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PubMed1989

[Inhibitory effect of procaterol (beta 2 agonist) on the release of cyclooxygenase products during antigen-induced bronchoconstriction in the guinea pig in vivo].

The purpose of this study was to investigate whether procaterol (beta 2 agonist) inhibits the release of cyclooxygenase products in bronchoalveolar lavage fluid (BALF) during in vivo allergic bronchoconstriction in passively sensitized guinea pigs. Antigen-induced bronchoconstriction was significantly inhibited by pretreatment with procaterol. The concentrations of 6-keto-PGF1 alpha, PGF2 alpha and TXB2 in BALF significantly decreased in guinea pigs pretreated with inhaled procaterol. The concentration of TXB2, which is the stable metabolite of TXA2, a strong bronchoconstrictor, was especially markedly decreased compared with that in the control animals. These data indicate that procaterol (beta 2 agonist) may inhibit the release of chemical mediators during allergic reactions as well as directly decrease the contractility of airway smooth muscle. Consequently, regular inhalation of procaterol may be clinically useful for prophylaxis of bronchial asthma.

Administration, Inhalation↗
PubMed1987

The effect of diet on the efficacy onset and duration of action of procaterol hydrochloride tablets.

Procaterol hydrochloride, a new potent beta-2 agonist drug, was evaluated for effects of food absorption, onset of action, and efficacy in a single-dose non-blinded placebo controlled crossover design in 18 subjects. Three diet conditions, separated by a three to seven day washout period, were used and compared to a placebo treatment. The diets were standardized and included high fat, low fat, and a fasting condition. Spirometric determinations and vital signs were obtained at 0, 15, 30 minutes, and at one, two, four, six, eight hours post-dose to evaluate therapeutic availability since no technique for measuring serum levels of procaterol hydrochloride is currently available. Spirometry results indicated significant improvement in pulmonary function during all diet conditions except with the placebo treatment. A delay in onset of action was seen in the low fat diet and to a certain extent in the high fat diet as compared to the fasting condition. There was no effect of diet on procaterol hydrochloride's peak response or duration of action with improvement in pulmonary function demonstrated for up to eight hours. Tremor and headache were the most frequent side effects, and were mild and transient. No significant effects were noted in electrocardiograms, heart rate, or blood pressure. An elevation in serum glucose was seen in three subjects during the fasting challenge and was felt to be secondary to the beta-agonist effects of procaterol hydrochloride. Procaterol was found to be an effective drug with a delayed onset of action when administered with food, but no effect on subsequent efficacy or duration of action.

Adolescent↗
PubMed1978

The metabolites of procaterol HCl in urine and faeces of dog and man.

1. The metabolites of procaterol HCl in dog urine and faeces and in human urine were qualitatively analysed by an improved g.l.c.-mass spectrometric method. 2. Trimethylsilylated derivatives of procaterol metabolites were identified by mass fragmentography as procaterol glucuronide, 5-(2-amino-1-hydroxybutyl)-8-hydroxycarbostyril (desisopropylprocaterol), 5-formyl-8-hydroxycarbostyril, 8-hydroxycarbostyril and unchanged procaterol. 3. The metabolic pattern of procaterol HCl was species-independent in rats, dogs and man.

Administration, Oral↗
PubMed1992

Clinical pharmacokinetics of procaterol: dose proportionality after administration of single oral doses.

Procaterol is a potent, orally active beta 2-agonist bronchodilator useful in the treatment of reversible bronchospastic disease. It is effective when administered as single or multiple (Q8H) 50 and 75 micrograms doses. As part of the clinical development of procaterol, the pharmacokinetics and dose proportionality of single 25, 50, 75, and 100 micrograms doses were investigated in 14 healthy subjects. Serial blood samples were collected for 16 h and urine was quantitatively collected for 48 h following administration of each dose. Procaterol concentrations in plasma and urine were determined using sensitive and specific radioimmunoassay methods. Mean values for tmax, the apparent elimination rate constant, Cl/F, renal clearance, and per cent of dose excreted unchanged in urine were similar for all doses. Dose-normalized AUC, Cmax, and amount excreted unchanged in urine (Ae) were also similar across dosage levels. Thus, the pharmacokinetics of procaterol appear to be proportional to dose over the range of doses studied.

Administration, Oral↗
PubMed1999

Large and small airway responses to procaterol hydrochloride administered through different extension devices in asthmatic patients.

