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Aminophylline (Aminophyllinum)

Parenterally. Asthmatic status: as part of complex therapy; a small additional effect for adults - intravenous infusion of 720-750 mg - and for children.

Apnea of newborns: administered via nasogastric tube in an initial dose of 5 mg/kg, maintenance dose - 2 mg/kg in 2 divided doses; the duration of treatment is several weeks or months. In premature newborns, a loading dose of 5-6 mg/kg intravenously, then 1.5 mg/kg every 8 hours for 48 hours.

Ischemic cerebrovascular accident (as part of complex therapy; insufficient evidence; no effect detected).

Edema syndrome in kidney diseases (as part of complex therapy).

Left ventricular failure, occurring with bronchospasm and Cheyne-Stokes breathing.

Inside.

Broncho-obstructive syndrome of various origins: bronchial asthma (drug of choice for exercise-induced asthma and additional remedy for other forms), COPD (pulmonary emphysema, chronic obstructive bronchitis). Pulmonary hypertension, cor pulmonale.

Sleep apnea (insufficient evidence; no effect detected).

Intravenously for adults in emergency conditions: 6 mg/kg, previously dissolved in 10-20 ml of 0.9% sodium chloride solution, administered slowly over 5 minutes.

Intramuscularly for adults: 100-500 mg/day.

Orally for adults: 100-200 mg 3-4 times a day, if necessary, increase the dose every 3 days.

Orally for adults in the form of prolonged forms: initial dose of 175 mg every 12 hours, then the dose is increased every 3 days until the optimal therapeutic effect is obtained.

In the acute phase of COPD for adults: initial dose 5-6 mg/kg (with a further increase in dose for every 0.5 mg/kg, the concentration of aminophylline in the blood increases by 1 μg/ml). The concentration in the blood should not exceed 20 mcg/ml. The maintenance dose for smoking patients is 4 mg/kg every 6 hours, for non-smokers and patients with liver pathology - 2 mg/kg every 8 hours.

Outside of exacerbation of COPD in adults: initial dose 6-8 mg/kg/day (maximum 400 mg/day) in 3-4 divided doses, possibly increasing the dose by 25% every 2-3 days to a maximum of 13 mg/kg/day (900 mg/day).

Rectally in the form of microenemas: 0.24-0.48 g in 20-25 ml of warm water; for children - according to age.

Maximum doses for adults orally, intramuscularly and rectally: single - 0.5 g, daily - 1.5 g; intravenously: single - 0.25 g, daily - 0.5 g.

Use in children

For maintenance therapy of asthma, taken orally; dosing according to the manufacturer's instructions.

To relieve a severe asthma attack.

Intravenous stream over 20 minutes (provided that the patient did not take theophylline before administration). 1 month-18 years: 5 mg/kg (maximum 500 mg), then intravenous infusion.

Intravenous infusion (the dose is selected by determining the concentration of theophylline in the blood plasma). 1 month-9 years: 1 mg/kg/hour. 9-16 years: 800 mcg/kg/hour. 16-18 years: 500 mcg/kg/hour.

The optimal effective concentration of theophylline in plasma for bronchial asthma is 10-20 mg/l. Children taking theophylline or aminophylline by mouth are usually given intravenous aminophylline only when plasma theophylline concentrations can be monitored.

For the treatment of neonatal apnea. Intravenous bolus over 20 minutes: initial dose 6 mg/kg, then 2.5 mg/kg every 12 hours, increasing if necessary to 3.5 mg/kg every 12 hours.

The optimal concentration of theophylline in plasma for the treatment of neonatal apnea is 8-12 mg/l. Children taking theophylline or aminophylline by mouth are usually given intravenous aminophylline only if plasma theophylline concentrations can be monitored.

In the acute phase of the disease, the initial dose is 5-6 mg/kg, and the maintenance dose (mg/kg) is calculated using the following formula. Up to 6 months: 0.07 × age in weeks + 1.7 (every 8 hours). 6-12 months: 0.05 × age in weeks + 1.25 (every 6 hours). 1-9 years: 5 mg/kg every 6 hours 9-12 years: 4 mg/kg every 6 hours 12-16 years: 3 mg/kg every 6 hours.

In the absence of exacerbation, the initial dose is 16 mg/kg/day (maximum 400 mg/day) in 3-4 doses, the dose can be increased by 25% every 2-3 days to the maximum daily dose, which is 0.3 × age up to 1 year in weeks + 8. In 1-9 years - 22 mg/kg. At 9-12 years old - 20 mg/kg. At 12-16 years old - 18 mg/kg. At 16-18 years old - 13 mg/kg.

Intramuscularly - 15 mg/kg/day.

