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PubMed2004

Effects of aminophylline on cytokines and pulmonary function in patients undergoing valve replacement.

OBJECTIVE: This study is to evaluate the effects of aminophylline on systemic inflammatory response after cardiopulmonary bypass in patients undergoing valve replacement. METHODS: Thirty patients undergoing elective valve replacement were randomized to receive either aminophylline treatment (aminophylline, n = 15) or no aminophylline (control, n = 15). Administration of aminophylline (5 mg/kg) was injected intravenously after induction of anesthesia and maintained with 0.5 mg/kg per h until the end of cardiopulmonary bypass. Perioperative cytokines (interleukin-8 and interleukin-10, tumor necrosis factor-alpha) and respiratory function, blood neutrophil count ratio of right atrium to that of left atrium, plasma malondialdehyde were measured during the experiment. RESULTS: Interleukin-8 and tumor necrosis factor-alpha levels after cardiopulmonary bypass were significantly lower in the aminophylline group than that in the control group (P < 0.05, for each group), and interleukin-10 level in aminophylline group was significantly higher than in control (P = 0.001). The respiratory index was greater in the control than in aminophylline group (P < 0.05). Neutrophil count ratio of right atrium blood to left atrium blood and plasma malondialdehyde level in aminophylline group were much lower (P = 0.02 and 0.001, respectively) than in the control 30 min after aortic declamping. Compared with control group, the duration of ventilation and intensive care unit stays were shorter in aminophylline group (P = 0.032 and 0.013, respectively). CONCLUSIONS: Intraoperative administration of aminophylline had anti-inflammatory effect and improved pulmonary oxygenation in patients undergoing valve replacement.

Adult↗
PubMed1986

Mechanical and electrical aspects of the relaxant action of aminophylline in guinea-pig isolated trachealis.

Aminophylline (1-1000 mumol l-1) suppressed the spontaneous tone of guinea-pig isolated trachealis in a concentration-dependent manner. In Krebs solution containing acetylcholine (1 mmol l-1), histamine (200 mumol l-1) or K+ (120 mmol l-1) isolated trachealis muscle developed near-maximal tension. The log concentration-effect curve for aminophylline was shifted 20 fold, 3 fold and 4 fold to the right, respectively, in the presence of these spasmogens. Three K+-channel inhibitors were tested: tetraethylammonium (TEA, 8 mmol l-1) did not modify the action of aminophylline, procaine (5 mmol l-1) shifted the log concentration-effect curve for aminophylline 2 fold to the left and 4-aminopyridine (5 mmol l-1) shifted the curve 2.5 fold to the right. Intracellular electrophysiological recording showed that aminophylline 10 mumol l-1 could cause relaxation in the absence of electrical changes. Higher concentrations of aminophylline (100-1000 mumol l-1) suppressed spontaneous slow waves and hyperpolarized the trachealis cells. In the presence of procaine (5 mmol l-1) or TEA (8 mmol l-1), the hyperpolarization induced by aminophylline (1000 mumol l-1) was significantly reduced but its relaxant effect was unchanged. In trachealis skinned of its plasma membranes, tension development induced by Ca2+ (20 mumol l-1) was unaffected either by aminophylline (1000 mumol l-1) or by isoprenaline (1 mumol l-1). In studies of the efflux of 86Rb+ from muscle-rich strips of trachea, aminophylline (100-1000 mumol l-1) was without effect whereas nicorandil (100 and 1000 mumol l-1) increased the efflux rate constant. It is concluded that aminophylline does not directly reduce the sensitivity of the contractile proteins to cytosolic Ca2+. In low concentration (1-10 mumol l-1) its relaxant action is not accompanied by membrane potential change but towards the upper end of its effective concentration range, aminophylline evokes hyperpolarization. This hyperpolarization may involve the opening of K+-channels which are inhibited by procaine and (to a lesser extent) by TEA. These K+-channels may be impermeable to 86Rb+.

Acetylcholine↗
PubMed1986

Aminophylline and fatigue of the sternomastoid muscle.

We examined the influence of intravenously infused aminophylline on the contractility of the sternomastoid muscle in 8 subjects. The muscle was stimulated directly using bipolar surface electrodes at 1, 10, 20, and 50 pulses per second (pps), and the force response was recorded. The ratio of force produced at 20 pps and 50 pps (20/50 ratio) was calculated. The effect of aminophylline on the 20/50 ratio was assessed at 2 dosages producing different blood serum levels (10.7 mg/L and 15.3 mg/L). At the lower dosage of aminophylline the potential prophylactic and curative influence of aminophylline was tested using 3 different experimental paradigms performed on separate days: (1) Baseline force frequency responses were determined before and 15 and 35 min after a headlifting maneuver; headlifting resulted in a decrease in the 20/50 ratio (low frequency fatigue). (2) The same sequence as in (1), with the addition of a continuous infusion of aminophylline started after the baseline force frequency responses. (3) The same sequence as in (1) except that the aminophylline infusion was begun only after the headlifting maneuver. After the fatiguing maneuvers, there were comparable and significant falls in the 20/50 ratio on all experimental days. The infusion of aminophylline did not significantly affect the baseline 20/50 ratio. In addition, aminophylline did not prevent the fatigue-related decrease in the 20/50 ratio or enhance its recovery. Experimental paradigms 1 and 2 were repeated at the higher aminophylline levels. Again, aminophylline did not prevent or reverse sternomastoid fatigue. We conclude that aminophylline in therapeutic dosages does not prevent or reverse low frequency fatigue of the sternomastoid muscle.