The effects of spacer devices on the magnitude and velocity of large and small airway bronchodilator responses in asthmatic patients who can correctly operate a metered dose inhaler (MDI) remain unclear. According to a double-blinded, randomized, crossover protocol, 14 asthmatic patients were studied on seven separate occasions. On each occasion, patients inhaled doubling methacholine concentrations until forced expiratory volume in 1 second (FEV1) had fallen by 20% of baseline. Changes in forced expiratory flow between 25% and 75% of vital capacity (FEF25-75) were also evaluated. Subsequently, patients were administered 20 or 50 micrograms of procaterol from an MDI either alone or in conjunction with a small- or large-volume spacer device. Changes in FEV1 and FEF25-75 corrected for baseline forced vital capacity (isoFEF25-75) were assessed at 3-minute intervals for 15 minutes and at 30 minutes. Spontaneous recovery was similarly evaluated. The time required to attain significant increases in both FEV1 and isoFEF25-75 was calculated in bronchodilator trials. With 20 micrograms of procaterol, both spacers allowed larger and faster FEV1 increases than the MDI alone (P < 0.01); with 50 micrograms, the velocity and magnitude of FEV1 increases were further enhanced in trials with the MDI alone. The lower procaterol dose via the large-volume spacer determined larger and faster isoFEF25-75 increases than the higher dose via both the small-volume spacer and the MDI alone (P < 0.01). Spacers enhance bronchodilation even in patients using MDIs optimally. Compared with both the small-volume device and the MDI alone, the large-volume spacer allows faster and larger small airway dilation with less than half of the procaterol dose.

Administration, Inhalation↗
PubMed1985

A comparative study of a new selective beta 2-adrenoceptor agonist, procaterol and salbutamol in asthma.

The effects of single oral doses of a new selective beta 2-adrenoceptor agonist procaterol (0.05 mg and 0.1 mg) and salbutamol (4 mg) on ventilatory function, were compared in 24 asthmatic patients. A bronchodilator effect of similar duration and magnitude followed all three treatments with no evidence of a dose-related response in the case of procaterol. There was no significant difference in blood pressure or heart rate responses or pattern of unwanted effects. We conclude that procaterol and salbutamol are clinically similar with oral dosing and that the maximum effective dose of procaterol is not greater than 0.05 mg.

Adolescent↗
PubMed1995

Ability of inhaled procaterol, a beta 2 adrenoceptor agonist, to attenuate eicosanoid-induced airflow obstruction and airway microvascular leakage.

Beta-2 adrenoceptor agonists are widely used as bronchodilators in the treatment of asthma mainly via inhalation. In the present study, we evaluated the ability of inhaled procaterol, a beta 2 adrenoceptor agonist, to reduce eicosanoid-induced airway microvascular leakage, and compared the ability with its inhibitory effect against bronchoconstriction. Tracheostomized guinea-pigs were given aerosolized procaterol (10 or 100 micrograms/ml) for 10 min under spontaneous breathing. Immediately after the end of inhalation, the animals were mechanically ventilated. Fourteen minutes after the end of inhalation, Evans blue dye (20 mg/kg) was given i.v. One minute later, 2 nmol/kg leukotriene D4 (LTD4), 50 nmol/kg U-46619, a thromboxane A2 mimetic, or vehicle was administered i.v. LTD4- or U-46619-induced increase in lung resistance was measured for 6 min. After removing the lungs, the amount of extravasated Evans Blue due in the lower airways was examined as an index of microvascular leakage. Inhaled procaterol significantly attenuated increases in both lung resistance and Evans Blue dye extravasation caused by these eicosanoids. The degree of inhibition was almost complete for lung resistance (approximately 90%), but it was only partial (range 18.5-61.2%) for the dye extravasation. No significant changes in mean systemic blood pressure and in heart rate was observed after an inhalation of 10 micrograms/ml procaterol. These results suggest that inhaled beta 2 adrenoceptor agonists may reduce airway microvascular leakage caused by inflammatory mediators such as eicosanoids without affecting systemic circulation.

Adrenergic beta-Agonists↗
PubMed2005

Adrenal influences on the inhibitory effects of procaterol, a selective Beta-two-adrenoceptor agonist, on antigen-induced airway microvascular leakage and bronchoconstriction in Guinea pigs.

