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PubMed1982

Effect of aminophylline on coronary functional hyperemia and myocardial adenosine.

The role of adenosine in coronary functional hyperemia was tested using the adenosine antagonist aminophylline. In 11 dogs left coronary blood flow (LCBF) and left ventricular oxygen extraction [(a-v)O2] were monitored. Myocardial oxygen consumption (MVO2) was calculated. Before aminophylline was administered, intracoronary infusion of 6.8 micrograms/min norepinephrine increased LCBF and MVO2 by 40-80%. Simultaneous infusion of adenosine further increased LCBF. Fifteen minutes after injection of 100 mg aminophylline, norepinephrine still increased LCBF, and the ratio delta LCBF/delta MVO2 was unchanged (P greater than 0.05). Although the functional hyperemia was not blunted, the response to infused adenosine was abolished by aminophylline. In 20 additional dogs myocardial adenosine was determined. Before norepinephrine infusion myocardial adenosine with and without aminophylline was 12.7 and 14.3 nmol/g dry wt, respectively (P greater than 0.05). During norepinephrine infusion an increase in adenosine correlated well with increases in MVO2 and LCBF, but the increase in adenosine was not greater after aminophylline. Thus the failure of aminophylline to blunt functional hyperemia was not due to a higher adenosine level after aminophylline. These results do not support a role for adenosine in functional hyperemia elicited by norepinephrine.

Adenosine↗

PubMed1987

The effects of aminophylline on sleep and sleep-disordered breathing in patients with obstructive sleep apnea syndrome.

The methylxanthine derivatives are known to have respiratory stimulant properties. To determine whether these drugs would improve obstructive sleep apnea, 10 male patients with obstructive sleep apnea (OSA) (Apnea Index greater than 15/h) were given infusions of aminophylline and a saline placebo on 2 separate nights a week apart, using a randomized crossover design. There was a significant decrease during aminophylline infusion in the frequency of those apneas, which contained periods of complete respiratory inactivity (central and mixed apneas; placebo, 4.3 +/- 1.8/h; aminophylline, 0.7 +/- 0.5/h; p less than 0.05). There was no change in either the frequency (placebo, 31.8 +/- 5.9/h; aminophylline, 28.7 +/- 8.7/h; NS) or duration of obstructive apneas. Mean and minimal arterial oxygen saturation values were also unchanged. Sleep architecture was markedly disturbed by aminophylline. There was a reduction in sleep efficiency (placebo, 84.8 +/- 2.0%; aminophylline, 60.2 +/- 5.0%; p less than 0.005), an increase in sleep fragmentation (sleep stage shifts/h: placebo, 11.6 +/- 1.3: aminophylline, 21.0 +/- 2.9; p less than 0.05) and less Stage 2 and more Stage 1 non-REM sleep. We conclude that aminophylline reduces central apnea and the central component of mixed apneas but has no effect on obstructive apnea. Theophylline is therefore unlikely to be therapeutically useful in patients with OSA, and because it leads to marked sleep disruption, its long-term use could conceivably increase the propensity to upper airway occlusion during sleep.

Aminophylline↗

PubMed1988

Aminophylline has little positive inotropic effect and a slightly negative diastolic effect on the left ventricle during hypoxic conditions in dogs.

We examined the effect of aminophylline on left ventricular (LV) mechanics and central hemodynamics under normoxic and hypoxic conditions in respective groups of dogs. In an open-chest preparation, LV end-systolic and diastolic dimensions were measured with ultrasonic crystal transducers seated subendocardially along the anterior to posterior and apex to base axes. In the group studied during hypoxia, measurements were obtained during 3 conditions: normoxia; hypoxia to a PO2 of 30 mm Hg; and during hypoxia when aminophylline was infused to a blood level of about 15 mg/L. In the group studied under normoxic conditions, measurements were initially obtained during normoxia after which aminophylline was also infused to a blood level of 15 mg/L. Intravascular volume was given or removed to maintain LV filling pressures at about 10 mm Hg during all conditions. In the normoxic group, aminophylline caused an increase in stroke volume (SV) and had a positive inotropic effect on the LV. End-systolic dimensions were reduced, while end-diastolic dimensions did not change with aminophylline. On the other hand, under hypoxic conditions, aminophylline did not have a positive inotropic effect: SV did not increase and end-systolic dimensions remained unchanged. Under hypoxic conditions, moreover, aminophylline caused a slight decrease in end-diastolic dimensions by augmenting hypoxia-induced increases in myocardial resting tension. Our results indicate that unlike normoxic conditions, aminophylline may have little beneficial effect on LV performance during hypoxic conditions.

