, PYRI, and saline, alone or in combination of MDMA with one of the antihistamines, 6 h apart and sacrificed 5 days later. Rectal temperature was measured prior to and hourly following the drug injections for 13 h. As compared to saline controls, MDMA increased body temperature and decreased levels of indoles, measured by HPLC, in several brain regions of rats. CPA attenuated and DIPH had no effect on MDMA-induced hyperthermia, yet both attenuated the depletion of indoles, whereas PYRI and TRIP potentiated these effects. CPA inhibited the binding of [(3)H]paroxetine and [(3)H]nisoxetine to the synaptosomes of cerebral cortex and of [(3)H]win 35,428 to the synaptosomes of striatum. CPA, DIPH, TRIP, and PYRI inhibited [(3)H]serotonin uptake. CPA, PYRI, and TRIP, but not DIPH, scavenge hydroxyl radicals. Possible mechanisms of the different effects of the antihistamines on MDMA-induced hyperthermia and depletion of serotonin are discussed. Published 1999 Wiley-Liss, Inc.

Effects of antihistamines on fenfluramine-induced depletion of indoles in the brain of rats.

Various effects of chlorpheniramine (CPA), diphenhydramine (DIPH), tripelennamine (TRIP), and pyrilamine (PYRI) on fenfluramine (FEN)-induced depletion of serotonin in the brain of rats were observed to be dependent on body temperature. Levels of 5-HT and 5-HIAA in the frontal cortex, hippocampus, and striatum of rats treated with FEN (10 mg/kg, once or twice daily x 4 days) decreased to approximately 30% (P < 0.01) that of controls with no significant changes after CPA, DIPH, TRIP, and PYRI. Treatment with FEN plus CPA (5, 10, 20 mg/kg) and FEN plus DIPH (20 mg/kg), but not FEN plus TRIP (20 mg/kg) and FEN plus PYRI (20 mg/kg), increased brain serotonin levels 2- to 3-fold more than those treated with FEN plus saline. Treatment with FEN plus CPA and FEN plus DIPH, but not FEN plus TRIP and FEN plus PYRI, decreased rectal temperature with no significant change after FEN. The antihistamines alone decreased temperature at a 1-hour period and enhanced FEN-induced reduction in body weight. Possible mechanisms of the different effects of antihistamines on FEN-induced depletion of serotonin are discussed.

Effects of epinastine on the antitussive and rewarding effects of dihydrocodeine in mice.

The effects of chlorpheniramine and epinastine on dihydrocodeine were examined in mice. Orally administered dihydrocodeine (3-30 mg/kg) dose-dependently inhibited the number of capsaicin-induced coughs. The dose-dependent antitussive effects of dihydrocodeine were enhanced by each corresponding dose of chlorpheniramine or epinastine delivered at a ratio generally similar to that found in over-the-counter antitussive preparations (dihydrocodeine:histamine H1 antagonist = 3:1). The ED50 value of dihydrocodeine in combination with chlorpheniramine was nearly the same as that for dihydrocodeine in combination with epinastine. On the other hand, while combination treatment with dihydrocodeine (3 mg/kg i.p.) and chlorpheniramine (1 mg/kg s.c.) significantly potentiated place preference, no potentiation was observed with the combination of dihydrocodeine (3 mg/kg i.p.) and epinastine (1 mg/kg s.c.). These results suggest that epinastine may be a useful constituent opioid-containing antitussive preparation that would not enhance the potential for psychological dependence.

A STUDY ON TREATMENT OF CHRONIC IDIOPATHIC URTICARIA WITH CETIRIZINE

In a prospective study a comparison has been made between the clinical efficacy and safety of cetirizine, a third generation H1 receptor antagonist with chlorpheniramine and cyprohepatadine, the most widely used antithistamines in the treatment of chronic idiopathic urticaria. One hundred and five patients with chronic idiopathic urticaria were studied where the effects of chlorpheniramine, 4 mg and cyproheptadine, 4 mg administered twice daily were compared with cetirizine, 10 mg given once daily for 4 weeks or earlier till the relief of symptoms and regression of lesions. Local therapy consisted of calamine lotion in all cases. Out of 35 patients receiving chlorpheniramine excellent response was achieved in 9 (25.7%) cases by subjective evaluation (SE) and 11 (31.4%) by objective evaluation (OE). Out of 35 cases, 7 (20%) and 10 (28.5%) cases treated with cyproheptadine have shown excellent response by SE and OE respectively. Out of 35 patients taking cetirizine 25 (71.4%) had shown excellent response by SE and 22 (62.8%) cases by OE. Drowsiness was an important side effect observed in 19 (54.2%) cases receiving chlorpheniramine, 22 (62.8%) patients taking cyproheptadine and 1 (2.8%) case getting cetirizine. These results suggest that cetirizine has got superior antiallergic activity than chlorpheniramine and cyproheptadine in the treatment of chronic idiopathic urticaria.