While the guinea pig has been the preferred choice for use as a model of allergic bronchial asthma in the evaluation of anti-asthmatic drugs, it has been shown that antigen-induced bronchoconstriction in guinea pigs is attenuated by epinephrine released from the adrenal gland. In order to investigate the possible influence of the adrenal gland on the effects of antiexudative and bronchodilative drugs on antigen-induced airway responses, we examined the inhibitory effects of procaterol, a selective beta(2)-adrenoceptor agonist, on antigen-induced airway microvascular leakage and bronchoconstriction in adrenalectomized guinea pigs and compared them with the drug's effects in sham-operated animals. Guinea pigs sensitized passively with anti-ovalbumin (OA) guinea-pig serum were adrenalectomized or sham-operated under urethane anesthesia and examined 30 min after surgery in the following experiments. (1) Animals were intravenously administered Evans blue dye to quantify airway plasma exudation, and then OA was inhaled for 10 min while measuring pulmonary inflation pressure, a parameter of bronchoconstriction. Procaterol (1, 3, 10, or 30 microg/kg) or saline (control) was administered into the airways 10 min prior to OA inhalation. The amount of extravasated Evans blue dye in the airways was calculated. (2) Venous blood samples were collected during OA or saline inhalation and plasma catecholamine levels were compared. In control animals, OA-induced increases in both the amount of Evans blue dye and in pulmonary inflation pressure were markedly greater in adrenalectomized animals than in sham-operated animals. Procaterol dose-dependently inhibited OA-induced airway microvascular leakage and bronchoconstriction, and its effects were more potent in adrenalectomized animals (significant at 1 microg/kg and higher) than in sham-operated animals (significant at 10 microg/kg and higher). Although the plasma concentration of epinephrine during OA inhalation was approximately 3 times higher than that during saline inhalation in sham-operated animals, no difference was seen in adrenalectomized animals. In conclusion, while procaterol essentially possesses pronounced inhibitory effects on antigen-induced airway microvascular leakage and bronchoconstriction in guinea pigs, the effects are considerably masked by epinephrine released from the adrenal gland.

Adrenal Glands↗
PubMed1990

Does a beta 2-stimulator really facilitate mucociliary transport in the human lungs in vivo? A study with procaterol.

The purpose was to study whether procaterol, a beta 2-stimulator, facilitated mucociliary transport on the ciliated airways in the human lungs. From immediately after inhalation of [99mTc]albumin aerosol, radioactivity of the thorax was continuously measured anteriorly by a gamma camera with the examinee in the supine position; the data were sequentially stored in a computer in 10-s frame mode. Three puffs (30 micrograms) of procaterol were inhaled from a metered dose inhaler at 60 min in the same supine position, and measurement of radioactivity was continued for 30 min more. Spirometry was performed before and after the measurement of radioactivity. A group of 8 normal subjects and 34 patients with various lung diseases, including 6 with bronchial asthma in remission, were studied. In addition to observation of mucus transport on the large airways by radioaerosol inhalation lung cinescintigraphy, the time-activity curve from the right lung was evaluated and the quantitative parameters for evaluating mucociliary clearance were calculated for the right lung. Following inhalation of procaterol, there were neither significant acceleration in mucus transport on the large airways by cinescintigraphy nor significant changes in the slope of time-activity curves. Quantitative parameters did not show any significant changes either, although spirometry indicated significant bronchodilation. We conclude that three puffs of inhaled procaterol neither necessarily accelerate mucus transport nor facilitate mucociliary clearance in the human lung.

Administration, Inhalation↗
PubMed1987

Oral clenbuterol and procaterol. A double-blind comparison of bronchodilator effects in children with chronic asthma.

In a double-blind crossover study, clenbuterol at a dose of 0.75 micrograms/kg, procaterol at a dose of 1.5 micrograms/kg, and placebo, all administered orally, were compared for bronchodilation efficacy. Twelve children aged from 6 to 13 years, with moderate to severe asthma, participated in the trial. Pulmonary function, heart rate, blood pressure, and tremor were evaluated at 30, 60, 90, and 120 minutes and then hourly for 8 hours after administration. Both clenbuterol and procaterol induced a significant change over their baseline values for all the pulmonary function parameters considered. For clenbuterol, the same was also observed in comparison with placebo, while for procaterol this was true only for FEV1 and FEF25-75, while no difference resulted from FVC and PEF. Mild and transient tremor was the only side effect observed. Oral clenbuterol and procaterol were both demonstrated to be safe and effective. However, at the doses studied, clenbuterol had a significantly higher bronchodilator activity lasting up to 8 hours.

Administration, Oral↗
PubMed1995

A beta 2-agonist, procaterol, inhibits basophil migration.