Aminophylline↗

PubMed1994

Treatment of acute asthma. Lack of therapeutic benefit and increase of the toxicity from aminophylline given in addition to high doses of salbutamol delivered by metered-dose inhaler with a spacer.

We conducted a randomized, double-blind, placebo-controlled study to determine if intravenous aminophylline adds any benefit to high doses of inhaled salbutamol in patients who presented for treatment of acute asthma. We studied 94 patients (mean age, 35.6 +/- 11.2 years) with moderate to severe acute asthma. All patients received therapy with salbutamol delivered with metered-dose inhaler (MDI) into a spacer device (Volumatic) in four puffs (400 micrograms) at 10-min interval, and intravenous hydrocortisone (500 mg). Patients were randomly assigned to receive either a loading dose of intravenous aminophylline followed by a routine infusion (n = 45) or an equal volume of placebo as a loading dose and infusion (n = 49). The two groups showed no differences in measurements of peak expiratory flow, FEV1, and FVC at baseline and at the end of treatment. However, the patients treated with aminophylline had significantly more adverse effects (p < 0.05). There were no differences in the final mean dose of salbutamol (6.3 +/- 44.5 mg for the placebo group and 5.8 +/- 4.2 mg for the aminophylline group), hospital admission rate (10.2 percent for the placebo group and 9.0 percent for the aminophylline group), and mean duration of Emergency Department treatment (2.5 +/- 1.83 h for the placebo group and 2.37 +/- 1.75 h for the aminophylline group). The results were similar when the patients were divided in accord with the degree of respiratory obstruction (baseline FEV1 < 30 percent of predicted) and theophylline level at 30 min of treatment (placebo group patients with theophylline level < 10 mg/L vs aminophylline group patients with theophylline level > or = 10 mg/L). We conclude that intravenous aminophylline adds to the toxicity but not the efficacy of inhaled salbutamol in the treatment of acute exacerbations of asthma.

Acute Disease↗

PubMed1990

Inhaled albuterol and oral prednisone therapy in hospitalized adult asthmatics. Does aminophylline add any benefit?

STUDY OBJECTIVE: To determine the efficacy of intravenous aminophylline in the treatment of adult patients hospitalized for exacerbation of asthma. DESIGN: Randomized, double-blind, placebo-controlled trial throughout the study. SETTING: University Hospital Clinical Research Center. PATIENTS: Forty-four patients admitted from the emergency room with a primary diagnosis asthma; 39 patients completed the study. INTERVENTIONS: Patients received either intravenous aminophylline or placebo in addition to frequent nebulized albuterol; prednisone 0.5 mg/kg body weight every 6 h orally; and supplemental oxygen. Aminophylline infusion rates were adjusted to achieve serum theophylline concentrations of 10 to 20 micrograms/ml. Changes were made in placebo infusion rates to maintain the double blind design. MEASUREMENTS AND RESULTS: Forced expiratory volume in 1 s (FEV1) and other spirometric measurements every 8 h by a blinded investigator or trained respiratory therapist. Subjective patient response and duration of hospitalization were compared. No difference in spirometric measurements was observed between the two groups at any time point. On admission to the study, FEV1 in the placebo group was 41.5 (+/- 2.9) percent predicted and in the aminophylline group 34.7 (+/- 2.3) percent predicted (p = 0.08). At discharge, FEV1 was 70.4 (+/- 2.9) percent predicted in the placebo group and 63.7 (+/- 2.8) percent predicted in the theophylline group (p = 0.10). There was no difference in subjective patient rating or duration of hospitalization between the two groups (placebo 1.95 days and aminophylline 1.78 days, p = 0.51). CONCLUSIONS: Our results suggest that aminophylline therapy does not add significant benefit to other standard therapies in hospitalized adult asthmatic patients. Because of the risks and cost of aminophylline treatment in the hospital setting, further research is needed to determine if there are subgroups of adult asthmatics who may benefit from the addition of aminophylline to other standard optimal therapies.