Inhibitory effects of chlorpheniramine and astemizolum on contraction of isolated rat and rabbit uteri induced by oxytocin and PGF2 alpha.

The contraction of isolated rat and rabbit uteri induced by oxytocin and PGF2 alpha was markedly inhibited by chlorpheniramine (Chl) and astemizolum (Ast), both of which also decreased the resting tension of uteri, and their spontaneous contraction. The inhibitory effects of both drugs were dose-dependent. At high concentrations, Chl 7.4 x 10(-4) mol/L and Ast 10(-4) mol/L could counteract the contraction of the uteri induced by Oxy and PGF2 alpha, and their spontaneous contraction as well. They decreased the resting tension to the lower level. The mechanism of their non-special relaxed action on uteri could not be completely explained only by their H1-receptor blocking action. Whether they act by blocking calcium channel or by inhibiting calmodulin (CaM) remains to be further explored.

Psychomotor stimulant effects of the stereoisomers of chlorpheniramine

The behavioral effects of the histamine H1 antagonists d- and l-chlorpheniramine and of the H2 antagonist zolantidine were determined in squirrel monkeys responding under a fixed-interval (FI) 3-min schedule of stimulus-shock termination. Although d-chlorpheniramine is known to be much more potent than l-chlorpheniramine for antagonizing H1 receptor-mediated effects of histamine or displacing [3H]-mepyramine from histamine H1 receptors, similar doses of racemic chlorpheniramine and the d- and l-isomers (3.0-10.0 mg/kg) produced comparable increases in rates of responding. Zolantidine (1.0-17.0 mg/kg) did not alter or, at the highest dose, markedly decreased responding. These findings suggest that the psychomotor stimulant effects of chlorpheniramine involve actions other than the blockade of histamine H1 or H2 receptors. Selected H1 antagonists and cocaine are known to have comparable rate-increasing, reinforcing, and discriminative stimulus effects and, recently, the enantiomers of chlorpheniramine have been shown to displace [3H]-cocaine from binding sites in CNS with approximately equal potency. Possibly, such actions mediate behavioral effects common to H1 antagonists and cocaine.

Autoregulatory escape from norepinephrine infusion: roles of adenosine and histamine

Stimulation of sympathetic fibers or infusion of norepinephrine (NE) into the superior mesenteric artery (SMA) leads to an initial decrease in intestinal blood flow, which is followed by a return of flow toward the base-line value (autoregulatory escape) despite continued nerve stimulation or NE infusion. Although the mechanisms responsible for "autoregulatory escape" have not been defined, accumulation of vasodilator metabolites is frequently invoked to explain this phenomenon. Inasmuch as histamine and adenosine exist in high concentrations in the intestinal mucosa and both are potent vasodilators, we examined the effects of chlorpheniramine (an H1 blocker) and adenosine deaminase (degrades adenosine) on autoregulatory escape from NE infusion. In autoperfused piglet intestinal preparations, we measured SMA blood flow and the arteriovenous oxygen difference during intra-arterial NE infusion before and after blockade with chlorpheniramine or adenosine deaminase. Adenosine deaminase pretreatment increased the peak vasoconstrictor and reduced the steady-state escape responses to NE infusion. Chlorpheniramine did not affect either the vasoconstrictor or escape responses. The oxygen uptake changes induced by NE infusion were not dramatically modified by either treatment. These results indicate that adenosine but not histamine is responsible for at least part of the escape of intestinal blood flow from NE infusion.

