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PubMed1978

The metabolism of a bronchodilator procaterol HCL in the rat in vitro and in vivo.

1. The metabolism of the bronchodilator, 5-(1-hydroxy-2-isopropylamino-butyl)-8-hydroxycarbostyril hydrochloride hemihydrate (procaterol HCl), has been studied in vitro and in vivo after oral and intravenous administration to rats. 2. The recovery of [14 C] procaterol HCl and its metabolites in 72 h was about 42% each in urine and faeces for an oral dose (30 mg/kg) and about 53% in urine and 33% in faeces for an intravenous dose (30 mg/kg). 3. Six metabolites in rat excreta were identified as procaterol glucuronide, 5-(2-amino-1-hydroxybutyl)-8-hydroxycarbostyril (desisopropylprocaterol), 5-formyl-8-hydroxycarbostyril (5-formyl-8-HCS), 8-hydroxycarbostyril (8-HCS), procaterol sulphate and unchanged procaterol. 4. In experiments in vitro, procaterol HCl was metabolized into desisopropylprocaterol, 5-formyl-8-HCS, and their conjugates, by rat liver 9000 g supernatant fraction, but not by preparations of kidney, lung and small intestine. Conjugation of procaterol HCl with glucuronic acid occurred in liver and small intestine preparations.

Amino Alcohols↗
PubMed1988

A comparison of oral procaterol and albuterol in reversible airflow obstruction.

The efficacy and safety of orally administered procaterol hydrochloride, a potent beta 2-adrenergic bronchodilator, was compared with that of albuterol in an eight-center, double-blind study conducted in 223 patients with mild to moderate, reversible bronchial airway obstruction. After a 1-wk placebo washout period, patients were administered either procaterol 0.05 mg twice daily for 2 wk followed by 0.10 mg twice daily for 10 wk or albuterol 2 mg three times a day for 2 wk followed by 4 mg three times a day for 10 wk. Spirometry determinations 1.5 h postdose showed consistently greater percent improvements from predose in FVC, FEV1, and FEF25-75 with procaterol than with albuterol at Weeks 1, 2, 4, 8, and 12. Treatment differences were statistically significant (alpha = 0.05) after 2 wk, 2 months, and 3 months of treatment. Bronchodilatation was evident 0.5 h after dosing and peaked at 1.5 to 3 h postdose for both treatments. The duration of action (i.e., time until spirometry determinations were lower than those at 0.5 h postdose) was at least 5 h after procaterol but only 3 h after albuterol. There was no evidence of tolerance with continued procaterol treatment, whereas a diminished duration of response to albuterol was observed with long-term treatment. Tremor was reported statistically more frequently in patients receiving procaterol than in those receiving albuterol (alpha = 0.05); the frequencies of other adverse events were similar for the two groups. No statistically significant treatment differences were noted for asthma symptoms, global evaluations, ECG results, vital signs, or clinical laboratory measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1988

The utility of a long-acting sympathomimetic agent, procaterol, for nocturnal asthma.

Patients with nocturnal asthma have their lowest pulmonary function and lowest serum epinephrine level at 4 to 6 AM. We studied a new long-acting beta-adrenergic agonist, procaterol, in ten patients with nocturnal asthma. The patients received 0.1 mg of procaterol one night and a placebo the other night in random order. Pulmonary function tests were performed every two hours from 10 PM to 8 AM. Pulmonary sounds were recorded using a modified stethoscope and were subsequently analyzed to estimate the proportion of time occupied by wheezing (est Tw/Ttot). The forced expiratory volume in one second (FEV1) while receiving the placebo and procaterol were similar at 10 PM (placebo, 1.35 +/- 0.18 L [mean +/- SE]; procaterol, 1.48 +/- 0.20 L); however, by 4 AM, the FEV1 had dropped significantly lower on the night with the placebo (1.01 +/- 0.14 L) than the night with procaterol (1.30 +/- 0.19 L; p less than 0.05). The est Tw/Ttot was similar at 12 AM for both nights, but at 4 AM, there was a significant increase in the est Tw/Ttot for the group with placebo but not the group with procaterol. The use of a long-acting beta-adrenergic sympathomimetic agent reversed the obstruction of the airways seen with nocturnal asthma.

