[Effect of procaterol in dosed aerosol and the procaterol-theophylline combination].
Explore the source record for details and available documents.
Aerosols↗
SEARCH · PubMed Health
Results for “Procaterol”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[A new aerosol adrenergic bronchodilator, procaterol. Comparative study of salbutamol and procaterol].
Explore the source record for details and available documents.
Adrenergic beta-Agonists↗
Comparison between oral procaterol and salbutamol in patients with bronchial asthma.
The efficacy of procaterol, a new beta 2-selective sympathomimetic drug, was compared with that of salbutamol and placebo in a double-dummy crossover study in 20 asthmatic patients. Procaterol (0.1 mg orally) was given twice daily and salbutamol (4 mg orally) 3-times a day. The study was made up of four consecutive 4-day treatment periods including two periods of plain placebo. A significant direct bronchodilating effect of both procaterol and salbutamol could be seen in PEF values, measured 4-times a day, compared with the effect of placebo (p less than 0.01 for both). Procaterol was slightly superior to salbutamol. The afternoon and evening PEF values during the procaterol period did not differ from the values during the placebo period. In symptom scores, there was significantly more tremor during the procaterol period than during the placebo period (p less than 0.01). Both procaterol and salbutamol produced more palpitation than placebo (p less than 0.05). The study shows that oral procaterol is a potent bronchodilator. The doses of procaterol and salbutamol were not equivalent. Procaterol with the dose used in the study was more potent. Despite this, the duration of the bronchodilator effect of procaterol on a twice daily dosage did not seem to be long enough in all patients.
Administration, Oral↗
Facilitation by procaterol, a beta-adrenoceptor agonist, of noradrenaline release in the pithed rat independently of angiotensin II formation.
1. The effects of the beta 2-adrenoceptor agonist, procaterol, on sympathetic neuroeffector transmission were studied in the pithed adrenal demedullated rat to determine if generation of angiotensin II was involved in its effect. Pressor responses were elicited by either electrical stimulation (20 V, 2 Hz) of the entire spinal sympathetic outflow or methoxamine (0.1 mg kg-1, i.v.). 2. Sodium nitroprusside (3 and 5 micrograms kg-1 min-1, i.v.) produced hypotension and the pressor responses to both sympathetic nerve stimulation and methoxamine were reduced. This indicates that decreasing blood pressure in pithed rats reduces pressor responses. Procaterol (10 and 30 ng kg-1 min-1, i.v.) also produced hypotension but did not alter pressor responses to sympathetic nerve stimulation. Nevertheless, procaterol (10 and 30 ng kg-1 min-1, i.v.) did reduce pressor responses to to methoxamine. Together these results suggest that procaterol may have enhanced sympathetic neurotransmitter release. This was confirmed in another series of experiments where procaterol (30 ng kg-1 min-1, i.v.) increased plasma noradrenaline levels during sympathetic nerve stimulation. 3. Captopril (5 mg kg-1, i.v.) produced hypotension and as expected reduced pressor responses to sympathetic nerve stimulation. When the hypotensive effect of captopril was abolished by concomitant vasopressin infusion (1.5-4.5 i mu kg-1 min-1, i.v.), pressor responses to sympathetic nerve stimulation were restored to pre-captopril levels. In this situation procaterol (10 and 30 ng kg-' min', i.v.) reduced basal blood pressure and did not alter pressor responses to sympathetic nerve stimulation whereas the pressor responses were reduced by an equihypotensive infusion of sodium nitroprusside (3 and 5 jig kg-' min' , i.v.). The lack of reduction of pressor responses after procaterol in the presence of captopril is indirect evidence that procaterol may have enhanced noradrenaline release independently of angiotensin II.4. In another series of experiments, plasma noradrenaline levels elicited by sympathetic nerve stimulation were not altered by captopril (5 mg kg', i.v.). In the presence of captopril (5 mg kg-', i.v.),procaterol (30 ng kg- min-1, i.v.) no longer enhanced plasma noradrenaline levels during sympathetic nerve stimulation. However, since the dose of captopril is well above that required to block angiotens in converting enzyme (ACE) the effect may be non-specific. Therefore, the selective AT, receptor antagonist, losartan (10mgkg'1, i.v.), was also used. Losartan (10mgkg'1, i.v.) did not alter plasma noradrenaline levels during sympathetic nerve stimulation, and in the presence of losartan procaterol(30 ng kg-I min-', i.v.) enhanced plasma noradrenaline levels during sympathetic nerve stimulation. This result further suggests that 1-adrenoceptor facilitation of noradrenaline release from sympathetic nerves in the pithed rat occurs by a mechanism independent of angiotensin II generation.