The Effects of Chlorpheniramine and Antiallergic Drugs on Ascaris suum Antigen-Induced Active Cutaneous Anaphylaxis in Dogs

Effects of chlorpheniramine and two antiallergic drugs on the active cutaneous anaphylaxis (ACA) reaction induced by intradermal injection of Ascaris suum antigen in naturally sensitized dogs were investigated. Chlorpheniramine (10 mg/kg, intraduodenally (i.d.)) almost abolished the ACA reaction. NCO-650 (100 mg/kg, i.d.) had no inhibitory effect while tranilast (300 mg/kg, i.d.) showed a weak inhibitory effect. These findings show that (i) the ACA reaction is almost totally mediated by histamine and (ii) ACA reaction is considerably resistant to antiallergic drugs such as tranilast and NCO-650.

P4H0116) - Effects of chlorpheniramine and cimetidine on the disposition of histamine in the various tissues in active anaphylaxis

P4H0116) - Effects of chlorpheniramine and cimetidine on the disposition of histamine in the various tissues in active anaphylaxis

Histamine H1 receptor antagonists inhibit autoregulation of renal blood flow in the dog.

Histamine H1 and H2 receptors are present in the canine renal circulation. We have examined the effects of H1 and H2 receptor antagonists on autoregulation of renal blood flow in the dog. Renal arterial pressure was reduced in a step-wise fashion to 80 mm Hg by means of an adjustable aortic clamp positioned above the left renal artery. Infusion of H2 antagonists, cimetidine or ranitidine, into the left renal artery at 10(-5) mol/min had no effect on autoregulation of renal blood flow or on the reactive hyperemia that occurred when the aortic constriction was released. By contrast, intrarenal infusion of 10(-5) mol/min chlorpheniramine, an H1 receptor antagonist, reversibly attenuated reactive hyperemia and the ability of the kidney to autoregulate renal blood flow. Similar results were obtained with other, chemically dissimilar H1 antagonists (terfenadine, diphenhydramine, and pyrilamine). The effects of chlorpheniramine on autoregulation of glomerular filtration rate also were evaluated. Before chlorpheniramine was infused (at 10(-5) mol/min), the reduction of renal arterial pressure to 90 mm Hg had no effect on the glomerular filtration rate, whereas, during infusion of the H1 antagonist, the glomerular filtration rate fell significantly when renal arterial pressure was reduced to 90 mm Hg. Infusion of histamine (1 microgram/kg per min) with increasing amounts of cimetidine, chlorpheniramine, diphenhydramine, or pyrilamine resulted in virtually identical dose-dependent decreases in histamine-induced renal vasodilation. However, even with 10(-5) mol/min cimetidine or 10(-5) mol/min chlorpheniramine, diphenhydramine, or pyrilamine, a significant histamine-induced renal vasodilation was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of chlorpheniramine, pyrilamine and astemizole on intracranial self-stimulation in rats

Rats implanted in the lateral hypothalamus were used to assess lever pressing for brain stimulation. Lever pressing was increased dose-dependently by chlorpheniramine and decreased dose-dependently by pyrilamine. Astemizole, a new orally long-acting antihistamine did not affect self-stimulation. Evidence from pharmacological tests based on altered neurotransmitter functions suggests that the central anticholinergic activity of chlorpheniramine is probably responsible for the increased response rate, whereas the central dopamine receptor blocking activity of pyrilamine may be responsible for the decreased response rate. Astemizole is a specific antihistamine devoid of any central activity.

The bronchodilator effects of chlorpheniramine in childhood asthma

Significant improvement in lung function has been demonstrated following the inhalation of chlorpheniramine. The doses which were used caused local irritation and are probably unsuitable for routine clinical use. Nevertheless, we believe that antihistamines deserve further investigation in the treatment of childhood asthma.

Effects of Chlorpheniramine and Pyrilamine on the Atrial Actions of Acetylcholine, Tyramine, and Ephedrine

The experiments described herein were performed on isolated, spontaneously beating rabbit atria. The muscarinic actions of acetylcholine in the presence of physostigmine were antagonized by pyrilamine, chlorpheniramine and procaine which demonstrates that these drugs have an “antimuscarinic” action. The nicotinic (positive inotropic and chronotropic) actions of acetylcholine in the presence of atropine were also antagonized by pyrilamine and chlorpheniramine. Cocaine, pyrilamine, and chlorpheniramine inhibited the atrial stimulation by tyramine and ephedrine. The fact that the antimuscarinic and antinicotinic effects of pyrilamine and chlorpheniramine show similar slopes may indicate that similar receptors are involved. Cocaine and pyrilamine also have parallel slopes indicating that pyrilamine has a cocaine-like effect which is not related to local anesthesia.