Asthma↗
PubMed2004

[Beta 2-adrenoceptor polymorphism and effects of inhaled beta 2-stimulant (procaterol) and an anti-cholinergic drug (oxitropium) on the airway resistance].

It has been suggested that the Arg 16/Gly 16 allele at codon 16 of beta 2-adrenoceptor polymorphism plays a role in down-regulating the stimulus of bronchodilatation caused by beta 2-agonists. This study was designed to evaluate the difference of bronchodilator responsiveness to beta 2-agonist (procaterol) and anti-cholinergic drug (oxitropium) between those who have Arg 16/Gly 16 allele (hetero type) and those who have Gly 16/Gly 16 allele (variant type) at codon 16 of in healthy women. Airway resistance and other pulmonary function tests were measured by a body plethysmography before and 5, 10, 15, 20, and 30 minutes after inhalation of procaterol or inhalation of procaterol and oxitropium. In healthy women inhaled procaterol, percent changes of respiratory airway resistance compared with values before inhalation were -2.8 after 5 minutes, -7.5 after 10 minutes, -11.2 after 15 minutes, -15.4 after 20 minutes, and -12.6 after 30 minutes. In healthy women inhaled porcaterol and oxitropium, percent changes of respiratory airway resistance compared with values before inhalation were -14.5 after 5 minutes, -18.9 after 10 minutes, -17.0 after 15 minutes, -20.8 after 20 minutes, and -20.4 after 30 minutes. Patterns of decrease of respiratory airway resistance differed between women who have Arg 16/Gly 16 allele (hetero type) and those who have Gly 16/Gly 16 allele (variant type). In women who have Gly 16/Gly 16 allele (variant type), although acute decrease of respiratory airway resistance was observed, the duration of bronchodilator effect by inhaled procaterol and oxitropium was shorter than those observed in Arg 16/Gly 16 allele (hetero type). The present study showed inhalation of procaterol and oxitropium had a differential bronchodilator effect in healthy women, depending on their genotype of beta 2-adrenoceptor polymorphism at codon 16.

Administration, Inhalation↗
PubMed1992

Evaluation of procaterol and albuterol (salbutamol) aerosol in the treatment of asthma.

Procaterol aerosol (10 micrograms/inhalation) was compared to albuterol (salbutamol) aerosol (100 micrograms/inhalation), two inhalations t.i.d. or q.i.d., in 333 outpatients with reversible bronchial airway obstruction over a 12-week period in a double-blind randomized and parallel study. Predose and postdose pulmonary function tests (PFTs) were performed initially and after 2, 4, 8, and 12 weeks of therapy. Patients maintained a daily diary of asthma symptom scores. A significantly higher percentage of patients receiving procaterol (59%) continued therapy on a t.i.d. schedule rather than a q.i.d. schedule compared with patients receiving albuterol (48%, P less than .05). Pulmonary function tests indicated similar improvement in both groups. Clinically significant improvement in mean FEV1 was maintained for four to seven hours postdose for procaterol and for three to six hours for albuterol. Adverse experiences were reported in 15% of procaterol-treated patients and 17% of albuterol-treated patients. Headache and tremor were most frequent, with no significant differences in frequencies between groups. Both procaterol and albuterol were highly effective in improving pulmonary function and controlling symptoms of asthma; both were well tolerated. Procaterol had a longer duration of action, and more patients were controlled on a t.i.d. dosage regimen.

Adolescent↗
PubMed1985

Responses to the beta 2-selective agonist procaterol of vascular and atrial preparations with different functional beta-adrenoceptor populations.