Angiotensin II↗
Relaxing actions of procaterol, a beta 2-adrenoceptor stimulant, on smooth muscle cells of the dog trachea.
1. The effects of procaterol, a beta 2-adrenoceptor agonist, on smooth muscle cells of the dog trachea were investigated by use of microelectrode and isometric tension recording methods, and by measurement of Ca transients as estimated from the fura-2 fluorescence, adenosine 3':5'-cyclic monophosphate (cyclic AMP) and breakdown of phosphatidylinositols. 2. Procaterol hyperpolarized the membrane and increased the ionic conductance (above 10 nM) in a dose-dependent manner. These actions were inhibited by propranolol. 3. Procaterol inhibited the mechanical responses evoked by acetylcholine (ACh), histamine or 5-hydroxytryptamine (5-HT), in the presence or absence of Ca2+ in the bath solution, but not that evoked by high concentrations of ACh (1 microM). The ID50 value of procaterol for the peak amplitude of the ACh-induced contraction (30 nM) was 0.3 nM. The equivalent values for the histamine-induced phasic and tonic responses (10 microM) were 0.15 and 0.01 nM), respectively. 4. Procaterol (over 1 nM) increased the amount of cyclic AMP in a dose-dependent manner which was blocked by prior application of propranolol. 5. Procaterol did not alter the changes in the amounts of phosphatidylinositol 4,5-bisphosphate (PI-P2) and phosphatidic acid (PA) induced by ACh, histamine or 5-HT. Thus, the synthesis of inositol 1,4,5-trisphosphate is not affected by stimulation of the beta 2-adrenoceptor. 6. ACh increased the free Ca2+ concentration to a greater extent than that produced by histamine or 5-HT. These changes were reduced by procaterol, except for those induced by high concentrations of ACh (over 1 microM). 7. It is concluded that procaterol relaxes tissues precontracted by various agonists due to a reduction in the free Ca2+. This inhibitory action may be due to an increase in the amount of cyclic AMP but does not result from an inhibition of the hydrolysis of phosphatidyl inositols. The hyperpolarization induced by procaterol may partly contribute to the observed relaxation.
Adrenergic beta-Agonists↗
Effect of inhaled procaterol on cough receptor sensitivity to capsaicin in patients with asthma or chronic bronchitis and in normal subjects.
BACKGROUND: To evaluate the effect of inhaled beta 2 adrenergic agonists on the sensitivity of airway cough receptors, the effect of inhaled procaterol on cough induced by aerosolised capsaicin, a stimulant of C fibres, was studied in patients with asthma or chronic bronchitis and in normal subjects. METHOD: Eleven patients with asthma and 10 with chronic bronchitis and 14 normal subjects participated. Increasing concentrations of capsaicin solution were inhaled for 15 seconds by tidal breathing through the mouth at one minute intervals until five or more coughs were elicited, before and 30 minutes after inhalation of 20 micrograms procaterol or placebo (freon gas alone) through a metered dose inhaler. Cough threshold was defined as the lowest concentration of capsaicin that elicited five or more coughs. To evaluate the bronchodilator effect of procaterol and the bronchoconstrictor effect of inhaled capsaicin, forced expiratory volume in one second (FEV1) was measured before and one minute after a capsaicin provocation test. This test was carried out both before and 30 minutes after treatment with procaterol or placebo. RESULTS: The geometric mean value of cough threshold to capsaicin was significantly increased by procaterol and placebo in both groups of patients but not in the control subjects. The increment in the cough threshold was not significantly different between the treatments with procaterol and placebo in each group. FEV1 was significantly increased by procaterol but not by placebo in all three groups. CONCLUSIONS: Inhaled procaterol has no effect on airway cough receptor sensitivity to capsaicin. The attenuation of the cough sensitivity seen after inhalation of procaterol in patients with asthma and bronchitis may result from tachyphylaxis to capsaicin.
Administration, Inhalation↗
Pre- and post-junctional actions of procaterol, a beta 2-adrenoceptor stimulant, on dog tracheal tissue.