Acute Disease↗

PubMed2003

Aminophylline for the prevention of apnea during prostaglandin E1 infusion.

BACKGROUND: Apnea is associated with prostaglandin E1 infusion (PGE1) used in the palliation of ductal-dependent congenital heart lesions. HYPOTHESIS: Aminophylline is a central respiratory stimulant and will decrease the incidence of PGE1-associated apnea and the need for intubation for apnea in infants with ductal-dependent congenital heart disease. METHODS: Informed consent was obtained for all patients. In a prospective, double-blinded, placebo-controlled study, newborn infants with ductal-dependent congenital heart disease were randomized to receive either aminophylline or placebo during initiation and maintenance of PGE1, which was started at 0.01 microg/kg/min and increased to 0.03 microg/kg/min. Aminophylline was given as a bolus dose of 6 mg/kg before or during initiation of PGE1, and continued at 2 mg/kg dose every 8 hours for 72 hours. Serum aminophylline levels were checked at 18 and 36 hours. The primary study endpoint was intubation for apnea, with a secondary endpoint of apnea, as defined as acute cessation of breathing with associated hypoxia and bradycardia. RESULTS: The study evaluated 42 infants. The 2 groups were similar for gestational age, weight, hematocrit, and use of sedation. In the aminophylline group, serum levels were 7.6 +/- 1.2 microg/mL. No significant side effects of aminophylline were seen. Infants receiving aminophylline (n = 21) were less likely to have apnea (2 vs 11) or be intubated for apnea (0 vs 6). Length of postoperative stay and survival to discharge were similar between the 2 groups. CONCLUSIONS: Aminophylline was effective for the prevention of apnea and intubation for apnea associated with PGE1 in infants with ductal-dependent congenital heart disease.

Alprostadil↗

PubMed2003

The current role of intravenous aminophylline in acute paediatric asthma.

Intravenous aminophylline is effective in children with acute asthma and was the bronchodilator of choice for many years. However, with the advent of inhaled b agonists and anticholinergic agents an alternative, less invasive, therapeutic strategy is currently available. If children with acute asthma fail to respond to inhaled therapy clinicians may consider aminophylline a controversial treatment. The published evidence on whether aminophylline produces further beneficial effect in children already receiving inhaled therapy for acute asthma is reviewed in this paper. The published randomised controlled trials comparing aminophylline with placebo are of good methodological quality, although the numbers of children in many of the studies are small. Trial outcomes included lung function (FEV1 and PEF) and clinical scoring of asthma severity. Aminophylline improved percentage predicted FEV1 by 6 hours, and this effect was maintained for 24 hours. Improvements were also seen in clinical asthma severity scores at 6 hours. Despite improvements in lung function and asthma severity, there was no reduction in hospital stay or the number of nebulisers required. The main side effect of aminophylline therapy was an increased incidence of vomiting. In conclusion, the addition of intravenous aminophylline should be considered early in the treatment of children hospitalised with acute severe asthma with suboptimal response to the initial inhaled bronchodilator therapy. Further research should be carried out to examine whether intravenous aminophylline may have a beneficial effect in other settings such as intensive care to determine if it may reduce intubation and ventilation rates.

Acute Disease↗

PubMed2006

Photodynamic inactivation of trypsin by the aminophylline-riboflavin system: involvement of hydroxyl radical.

BACKGROUND: Riboflavin finds ubiquitous occurrence in plants and animals and functions as a coenzyme participating in various oxidation-reduction reactions during the course of metabolism. Photosensitized riboflavin generates reactive oxygen species (ROS). Aminophylline is an antiasthmatic drug and a known phosphodiesterase inhibitor. In this study we examined the effect of photoilluminated riboflavin on aminophylline using trypsin as the target molecule. MATERIAL/METHODS: The possible loss of trypsin activity due to autolysis was assayed after incubation in fluorescent light. Changes in trypsin activity caused by photoilluminated riboflavin alone and with aminophylline were monitored as functions of concentration and time. These effects were also analyzed by SDS-PAGE to visualize protein degradation. Spectra of riboflavin, alone and with aminophylline, under different conditions were taken to monitor the structural changes for elucidating the possible reaction mechanism involved. Free radical scavengers were also included in some experiments. RESULTS: Aminophylline alone is not known to posses any photosensitizing characteristics. However, in the presence of riboflavin and fluorescent light, aminophylline caused inactivation and fragmentation of trypsin. This fragmentation was found to be concentration dependent and was mediated by ROS. In all cases, thiourea, a scavenger of hydroxyl radicals, was most effective in scavenging the damaging effect of the riboflavin-aminophylline combination. CONCLUSIONS: Based on our results we suggest that photoilluminated riboflavin generates the singlet and triplet excited states that, upon energy transfer, generate (1)O(2). and (3)O(2). oxygen. These activated oxygen species probably attack aminophylline leading to its oxidation, generating hydroxyl radicals which presumably cause inactivation and fragmentation of trypsin.