Intravenously (duration of parenteral administration does not exceed 14 days). Under 3 months: 30-60 mg/day. 4-12 months: 60-90 mg/day. 2-3 years: 90-120 mg. 4-7 years: 120-240 mg. 8-18 years: 250-500 mg/day.

The highest doses for children orally, intramuscularly and rectally: single - 7 mg/kg, daily - 15 mg/kg; intravenously: single dose - 3 mg/kg.

Brand names

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Eufillin
Phyllocontin
Trufillin
Minomal R 175 mg tab
Minomal R 350 mg tab
Minomal SR 600 mg tab.

Recommendations

"Professional monograph of aminophylline." Drugs.com
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Mader T. J., Smithline N. A., Durkin L., Skriver G. (March 2003).
"Randomized controlled trial of intravenous aminophylline for the treatment of atropine-resistant out-of-hospital asystolic cardiac arrest." Academic Emergency Medicine
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(3): 192–7. Doi:10.1197/aemj.10.3.192. PMID 12615581.
"Aminophylline for injection." Drugs.com
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"Aminophylline for the prevention of bradyarrhythmias during orbital or rotational atherectomy of the right coronary artery." invasivecardiology.com
. Received 2018-06-15.
Caruso, M. K., Pekarovic, S., Raum, W. J., Greenway, F. (May 2007). "Topical reduction of fat in the waist area." Diabetes, obesity and metabolism
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(3): 300–3. Doi:10.1111/j.1463-1326.2006.00600.x. PMID 17391155.
Blackbourne L.H. Surgical review. Lippincott Williams and Wilkins, 2009, p. 169.
Hayward E; Showler L; Soar J (2007), “Aminophylline for bradyasystolic cardiac arrest”, Emerg.
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(8): 582–3, doi:10.1136/emj.2007.051342, PMC 2660094, PMID 17652689
Hurley KF, Magee K, Green R (November 2015). "Aminophylline for bradyasystolic cardiac arrest in adults." Cochrane Database of Systematic Reviews
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(11): CD006781. Doi:10.1002/14651858.CD006781.pub3. PMID 26593309.
Turan A, Kasuya Y, Govinda R, Obal D, Rauch S, Dalton JE, et al (February 2010). "Effect of aminophylline on loss of consciousness, bispectral index, propofol requirement and minimum alveolar concentration of desflurane in volunteers." Anesthesia and analgesia
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Luszczki JJ, Jankiewicz K, Jankiewicz M, Czuczwar SJ (May 2007). "Pharmacokinetic and pharmacodynamic interactions of aminophylline and topiramate in a mouse model of maximal shock-induced seizure." European Journal of Pharmacology
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Essayan DM (November 2001). "Cyclic nucleotide phosphodiesterases". Journal of Allergy and Clinical Immunology
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(January 2005). "Leukotrienes: underappreciated mediators of the innate immune response." Journal of Immunology
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Pharmacology

Like other methylated xanthine derivatives, aminophylline simultaneously

a competitive non-selective phosphodiesterase inhibitor[11] that increases intracellular camp, activates PKA, inhibits TNF-alpha[12][13] and leukotriene[14] synthesis and reduces inflammation and innate immunity[14] and
non-selective adenosine receptor antagonist.[15]

Aminophylline causes bronchodilation, diuresis†, Central nervous system cardiac stimulation, and gastric acid secretion by blocking phosphodiesterase, which increases tissue concentrations of cyclic adenosine monophosphate (cAMP), which in turn promotes catecholamine stimulation of lipolysis, glycogenolysis, and gluconeogenesis, and causes release adrenaline from adrenal medulla cells. †Note that diuresis is caused by an increase in cAMP, which acts in the CNS to inhibit the release of antidiuretic hormone (arginine vasopressin).

Adenosine is an endogenous extracellular messenger that can regulate myocardial oxygen demand.[2][16] It acts through cell surface receptors that influence intracellular signaling pathways to increase coronary artery blood flow, decrease heart rate, block atrioventricular node conduction, inhibit cardiac automaticity, and reduce β-adrenergic effects on contractility.[2][16] Adenosine also antagonizes the chronotropic and ionotropic effects of circulating catecholamines.[17] In general, adenosine reduces heart rate and contraction force, which increases blood flow to the heart muscle. Under certain circumstances, this mechanism (which is designed to protect the heart) can cause atropine-resistant refractory bradyasystole.[2] The effects of adenosine are concentration dependent. Adenosine receptors are competitively antagonized by methylxanthines such as aminophylline.[2][16][17] Aminophylline competitively antagonizes the cardiac effects of adenosine at cell surface receptors.[16] Thus, heart rate and contractility increase.