1. The effects of procaterol, a beta 2-adrenoceptor agonist, on excitatory neuro-effector transmission in the dog trachea were investigated and the findings were compared to those seen with isoprenaline, with microelectrode, double sucrose gap and tension recording methods. 2. Procaterol (10(-10)-10(-9) M) and isoprenaline (10(-9) M) had no effect on the resting membrane potential or on the input resistance of the smooth muscle cells of dog trachea. However with increased concentrations (greater than 10(-8) M), these agents hyperpolarized the membrane and decreased the input resistance of the membrane. 3. Procaterol (10(-10)-10(-7) M) and isoprenaline (10(-9)-10(-7) M) dose-dependently reduced the amplitude of the twitch contractions evoked by field stimulation in the combined presence of indomethacin (10(-5) M) and guanethidine (10(-6) M). In parallel with actions on twitch contractions, procaterol (10(-10)-10(-7) M) and isoprenaline (10(-9)-10(-7) M) reduced the amplitude of the excitatory junction potentials (e.j.ps), evoked by single pulse field stimulation in the dog trachea. 4. Procaterol (10(-8) M) had no effect on the post-junctional response of smooth muscle cells to exogenous acetylcholine (ACh) (10(-7)-10(-6) M). 5. Pretreatment with ICI-118551, a beta 2-adrenoceptor blocking agent, reduced the inhibitory action of procaterol on the amplitude of twitch contractions evoked by field stimulations in the dog trachea. 6. These results indicate that procaterol in low concentrations has a prejunctional action inhibiting the excitatory neuro-effector transmission in addition to a postsynaptic action, presumably by suppressing transmitter release from the vagus nerve terminals through beta 2-adrenoceptors in the dog tracheal tissue. The pre- and post-junctional actions of procaterol explain its potent bronchodilator effects in clinical use.
Adrenergic beta-Agonists↗
The effect of procaterol treatment on beta-adrenergic bronchodilation and polymorphonuclear leukocyte responsiveness.
Procaterol is a new and effective beta-adrenergic bronchodilator. To determine if procaterol administration could cause tachyphylaxis, airway and leukocyte beta-adrenergic function were monitored in 10 patients with asthma during two 4-wk, double-blind treatment periods, each preceded by a 2-wk beta-agonist washout. Treatment periods were randomized to placebo or procaterol (2 wk, 0.1 mg/day; 2 wk, 0.2 mg/day). At each 7 biweekly evaluations, the patient's cumulative bronchodilator dose-response to inhaled isoproterenol (0.1 to 0.64%) was measured, and venous blood was collected to quantitate, in vitro, the polymorphonuclear leukocyte (PMN) beta-adrenergic receptor's 125Iodo-cyanopindolol (125I-CYP) ligand binding and the PMN cyclic AMP response to isoproterenol and procaterol. Neither the airway nor leukocyte beta-adrenergic characteristics were changed during placebo treatment. Procaterol treatment reduced (p less than 0.05) the maximal 125I-CYP binding to PMN membranes but only during the initial 2 wk at low dosage. The percent PMN cyclic AMP increase to procaterol (10(-5) M) was also significantly (p less than 0.05) less during active treatment (141 +/- 40%) than during washout (256 +/- 24%) or placebo (257 +/- 32%). In contrast, procaterol treatment did not alter the acute isoproterenol bronchodilation response as measured by either the percent improvement in FEV1 or the dose required to produce 50% maximal bronchodilation. The duration of bronchodilation was not measured. Therefore, although procaterol therapy of asthma is associated with decreased PMN beta-adrenergic function, airway smooth muscle function appears not to be altered.
Adult↗
Inhibitory effects of theophylline and procaterol on eosinophil function.
Eosinophils play a crucial role in bronchial asthma. As theophylline and procaterol (beta 2-agonist) are used for the treatment of bronchial asthma, the specific functions of eosinophils in the presence of granulocyte/macrophage colony-stimulating factor (GM-CSF) or platelet activating factor (PAF) were examined using theophylline and procaterol alone and in combination. Eosinophil degranulation induced by PAF or GM-CSF was inhibited by theophylline (10(-6) M-10(-3) M and 10(-6) M to 10(-3) M, respectively) and procaterol (10(-7) M-10(-5) M and 10(-7) M-10(-5) M, respectively). The combination of 10(-4) M theophylline and various concentrations of procaterol provided higher inhibition than 10(-4) M theophylline or procaterol (10(-7) M-10(-5) M). CD11b, which is a triggering molecule for human eosinophil degranulation, showed a significantly inhibited expression of PAF stimulation with 10(-4) M theophylline. CD11b and another triggering molecule for eosinophil degranulation, CD18, showed a significantly inhibited expression of PAF stimulation using a combination of 10(-4) M theophylline and various concentrations of procaterol (10(-5) M-10(-7) M) compared with the inhibition of 10(-4) M theophylline or procaterol (10(-5) M-10(-7) M), but GM-CSF-stimulated eosinophils were not inhibited. Taken collectively, theophylline and/or procaterol have anti-inflammatory effects.