Aminophylline↗

PubMed1975

Regulation of aryl hydrocarbon (benzo-(A)-pyrene) hydroxylase activity in mammalian cells. Induction of hydroxylase activity by N6,O2'-dibutyryl8 adenosine 3':5'-monophosphate and aminophylline.

Treatment of hamster BHK cells with N6,O2'-dibutyryl adenosine 3':5'-monophosphate (Bt2cAMP), aminophylline, theophylline, or papaverine increased the level of aryl hydrocarbon (benzo(a)pyrene) hydrolxylase activity. The highese increase, 100-fold, was obtained with Bt2cAMP plus aminophylline or theophylline. N2,O2-Dibutyryl guanosine 3':5'-monophosphate gave a lower induction than Bt2cAMP. The level of hydroxylase activity started to decrease 6 hours after treatment with the inducer and was reduced to almost the uninduced level after 24 hours. Repeated addition of Bt2cAMP and aminophylline did not prevent this decrease. The hydroxylase can also be induced by treating cells with benz(a)anthracene, and the level of this induced activity was maintained for 24 hours. Aminophylline gave a 2- to 8-fold stimulation of the induction by benz(a)anthracene. The enzyme activity induced by Bt2cAMP, aminophylline, and benz(a)anthracene converted benzo(a)pyrene to similar alkali-extractable metabolities with a fluorescence spectra similar to that of 3-hydroxybenzo(a)pyrene. These induced enzyme activities also showed a similar heat stability. Induction by Bt2cAMP and aminophylline, like induction by benz(a)anthracene, required continued protein synthesis and only an initial period of RNA synthesis. Compared to the benz(a)anthracene-induced hydroxylase with a Km of 4.3 muM, the hydroxylase induced by Bt2cAMP and aminophylline showed a Km of 0.14 muM, and was 100-fold more sensitive to inhibition by 7,8-benzoflavone. Increasing the serum concentration in the culture medium stimulated the induction by aminophylline but did not stimulate induction by benz(a)anthracene. The results indicate that aryl hydrocaarbon (benzo(a)pyrene) hydroxylase can be induced by compounds that increase the level of adenosine 3':5'-monophosphate and that this induction and induced enzyme activity differs from that caused by benz(a)anthracene.

Aminophylline↗

PubMed1988

Aminophylline treatment in severe, acute asthma. A meta-analysis.

Aminophylline is routinely recommended as a basic part of the emergency treatment of asthma. A comprehensive search found 13 reports of controlled trials of intravenous aminophylline therapy in severe, acute asthma. These studies compared aminophylline therapy with treatment with either albuterol (salbutamol), epinephrine, or other bronchodilators. The 13 reports did not agree. Seven reported no difference in spirometric values between aminophylline treatment and the control regimens. Three found aminophylline treatment superior. Three favored the control regimen. The results of the 13 trials were reanalyzed and pooled. Overall, there was no difference between the aminophylline-treated groups and the control groups. Sensitivity analysis suggests that aminophylline therapy is ineffective alone but may be more effective than single-drug therapy when combined with an injected beta-agonist. Despite widespread practice, available trials do not provide adequate evidence to support or reject the use of aminophylline in the treatment of severe, acute asthma.

Albuterol↗

PubMed1983

Potentiation of the antithrombotic effect of prostacyclin by simultaneous administration of aminophylline in a canine model of coronary artery thrombosis.