Relaxant responses to the beta-adrenoceptor agonist, procaterol, have been examined on preparations of guinea-pig pulmonary artery (beta 2-adrenoceptors only), rat and rabbit pulmonary artery and rat aorta (beta 2 greater than beta 1), and these responses have been compared with responses of dog left circumflex coronary artery (beta 1 only). Low concentrations of procaterol (3 nM to 100 nM) relaxed KC1-contracted preparations of rat aorta and pulmonary artery from rat, rabbit and guinea-pig whereas high concentrations (greater than 1 microM) were required to relax preparations of the dog left circumflex coronary artery. The dissociation constant (KP value) for procaterol on beta 1-adrenoceptors was 4.9 microM (determined on dog coronary artery) and on beta 2-adrenoceptors was 0.008 microM (rabbit pulmonary artery). Procaterol therefore had a beta 2:beta 1 selectivity value of 612. KP values obtained on guinea-pig atria for procaterol, on which the concentration-response curve was biphasic, confirmed that both beta 2- and beta 1-adrenoceptors mediate responses of this tissue. The KP values were 0.009 microM (data from the first phase of the control concentration-response curve) and 3.5 microM (data from the concentration-response curve in the presence of the beta 2-selective antagonist, ICI 118,551, 10 nM). Data obtained on rat atria indicated that chronotropic responses of preparations from some rats, but not others, involved a minor population of beta 2-adrenoceptors, but the beta 2-adrenoceptors, when present, were less important than in guinea-pig atria. 6 Procaterol appears to be a particularly useful drug for detecting a functional population of beta 2-adrenoceptors in tissues, whether they are the minor or the predominant receptor sub-type present.

Adrenergic beta-Agonists↗
PubMed1988

Possible site of bronchodilation due to inhaled procaterol aerosol in asthmatic patients.

We studied the effective site of an inhaled aerosol of procaterol, a beta 2-selective adrenergic bronchodilator, in 8 asthmatic patients whose basal lung functions are almost within the normal range in both slow vital capacity (VC) and forced expiratory volume in one second (FEV1.0), and are free from asthmatic attack. In patients who had received procaterol 30 min after inhalation of aerosol, there was no significant change in VC, although FEV1.0, maximal expiratory flow at 50% VC (V50), maximal expiratory flow at 25% VC (V25) and maximal expiratory flow at 30% VC of partial maximal expiratory flow volume curve (V30p) improved significantly. On the other hand, in those who had received placebo, none of the parameters changed. Furthermore, R1 decreased and C0.5 increased significantly during the first 5 min after inhalation of procaterol aerosol. After an interval of 5 min, R1 did not change any further, while C0.5 continued to improve until 30 min after inhalation of procaterol. These results suggest that procaterol may first dilate the large airway and then may gradually dilate the small airway in bronchial asthma.

Adult↗
PubMed2006

Preferable inotropic action of procaterol, a potent bronchodilator, on impaired diaphragmatic contractility in an intraabdominal septic model.

Intraabdominal sepsis can lead to acute respiratory failure, and concomitant diaphragmatic dysfunction may be aggravated by sepsis-induced airway hyperreactivity. We previously reported that isoproterenol, a nonselective beta-adrenoceptor agonist, increased diaphragmatic contractility and accelerated recovery from fatigue during sepsis. The purpose of this study was to demonstrate the direct inotropic effect of a potent bronchodilator and beta(2)-selective adrenoceptor agonist, procaterol, on fatigued diaphragmatic contractility in an intraabdominal septic model. Rats were divided into two groups: a cecal ligation and perforation (CLP) group and a sham group. CLP was performed in the CLP group whereas laparotomy alone was performed in the sham group. The left hemidiaphragm was removed at 16 h after the operation. The diaphragmatic tissues were exposed to procaterol (10(-8)-10(-6) M), and muscle contractility was assessed. Intracellular cyclic AMP levels were also measured in the CLP model. Procaterol caused an upward shift in the force-frequency curves in the CLP group whereas it had no effect on the curves in the sham group. Procaterol significantly increased cyclic AMP levels in the CLP model. We conclude that the potent bronchodilator procaterol had a direct and positive inotropic effect on the diaphragm in an intraabdominal septic model.