Asthma↗
Inhaled procaterol versus salbutamol in bronchial asthma.
Procaterol is a new, potent, long-acting beta-2-adrenergic bronchodilator. The magnitude and duration of the immediate bronchodilatation produced by inhaled procaterol aerosol have been compared with those produced by inhaled salbutamol aerosol in 20 asthmatic patients. Patients inhaled two puffs of procaterol (20 micrograms) or two puffs of salbutamol (200 micrograms) and PEF, FVC and FEV1 were measured after 5, 15, 30, 60, 120 and 180 min. The changes in mean PEF, FEV1 and FVC values were greater after procaterol than salbutamol, but the difference in bronchodilatation was not significant. The response to rimiterol after 180 min was greater in the salbutamol group. The increases in heart rate and systolic blood pressure were slightly higher after procaterol. Eleven patients reported adverse effects; 5 after procaterol, 3 after salbutamol, and 3 after both drugs. Thus, procaterol was a potent bronchodilator when inhaled as a single dose of 20 micrograms, but it did not appear to be an ultra long-acting preparation.
Administration, Inhalation↗
Lipomobilizing effects of procaterol and yohimbine in the conscious dog: comparison of endocrinological, metabolic and cardiovascular effects.
1. Lipid mobilization during a hypocaloric diet may be enhanced by a pharmacological approach using beta 2-adrenoceptor agonists or alpha 2-adrenoceptor antagonists. Studies were undertaken in the dog, an animal model presenting fat cell antilipolytic alpha 2- and lipolytic beta-adrenoceptors, in order, firstly, to demonstrate the presence of beta 2 subtype adrenoceptors on adipocytes and, secondly, to compare the effects of procaterol (beta 2-adrenoceptor agonist) and of yohimbine (alpha 2-adrenoceptor antagonist) on metabolic, endocrinological and cardiovascular parameters. 2. Procaterol strongly stimulates lipolysis in dog adipocytes in vitro. The utilisation of selective beta 1- and beta 2-adrenoceptor antagonists (bisoprolol and ICI 118,551) in both lipolysis and binding studies (displacement of [3H]-dihydroalprenolol binding) demonstrated the presence of the two beta-adrenoceptor subtypes in dog fat cells. 3. Infusion of either yohimbine or procaterol (10 and 0.4 nmol min-1 kg-1, respectively for 30 min), provoked an equivalent increase in plasma non-esterified fatty acids (+100%). Procaterol, but not yohimbine, induced hyperglycaemia (+120%). Plasma insulin was weakly enhanced by yohimbine (+120%) as compared to the increase given by procaterol (+500%). 4. Both drugs stimulated sympathetic nervous system activity, as indicated by the increased plasma noradrenaline concentration, but only yohimbine increased the plasma adrenaline level. 5. Cardiovascular measurements indicated that procaterol strongly enhances heart rate and transiently decreases mean blood pressure. Yohimbine exhibits a weaker effect on heart rate and slightly increases mean blood pressure. 6. The present work clearly indicates that lipid mobilization is enhanced during fasting in the dog by selective beta 2-adrenoceptor stimulation or by alpha 2-adrenoceptor blockade. This enhanced lipolytic effect may result either from a direct action of the drugs on the adrenoceptors of fat cells or from an activation of the sympathetic nervous system. Procaterol suffers major limitations since it strongly increases heart rate, immunoreactive insulin and glycaemia. On the other hand, yohimbine induces only minor modifications both in cardiovascular and endocrinological parameters.
Adipose Tissue↗
Effects of procaterol, a beta-2-adrenoceptor stimulant, on neuroeffector transmission in human bronchial tissue.