The antithrombotic efficacy of prostacyclin (PGI2) when administered in conjunction with the phosphodiesterase inhibitor aminophylline was evaluated in a canine model in which coronary artery thrombosis was induced by electrical stimulation of the intimal surface of the left circumflex (LCX) coronary artery. Infusions of PGI2 (25 or 50 ng/kg/min) into the left atrial appendage and aminophylline (20 micrograms/kg/min) or ethylene diamine into the left jugular vein were initiated 10 min before the start of LCX coronary artery stimulation and continued for the 6-hr stimulation period. Every animal in the control (Tris buffer plus ethylene diamine, n = 7), PGI2 (25 ng/kg/min) only (n = 6) and aminophylline only (n = 7) groups developed completely occlusive coronary artery thrombi. In contrast, none of the animals receiving PGI2 (25 ng/kg/min) plus aminophylline or PGI2 (50 ng/kg/min) plus aminophylline underwent occlusive thrombus formation. The average thrombus mass developed in response to intimal injury of the LCX coronary artery was 57 +/- 14 mg (X +/- S.E.M.) in the control group. Aminophylline administration in conjunction with PGI2 infusion at doses of 25 and 50 ng/kg/min significantly reduced thrombus mass to 11 +/- 2 and 10 +/- 1 mg, respectively (P less than .05). PGI2 (25 ng/kg/min) plus aminophylline reduced mean arterial pressure by 12% from 116 +/- 5 to 102 +/- 4 mm Hg. These data demonstrate that the combined administration of aminophylline with low-dose PGI2 provides antithrombotic efficacy while minimizing the detrimental hemodynamic effects of large-dose PGI2 administration.

Aminophylline↗

PubMed1982

Physiochemical properties of aminophylline-dextrose injection admixtures.

The compatibility and stability of aminophylline-dextrose injection admixtures were investigated. Aliquots of 5% dextrose injection, 0.9% sodium chloride injection, and 5% dextrose and 0.9% sodium chloride injection were studied for these physiochemical properties: pH, color, clarity, absorbance in a spectrophotometer at 400 nm, and hydroxymethylfurfural (HMF) content. Aminophylline injection was added to the solutions, and aliquots were withdrawn after 0, 6, 24, and 48 hours of storage at 5, 25, 35, and 55 degrees C for testing of the physiochemical properties and aminophylline content. An aminophylline admixture in 5% dextrose injection was passed through an in-line filter (IVEX-2), and eluents were collected for aminophylline assay and for testing the above physiochemical properties. HMF and theophylline were assayed to high-pressure liquid chromatography (HPLC). The aminophylline concentration remained constant in all admixtures studied. A yellow color developed in dextrose-containing aminophylline admixtures stored at 25, 35, and 55 degrees C for 48, 24, and 6 hours, respectively. HMF concentration, pH, and clarity remained within compendial limits. The in-line filter did not retain active ingredients or alter the physiochemical properties of the admixture. Solutions that were yellow showed additional peaks on HPLC. HMF seemed to be a precursor for this yellow color, inasmuch as HMF concentration increased with increasing color intensity. It is concluded that aminophylline-dextrose admixtures are visually and chemically stable for 48 hours when stored under refrigeration or at room temperature.

Aminophylline↗

PubMed1980

Aminophylline pharmacokinetics and cardiorespiratory effects during halothane anesthesia in experimental animals.

The pharmacokinetics and cardiorespiratory effects of aminophylline during halothane anesthesia are not well established and are the subject of this study. Eleven dogs were anesthetized with 1% halothane in air and given 10 mg/kg of intravenous aminophylline (theophylline ethylenediamine) over 5 minutes. Serum theophylline levels were measured over the next 60 minutes and were found to be in the therapeutic range (10-20 mg/L). Theophylline levels decayed according to a two-component exponential function. The half-time for the fast component was 4.5 minutes, while the slow component half-time was 134.5 minutes. Heart rate increased significantly (p less than 0.05) within 2 minutes following aminophylline, and remained significantly elevated for 60 minutes. Pulmonary capillary wedge pressure and systemic vascular resistance decreased 2 minutes after aminophylline, as did the arterial-mixed venous oxygen content difference. Cardiac index increased 2 minutes following aminophylline. All these changes were transient, and values returned to near control values within 10 minutes after aminophylline. Arterial oxygenation, venous admixture, and physiologic dead space were not significantly (p less than 0.05) altered by aminophylline. No cardiac arrhythmias occurred. Other than a sustained 12% increase in heart rate, and transient hemodynamic changes immediately following its administration, aminophylline in therapeutic doses did not have adverse effects on cardiorespiratory function during prolonged 1% halothane anesthesia in normoxic, eucapnic dogs.