Adrenergic beta-Antagonists↗
PubMed1985

A placebo-controlled trial of procaterol: a new long-acting oral beta 2-agonist in bronchial asthma.

Procaterol hydrochloride, a potent beta 2-adrenergic bronchodilator developed in Japan, was evaluated in a double-blind, placebo-controlled study for efficacy and safety in 45 patients (ages 18 to 55 yr) with chronic documented reversible airway disease. After a 1-week placebo washout period, patients were administered either 0.05 mg or 0.10 mg of procaterol or placebo twice daily for 2 wk. Spirometric determinations, vital signs, and ECGs were obtained at 1/2, 1, 2, 4, 6, and 8 hr after the first dose and at the same time intervals after 1 and 2 wk of treatment. Patients recorded on a daily basis peak flow rates, asthma symptoms, need for supplemental aerosol, concurrent medications, and side effects. Spirometry results indicated significant improvement in pulmonary function with both doses of procaterol compared with placebo (P less than 0.05). The larger dose was generally more effective. Bronchodilatation was evident 1/2 hr after dosing and peaked at 2 hr. At 8 hr after 0.10 mg of procaterol, FEV1 was still above predose values. Daily peak flow rates were significantly higher with 0.10 mg than with 0.05 mg (P less than 0.05) and placebo (P less than 0.001). Tremor and nervousness were the most frequent side effects. They occurred in a dose-related frequency, were mild and transient, and occurred early in treatment. No significant drug-related changes were noted in ECGs, heart rate, blood pressure, or clinical laboratory data. Procaterol was found to be an effective, well-tolerated oral bronchodilator with a long duration of action, especially at 0.10 mg twice daily.

Adolescent↗
PubMed1983

New pharmacological aspects of the bronchodilating activity of procaterol.

The selectivity of procaterol for beta 2-adrenoceptors vs beta 1-adrenoceptors in animals has been already described. In these studies the ability of procaterol to protect guinea-pig against bronchoconstriction induced by various spasmogens such as histamine, LTC4 and acetylcholine is demonstrated. The results obtained both in anaesthetized animals and in perfused lungs clearly show that procaterol antagonizes not only the direct effect of the bronchoconstrictors quoted above but also their ability to activate arachidonic acid metabolism and to augment the generation of TXA2. Procaterol (0, 3-3 micrograms/Kg i.v.) is more potent than salbutamol in protecting passively sensitized guinea-pig from massive bronchoconstriction following antigen challenge: a phenomenon which is paralleled by an increment of the circulating TXA2. The possibility that the adenylate-cyclase-stimulating properties of procaterol may explain its antiasthmatic activity is discussed.

Animals↗
PubMed2000

Synthesis and biodistribution of [11c]procaterol, a beta2-adrenoceptor agonist for positron emission tomography.