It has been reported that low concentrations of noradrenaline or isoprenaline reduce the resting tension of the smooth muscle cells and suppress acetylcholine release from the vagal nerve terminals through activation of beta 2-adrenoceptors. Procaterol, beta 2-adrenoceptor stimulant, has a high potency and selectivity for airway smooth muscle tissues. However, there is little documentation on the prejunctional actions of this chemical in airway smooth muscle, especially in man. In the present study, the effects of procaterol on excitatory neuroeffector transmission in the human bronchus were investigated. Procaterol (10(-10) to 10(-7) M) dose dependently reduced the amplitude of the contractions evoked by electrical field stimulation in the presence of indomethacin (10(-5) M), FPL-55712 (10(-6) M), and guanethidine (10(-6) M). By contrast, procaterol (10(-10) to 10(-9) M) had no effect on the postjunctional response of smooth muscle cells to exogenously applied acetylcholine. Pretreatment with ICI-118551 (10(-7) M), a beta 2-adrenoceptor-blocking agent, reduced the inhibitory action of procaterol on the amplitude of twitch contractions evoked by field stimulations in the human bronchus. These results indicate that procaterol at low concentrations has a prejunctional action, inhibiting the excitatory neuroeffector transmission and presumably suppressing transmitter release from the vagal nerve terminals through beta 2-adrenoceptors in the human bronchial tissue. The prejunctional action of procaterol explains partly its potent bronchodilator effects in clinical use.
Acetylcholine↗
Effect of procaterol on the isolated airway smooth muscle and the release of anaphylactic chemical mediators from the isolated lung fragments.
The effects of an orally active and selective beta 2-stimulant, procaterol (OPC-2009) on the isolated pulmonary smooth muscle and the release of chemical mediators from the passively sensitized lung fragments were studied and compared with those of isoprenaline (isoproterenol) and salbutamol. Procaterol potently relaxed the isolated guinea pig trachea and lung parenchyma in a concentration-dependent fashion. The drug at a similar range of concentrations antagonized the contraction of the isolated guinea pig trachea and lung parenchyma or human bronchus induced by leukotriene (LT) D4. Salbutamol and isoprenaline also showed similar effects to those of procaterol on the above experiments, but the potencies were consistently weaker than that of procaterol. The release of either histamine or LTs from the passively sensitized human lung fragments was markedly and dose-dependently inhibited by both the 5 min and 15 h treatment with procaterol (10(-10)-10(-7) mol/l) before antigen challenge. Isoprenaline and salbutamol in 5 min treatment experiments showed similar potency as and less potency than procaterol, respectively, on the release of these mediators, but the inhibition potencies of these drugs, particularly isoprenaline, were remarkably reduced by 15 h treatment. From these results, procaterol, besides the existing use as a bronchodilator, is expected to be a potentially prophylactic drug for allergic asthma because of the strong inhibition of the anaphylactic mediator release.
Albuterol↗
Comparative study of chronotropic and inotropic responses to 5-(-hydroxy-2-isopropylaminobutyl)-8-hydroxycarbostyril hydrochloride hemihydrade (procaterol), salbutamol, noradrenaline and isoprenaline in the dog heart.
1. The cardiac chronotropic and inotropic responses to 5-(1-hydroxy-2-isopropylaminobutyl)-8-hydroxycarbostyril hydrochloride hemihydrade (procaterol) and salbutamol have been compared to noradrenaline and isoprenaline in isolated blood-perfused canine atrial and ventricular preparations. 2. All four compounds induced dose-related positive chronotropic and inotropic effects, but different individual response patterns were observed. 3. Procaterol and salbutamol were partial agonists compared to noradrenaline and isoprenaline for causing chronotropic and inotropic responses. The order of efficacy for the adrenoceptors mediating both chronotropic and inotropic responses was isoprenaline, noradrenaline, salbutamol and procaterol. The slopes of the salbutamol dose-response curves were flatter than those for isoprenaline and noradrenaline; the slopes of the procaterol dose-response curves were flatter than those for salbutamol. 4. Because of these differences, the order of activity depended upon the level of response chosen for the comparison. When doses producing small chronotropic and inotropic responses were compared, the order of activity was isoprenaline, noradrenaline, procaterol and salbutamol; whereas with doses producing large responses the order was isoprenaline, noradrenaline, salbutamol and procaterol. 5. Procaterol was longer acting than salbutamol, and salbutamol was longer acting than noradrenaline.
Adrenergic beta-Agonists↗
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↗
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↗
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↗
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↗