Aminophylline↗

PubMed1996

Improvement of exercise-induced ischaemia and myocardial perfusion after aminophylline.

BACKGROUND: Previous studies have suggested that aminophylline improves exercise-induced ischaemia by preventing the redistribution of the coronary flow from ischaemic to non-ischaemic myocardium. The purpose of the study was to assess whether aminophylline improves myocardial perfusion in zones supplied by collateral circulation. METHODS: Twenty-three patients with an occluded coronary artery and collateral circulation from a non-diseased vessel underwent two symptom-limited exercise 99mTc-MIBI, single-photon emission computed tomography (SPECT) myocardial scintigraphy experiments, which were preceded by an intravenous infusion of either aminophylline (5 mg/kg over 20 min) or saline solution in a randomized double-blind control procedure. The MIBI SPECT images were analysed by two experienced observers who were blinded to each other's data. RESULTS: All patients underwent cardiac catheterization. For 16 patients this was because of stable angina and the remaining eight were post-myocardial infarction patients with a positive exercise test. Aminophylline significantly increased the time to the onset of ischaemia in the 15 patients with a positive exercise test (mean +/- SD, 6.5 +/- 1.9 compared with 5.3 +/- 1.8 min, P < 0.005); and ischaemia occurred at higher rate-pressure product (230 +/- 68 compared with 195 +/- 68 HB x mmHg, P < 0.03). After aminophylline, exercise ST-segment depression was 1.1 +/- 0.5 mV, compared with 1.5 +/- 0.8 mV after placebo (P < 0.01). All patients had perfusion defects that resolved partially or completely in the rest images. The imaging score was significantly lower after aminophylline infusion than after placebo (9.7 +/- 9 compared with 12.1 +/- 10, P < 0.01). CONCLUSIONS: Aminophylline significantly delayed the time to onset of exercise-induced ischaemia and improved perfusion in zones supplied by collateral circulation. Aminophylline-like drugs may be useful in the treatment of selected patients with ischaemic heart disease.

Aminophylline↗

PubMed1996

[Effect of beta 2-adrenergic agonists on neurotoxic action of aminophyllines].

The purpose of the present investigation was to evaluate whether the beta 2-adrenergic agonists affect the pharmacodynamics and pharmacokinetics of aminophylline-induced seizures. Adult male Albino Swiss mice were treated i.p. with salbutamol, fenoterol or terbutaline and 30 min. later they received i.p.aminophylline. During 90 min. observation clonic and tonic seizures and also mortality of mice were registered. Moreover the influence of beta 2-adrenomimetics on electroshock-induced seizure threshold (CS 50) and on plasma aminophylline concentration was estimated. It was found that pretreatment with salbutamol, fenoterol and terbutaline decreased the ED 50 (for clonic and tonic seizures) and LD 50 of aminophylline. Fenoterol decreased but terbutaline increased the CS 50 in mice. Only terbutaline elevated significantly the plasma concentration of aminophylline. The data indicate that concomitant treatment with beta 2-adrenergic agonists together with aminophylline increase the risk of aminophylline-induced seizures. Thus plasma monitoring of aminophylline concentration could be used in all patients treated simultaneously with beta-2-adrenergic agonists and aminophylline.

Adrenergic beta-Agonists↗

PubMed2001

Intravenous aminophylline for acute severe asthma in children over 2 years using inhaled bronchodilators.