The potent, subtype-selective radioligand (+/-)-erythro-5-(1-hydroxy-2-[11C]isopropyl-aminobutyl)-8-hydroxy-car bostyril ([11C]procaterol) was synthesized and evaluated for visualization of pulmonary beta2-adrenoceptors with positron emission tomography (PET). Procaterol was labelled by reductive alkylation of the desisopropyl precursor with [11C]acetone under the influence of NaCNBH3 and acetic acid. Synthesis and HPLC purification were performed in 34 min. Specific activities ranged from 26.5-39.3 TBq (about 700-1000 Ci)/mmol and the radiochemical yield was 2.4-8.6% (corrected for decay). Biodistribution studies were performed in male Wistar rats which were either untreated or predosed with (D,L)-propranolol hydrochloride (beta-adrenoceptor antagonist, 2.5 mg/kg), ICI 118551 (beta2-adrenoceptor antagonist, 0.15 mg/kg), CGP 20712A (beta1-adrenoceptor antagonist, 0.15 mg/kg) or isoprenaline (beta1-adrenoceptor agonist, 15 mg/kg). Specific binding was observed in lungs, spleen and red blood cells, tissues known to contain beta2-adrenoceptors. Pulmonary binding was blocked by propranolol, ICI 118551 and isoprenaline, but not by CGP 20712A. This binding pattern is consistent with the beta2 selectivity of the radioligand. The clearance of [11C]procaterol was biphasic, with a rapid distribution phase (t1/2 0.17 min) representing 90% of the injected dose followed by an elimination phase (t1/2 18.1 min). About 45% of the plasma radioactivity was unmetabolized procaterol at 15 min postinjection. In a dynamic PET-study, the lungs of untreated control rats could barely be detected and total/non-specific binding ratios rose to only 1.2 at 20 min postinjection. Although labelling and administration of (-) erythroprocaterol, the most active of 4 stereoisomers, may produce better results, [11C]procaterol seems unsuitable for beta-adrenoceptor imaging.

Adrenergic beta-Agonists↗
PubMed1993

Clinical pharmacokinetics and relative bioavailability of oral procaterol.

The pharmacokinetics and relative oral bioavailability of procaterol, an orally active beta 2-adrenergic agonist bronchodilator were evaluated in healthy volunteers. Procaterol was rapidly absorbed after oral administration. Mean plasma procaterol concentration-time profiles and pharmacokinetic parameters for both formulations were essentially superimposable. Following tablet administration, the mean Cmax was 358 pg/mL and the corresponding mean tmax was 1.6 hr. Mean renal clearance was 163 mL/min and accounted for approximately one-sixth of the mean apparent oral plasma clearance (988 mL/min). The mean apparent elimination half-life of procaterol was 4.2 hr. Hepatic metabolism appears to be the primary mechanism for elimination of procaterol from the body, and first-pass metabolism may limit systemic bioavailability.

Absorption↗
PubMed1991

Inhibitory effect of inhaled procaterol on anaphylactic bronchoconstriction and thromboxane A2 production in guinea-pigs.

This study was designed to examine whether an inhaled beta 2-agonist, procaterol, inhibits thromboxane A2 (TXA2) production induced by antigen challenge in passively sensitized guinea-pigs in vivo. Antigen-induced bronchoconstriction was markedly inhibited by pre-treatment with procaterol. Inhaled procaterol significantly reduced in a dose-dependent manner the increment in TXB2 concentration in bronchoalveolar lavage fluid obtained 5 min after antigen challenge. Aerosol administration of procaterol significantly inhibited bronchoconstriction induced by inhaled histamine. These results suggest that inhalation of procaterol has an inhibitory effect on antigen-induced TXA2 production as well as a protective effect against bronchoconstriction induced by bronchoactive agents.

Administration, Inhalation↗
PubMed1985

Procaterol and terbutaline in bronchial asthma. A double-blind, placebo-controlled, cross-over study.

Procaterol, a new beta-2 adrenoceptor stimulant, was studied in a double-blind, placebo-controlled, cross-over trial in patients with bronchial asthma. Oral procaterol 50 micrograms b.d., procaterol 100 micrograms b.d., and terbutaline 5 mg t.i.d., were compared when given randomly in 1-week treatment periods. The best clinical effect was found with terbutaline. Both anti-asthmatic and tremorgenic effects of procaterol were dose-related. Procaterol appeared effective in the doses tested, and a twice daily regimen would appear to be suitable with this drug.

Adolescent↗
PubMed2006

Procaterol upregulates peroxisome proliferator-activated receptor-gamma expression in human eosinophils.

Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a nuclear receptor that regulates immune reaction. We have previously demonstrated that human eosinophils express PPARgamma and that stimulation with a synthetic agonist for PPARgamma attenuated the factor-induced eosinophil activations. However, the modulator of PPARgamma expression in eosinophils has not yet been studied. In this study, we investigated the effect of procaterol, the synthetic beta2-adrenoceptor agonist widely used as bronchodilators in asthma, on the PPARgamma expression in eosinophils. Purified human peripheral blood eosinophil and the eosinophilic cell line EoL-1 were cultured with procaterol. This was followed by PPARgamma measurement using flow cytometer and quantitative real-time RT-PCR. We observed that PPARgamma was constitutively expressed by EoL-1 and the purified eosinophils and that the therapeutic concentration (10(-9)M) of procaterol markedly enhanced PPARgamma protein expression, which was reversed by the selective beta2-adrenoceptor antagonist ICI-118551. The PPARgamma mRNA expression in EoL-1 and eosinophils was also induced by procaterol. These findings suggest that procaterol could modulate the eosinophil function by increasing the expression of PPARgamma.

Adrenergic beta-Agonists↗
PubMed1985

Effect of inhaled procaterol hydrochloride in children with bronchial asthma, with particular reference to duration of effect.

This double-blind crossover trial evaluated the prolonged clinical effect of procaterol inhaled in a dose of 10 micrograms by nine asthmatic children with mild and stable respiratory disturbance. To compare procaterol with the placebo administered with a pressurized metered-dose inhaler 48 hr before or after procaterol, FVC, FEV1, V50, and V25 were followed up for 10 hr. FVC did not indicate a significant difference between the two treatments, while FEV1, V50, and V25 showed significantly greater changes after procaterol administration. The duration of action of procaterol in terms of FEV1, V50, and V25 was 6, 10, and 4 hr, respectively.

Adolescent↗
PubMed1992

[Clinical evaluation of procaterol and salbutamol in patients with bronchial asthma].

When the beta-2-selectivity of beta-agonists is assessed in man it is always considerably less than would be expected from studies on isolated tissues. That was a reason why this study was taken. As we know procaterol has been included into group of beta-2-selective non-catecholamines with a reasonably long duration of action. We performed clinical evaluation of procaterol and salbutamol on 24 patients with bronchial asthma. Procaterol was administered per os (tabl. a 50 micrograms twice daily) during 4 weeks, and next salbutamol was replaced above mentioned (tabl. a 8 mg twice daily) also during 4 weeks. Clinical symptoms and spirometric values were analyzed. Obtained results indicated that procaterol and salbutamol showed a similar potency in spirometric examination in patients with bronchial asthma. Observed side effects after procaterol were less often than after salbutamol.

Adolescent↗
PubMed1989

Procaterol metered-dose inhaler: a multiclinic study evaluating the efficacy and safety in patients with asthma.

Procaterol hydrochloride aerosol, a potent beta 2-adrenergic bronchodilator, was evaluated in a double-blind, placebo-controlled study for efficacy and safety in 210 patients with documented mild to moderate reversible airway obstruction. Patients were randomized to receive procaterol in two inhalations (high dose) or one inhalation (low dose), 0.01 mg/inhalation, three times daily, or placebo. Pulmonary function tests were recorded at five and 30 minutes and hourly for eight hours after the first dose and following 1 and 2 weeks of treatment. Both doses of procaterol produced significantly greater improvement in PFTs at one hour and for up to seven hours after dosing compared with placebo (p less than 0.05). Mean percent increases in FEV1 were 35% in the high-dose group and 29% in the low-dose group at week 2. The high-dose group showed no loss of duration of bronchodilation with continued dosing. Improvement in PFTs and peak flow rates was significantly greater in the high-dose than in the low-dose group (p less than 0.05). Tremor was the most frequent side effect. Procaterol had no effect on electrocardiograms, heart rate, blood pressure, or clinical laboratory tests. The high dose of procaterol aerosol was shown to be an effective and well-tolerated bronchodilator with a rapid onset and long duration of action.

Adolescent↗