Beta 2-receptor agonists have recently been reported to be effective on allergen-induced late-phase reaction (LPR) in addition to their inhibitory effect on immediate-phase reaction, although the precise mechanism is not fully understood. In this study, we tested the effect of a selective beta 2-agonist, procaterol, on human basophil migration, which may be an important characteristic of LPR. Procaterol inhibited IL-8- and C5a-induced basophil migration in a dose-dependent fashion; 10(-7) M of procaterol reduced 30% of migration induced by both factors. The action of procaterol was rapid since the inhibition of migration was detected without preincubation and was not via the toxic effect on basophils as assessed by trypan blue test. The results of this study extend the repertoire of anti-inflammatory actions of beta 2-agonists.

Adrenergic beta-Agonists↗
PubMed2000

Determination of procaterol in human plasma by gas chromatography/electron impact ionization mass spectrometry.

AIM: To improve a gas chromatography/electron impact ionization mass spectrometry (GC/MS) method for determining the concentration of procaterol in human plasma. METHODS: GC/MS was developed with capillary column. Samples were extracted by liquid phase before derivated. Imipramine was used as an internal standard. The injector and GC/MS interface temperatures were set at 280 degrees C and 250 degrees C, respectively. The carrier gas (helium) was 0.8 mL.min-1, and injections were made in the pulse-splitless mode. The MS source and MS Quad temperature were 230 degrees C and 150 degrees C, respectively. RESULTS: The detection limit of plasma procaterol was 5 ng.L-1. The assay was linear over the range of 10-10,000 ng.L-1 with correlation coefficient of 0.9987. The coefficients of variation were less than 10% for procaterol detection at high, medium and low concentration levels (n = 5). The average recovery of the assay was 99.1% +/- 1.3%. CONCLUSION: This assay was sensitive, precise, and accurate for evaluating the clinical pharmacokinetics of procaterol.

Bronchodilator Agents↗
PubMed1991

Cardiac effects of beta-2 adrenoceptor stimulation with intracoronary procaterol in the absence and presence of regional myocardial ischemia in dogs.

To evaluate consequences of cardiac beta-2 adrenoceptor stimulation on coronary hemodynamics and regional myocardial function assessed by sonomicrometry in the normal and regionally ischemic heart, the effects of administration of procaterol, a selective beta-2 adrenoceptor agonist, into the left circumflex coronary artery (LCX) were examined in the absence and presence of a stenosis of the LCX in anesthetized open-chest dogs. The stenosis of the LCX was made sufficient to decrease percent segment shortening in the LCX-perfused region to around 2 to 3%. When coronary stenosis was absent, intracoronary infusion of procaterol (6.7 ng/min for 15 min) produced significant increases in LCX flow and myocardial segment shortening in the infused region without changes in global hemodynamics. During coronary stenosis, on the contrary, intracoronary procaterol at the same dose significantly deteriorated regional myocardial dysfunction without changing LCX flow, global hemodynamics and cardiac lactate metabolism. These changes induced by procaterol were not observed in the dogs treated with a selective beta-2 antagonist, erythro-(+/-)-1-(7-methylindan-4-yloxy)-3-isopropylaminob utan-2-ol. These results suggest the presence of functional beta-2 adrenoceptors in the canine heart both with and without myocardial ischemia.

Adrenergic beta-Agonists↗
PubMed1990

Effects of albuterol and procaterol on exercise-induced asthma.

Procaterol and albuterol, beta agonists, were studied using a placebo-controlled, repeated exercise challenge design in order to assess their duration of effectiveness in both bronchodilation and in modifying exercise-induced asthma (EIA). Fifty-three subjects aged 12 to 50 years who had at least a 20% drop in FEV1 during a screening exercise tolerance test were entered. Subjects took two inhalations of procaterol (10 micrograms/inhalation), albuterol (90 micrograms/inhalation), or placebo. Thirty minutes later they exercised on a treadmill at a workload sufficient to induce greater than or equal to 80% aerobic O2 consumption for six minutes. Pulmonary function was measured before and serially for 30 minutes after exercise. The same exercise challenge was repeated three, six, and nine hours after drug administration. Both procaterol and albuterol bronchodilated and modified EIA at 30 minutes and three hours, mean drops in FEV1 being 8.2 and 9.7% respectively at 30 minutes and 16.8 and 16.3% at three hours. This was compared with placebo falls of 30% and 26%. At six hours the subjects' response was similar after both procaterol and albuterol, and fewer subjects had a 20% fall in FEV1 than with placebo, although protection afforded by both beta agonists was substantially less than at three hours. Both drugs were tolerated well.

Adolescent↗
PubMed1986

Duration of oral procaterol protection from methacholine-induced bronchial obstruction.