BACKGROUND: Intravenous aminophylline was the bronchodilator of choice for many years until supplanted by more effective bronchodilators in the treatment of acute paediatric asthma. Recently there has been renewed interest in this therapy for children with acute severe asthma. OBJECTIVES: To determine whether addition of intravenous aminophylline produces a beneficial effect in children with acute severe asthma receiving oxygen, maximised inhaled bronchodilators and oral/intravenous glucocorticoids. SEARCH STRATEGY: The Cochrane Airways Group register of trials (based on MEDLINE, EMBASE, CINAHL and hand searched respiratory journals) and reference lists of relevant articles were used to identify relevant studies. The latest search was carried out in October 2000. SELECTION CRITERIA: Only randomised-controlled trials comparing intravenous aminophylline with placebo in children treated with inhaled bronchodilators and systemic glucocorticoids for acute asthma were considered for this review. DATA COLLECTION AND ANALYSIS: Full text of 35 trials were anonymized for author, date and publication and two blinded independent reviewers selected eligible studies for inclusion. Disagreement was resolved through consensus. Seven trials met the inclusion criteria. Attempts were made to contact authors to verify accuracy. Results were reported as weighted mean differences (WMD) or relative risk (RR) with 95% confidential intervals (CI). MAIN RESULTS: Patients in these trials were predominantly school-aged children hospitalised for acute severe asthma with a baseline FEV1 at 35-40% of predicted and/or a baseline Pulmonary Index of 6-7. Aminophylline significantly improved percentage predicted FEV1 by 6 - 8 hours (WMD 8.4%; 95% CI: 0.82, 15.92%). The effect was maintained for 24 hours. Improvements were also seen in symptom scores at 6-8 hours (WMD= -0.71; 95% CI: -0.82,-0.60). There was no reduction in hospital stay or in number of nebulisers required. Vomiting was more likely with aminophylline therapy (Relative Risk = 3.69; 95% CI: 2.15, 6.33). REVIEWER'S CONCLUSIONS: Addition of intravenous aminophylline should be considered early in the treatment of children hospitalised with acute severe asthma with sub optimal response to the initial inhaled bronchodilator therapy. Although the improvement is sustained for 24 hours, there is no apparent reduction in length of hospital stay or number of inhaled beta2-agonists nebulisations. Treatment with aminophylline is associated with an increased risk of vomiting.

Acute Disease↗

PubMed1998

Effect of aminophylline in patients with atropine-resistant late advanced atrioventricular block during acute inferior myocardial infarction.

BACKGROUND: Advanced atrioventricular (AV) block is a frequent complication in patients with acute inferior myocardial infarction (AIMI). This conduction abnormality is associated with narrow QRS complex in conducted or junctional escape beats, suggesting that the site of block is the AV node; however, its pathophysiology has not been properly established. HYPOTHESIS: This study investigated the effect of aminophylline in eight patients (5 men, 3 women, age range 51 to 78 years, mean 67.5 +/- 8.8 years) with atropine-resistant late advanced AV block during AIMI. METHODS: Advanced AV block was late in appearance in all patients, starting 2 to 5 days after AIMI, and consisted of second-degree Mobitz II type in two patients and of complete AV block in six patients; all patients had narrow QRS complexes. Before aminophylline administration, all patients had a temporary pacemaker installed which was switched off throughout the study. They were given intravenous atropine (1 mg) that was found to be ineffective. One-half h after atropine, the first aminophylline injection (240 mg) was given intravenously over 10 min. One h following the first injection, a second aminophylline dose (240 mg) was administered. Electrocardiographic rhythm strips were obtained before and after drug administration, and the type of AV block and atrial and ventricular rate were noted. RESULTS: Aminophylline restored 1:1 conduction with first-degree AV block in six patients, Mobitz I AV block in one patient, and normal sinus rhythm in one patient. Mean atrial and ventricular rates before aminophylline were 104 +/- 16 beats/min and 57 +/- 9 beats/min, respectively, and after drug administration 95 +/- 25 beats/min and 89 +/- 17 beats/min, respectively, (p = 0.012). CONCLUSION: These results indicate that aminophylline improves AV conduction in atropine-resistant late advanced AV block complicating AIMI.

Aged↗

PubMed1979

Antepartum aminophylline treatment for prevention of the respiratory distress syndrome in premature infants.

The frequency of idiopathic respiratory distress (IRD) among premature offspring born of women who were given aminophylline before the thirty-fourth week of pregnancy was evaluated. Sixty-seven premature deliveries were included in the aminophylline group and 75 in the control group. The perinatal death rate was 7.1% in the aminophylline group and 17.9% in the control group (p less than 0.05). A statistically significant difference was noted between the aminophylline and control groups in the frequency of IRD which was three times lower (10%) in the aminophylline group than in the control group (29.5%) for the total of premature infants. If the time of rupture of membranes is taken into consideration, a significant decrease in the frequency of IRD following aminophylline administration is noted in the infants, whose mothers had ruptured membranes for more than 24 hours. No complications or side effects of aminophylline administration were noted in the mothers or their infants.

Aminophylline↗