The duration of action of procaterol, a beta-2-adrenoceptor agonist with an entirely new chemical structure, was assessed, in comparison to that of salbutamol, by inhalation of 43 inhalation units of methacholine at time intervals of 1, 3, 5, 7, and 9 hours after intake of the drugs. Procaterol and salbutamol were given in a double-blind random fashion, on different days, to 12 asthmatic children; pulmonary function tests (FVC, FEV1, MEF50, MEF25), skeletal muscle tremor, and vital signs (heart rate and blood pressure) were measured. Although there was no statistical significant difference between procaterol and salbutamol, protection of large and medium airways lasted for about five hours, while normal small airway patency was still present at seven hours. It is concluded that procaterol can be a good alternative beta-2-adrenoceptor agonist when the oral route is needed.

Adrenergic beta-Agonists↗
PubMed1987

Procaterol metered aerosol in patients with chronic obstructive pulmonary disease.

The activity and tolerability of procaterol, a recently introduced beta 2-adrenergic drug, were evaluated in comparison with fenoterol and a placebo in a single blind, cross-over study, using a metered aerosol formulation. Twelve patients suffering from chronic obstructive pulmonary disease with reversible bronchial obstruction were enrolled. Before and 30, 120, 240, 360, 480 min after drug administration, forced vital capacity (FVC), forced expiratory volume at the first second, forced expiratory flow at 25-75% and 75-85% respectively of the FVC, thoracic gas volume and the specific airways conductance were calculated. Procaterol 20 mcg showed a significant bronchodilating activity as well as fenoterol 400 mcg. This activity was already significant within 30 min, achieved its maximum after two hours and lasted more than eight hours. Side-effects were complained of by 41% of patients treated with procaterol and by 50% treated with fenoterol; procaterol showed less cardiovascular effects than fenoterol.

Adrenergic beta-Agonists↗
PubMed1986

A new bronchodilating agent, procaterol, in preventing exercise-induced asthma.

The aim of the present study was to verify the effectiveness of procaterol, a recent and specific beta-2-adrenoceptor stimulant, in preventing exercise-induced asthma (EIA). Twelve asthmatic patients were selected aged 18.6 +/- 5.6 years with a positive response to EIA and a basal forced expiratory volume of the first second (FEV1) better than 80% of predicted. The patients underwent four bronchoprovocation challenges on four consecutive days. On the first day they performed an inclusion test, and, on the three subsequent days, they were submitted, to three identical standardized challenges according to a randomized design. Fifteen minutes before, procaterol (20 mcg), salbutamol (200 mcg) and a placebo were administered as metered aerosol. No pharmacological treatment was given for 24 h (48 h for antihistamines) before each challenge. The test was carried out running on treadmill (10% grade) for 7 min. Room temperature (20-25 degrees C) and relative humidity (40-55%) were maintained constant. At baseline, 15 min before, 5, 10, 15, 30 and 60 min after the exercise, lung function was assessed. Basal mean values of FEV1 were 94.7, 94.9, 90.7 and 91.5% of predicted for the inclusion and the three protected tests, respectively, without significant differences. The FEV1 mean values showed a mild bronchodilation 15 min after salbutamol (+13.2%, p less than 0.006) and procaterol (+8%, NS). At every considered time all indices showed a significant gap (p less than 0.01) between drugs and the placebo with no appreciable differences between procaterol and salbutamol.

Adolescent↗
PubMed1982

[Preclinical study of third generation beta 2-stimulant (procaterol) on inhibition of uterine contraction (author's transl)].

A preclinical study was carried out on the beta 2-effect of procaterol, a new third generation beta 2-stimulant, by testing its inhibitory effect on uterine contraction. 1) The inhibitory effect of procaterol on uterine contraction in pregnant rats showed the same pattern as did treatment with second generation beta 2-stimulants (terbutaline, ritodrine). Procaterol showed the inhibitory effect at the lowest dose (0.05 microgram/ml) of the 20 inhibitory substances. 2) As for changes in c-AMP and c-GMP after administering procaterol to rats in the later stage of pregnancy, an increase in c-AMP and a decrease in c-GMP were observed, and the % changes were lower than the second generation beta 2-stimulants (in vitro). Likewise, in the in vivo study, changes in serum c-AMP in pregnant rats showed the same tendency as did the in vitro study. The c-AMP values in uterus, placenta and fetus increased as they did after treatment with ritodrine. Changes in c-GMP, however, showed different results after treatment with ritodrine, and an increase in the uterus and liver was observed but no changes were observed in the placenta and fetus.

Adrenergic beta-Agonists↗