Adult↗
PubMed1980

Arrhythmogenic effects of aminophylline during halothane anesthesia in experimental animals.

Arrhythmogenic effects of aminophylline (theophylline ethylenediamine) during halothane anesthesia have been reported but have not been related to serum theophylline levels. This study was designed to determine the arrhythmogenicity of therapeutic and toxic serum theophylline levels during halothane anesthesia. The study consisted of three parts. In part 1 (induction) six dogs were anesthetized for 15 minutes with 1% halothane in air and then given intravenous aminophylline, 50 mg/kg. In part 2 (maintenance) eight dogs were anesthetized for 2 hours with 1% halothane and then given intravenous aminophylline, 10 mg/kg. In part 3, after four additional hours of steady-state 1% halothane anesthesia, additional intravenous aminophylline, 25 mg/kg, was given to these eight animals. Three of six dogs in part 1 had arrhythmias following aminophylline, with serum theophylline levels ranging from 48 to 66 mg/L. No dog in part 2 had arthythmias following the 10 mg/kg dose of aminophylline, with serum theophylline levels of 14 to 23 mg/L. Six of eight dogs in part 3 had arrhythmias shortly after aminophylline, 25 mg/kg, with serum theophylline levels of 36 to 72 mg/L. Aminophylline administration after prolonger 1% halothane anesthesia appears free from arrhythmogenic effects if serum theophylline levels remain near the therapeutic range (10 to 20 mg/L). Aminophylline administration resulting in high serum theophylline levels (above 36 mg/L) causes ventricular arrhythmias when aminophylline is given during induction or maintenance of 1% halothane anesthesia. Arrhythmias usually (89%) begin with 5 minutes of aminophylline administration, and these arrhythmias always resolve spontaneously within 2 minutes of onset.

Aminophylline↗
PubMed1982

The failure of aminophylline to modulate glucagon release in man.

There are conflicting results regarding the impact of cyclic AMP on pancreatic glucagon release. The effect of aminophylline, a phosphodiesterase inhibitor, on glucagon secretion was studied in four non-obese, non-diabetic, healthy young male volunteers. The subjects received separate infusions of: 1) aminophylline; 2) aminophylline and propranolol; 3) arginine; 4) aminophylline and arginine; 5) insulin; 6) aminophylline and insulin; and 7) aminophylline and isoproterenol. Aminophylline not only failed to alter glucagon levels but also did not affect the glucagon responses observed after arginine and insulin-induced hypoglycemia. The concurrent infusion of isoproterenol and aminophylline also failed to cause a glucagon response. Although glucagon release has been evoked by cyclic AMP in some in vitro system, administration of aminophylline to human subjects does not enhance secretion. These results indirectly suggest that cyclic AMP is of little importance in the control of glucagon secretion in man, though the effects of aminophylline at the cellular level may be complex.

Adolescent↗
PubMed1994

Aminophylline fails to improve the outcome of cardiopulmonary resuscitation from prolonged ventricular fibrillation: a placebo-controlled, randomized, blinded experimental study.

OBJECTIVES: The purpose of this study was to evaluate systematically the effects of the adenosine antagonist aminophylline on resuscitation outcome in a canine model of postcardioversion nonperfusing rhythm. BACKGROUND: Theoretic considerations and experimental studies indicate that myocardial adenosine accumulation during prolonged ventricular fibrillation might play a significant role in postcardioversion asystole and electromechanical dissociation. A recent uncontrolled clinical trial has suggested that the adenosine antagonist aminophylline might improve the outcome of cardiopulmonary resuscitation from refractory bradyasystolic cardiac arrest. METHODS: Two placebo-controlled, randomized, blinded experimental studies were performed. In protocol 1 (20 dogs), ventricular fibrillation was induced and maintained for 7.5 min. Sixty seconds before cardioversion, dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In protocol 2 (20 dogs), dogs were cardioverted to electromechanical dissociation after 5 min of unsupported ventricular fibrillation. Sixty seconds later, all dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In both experiments, resuscitation efforts were continued until return of spontaneous circulation, or up to 30 min. The primary end point was survival to 1 h. RESULTS: In protocol 1, 4 of 10 dogs survived in the aminophylline group, whereas 7 of 10 dogs survived in the placebo group, a nonsignificant trend toward unfavorable outcome from aminophylline. Pretreatment with aminophylline increased the number of cardioversion applications required to terminate ventricular fibrillation. In protocol 2, 5 of 10 and 6 of 10 dogs survived in the aminophylline and placebo groups, respectively. CONCLUSIONS: The results of this study suggest that aminophylline fails to improve the outcome of resuscitation from prolonged ventricular fibrillation. It does not reverse established electromechanical dissociation and may in fact increase the number of cardioversion applications required to terminate ventricular fibrillation. The rationale for conducting clinical trials with aminophylline during cardiopulmonary resuscitation is questionable.

Aminophylline↗
PubMed2000

A comparison of the spasmolytic effects of olprinone and aminophylline on serotonin-induced pulmonary hypertension and bronchoconstriction with or without beta-blockade in dogs.

In the present study in dogs, we compared with aminophylline the spasmolytic effects of olprinone, a novel phosphodiesterase 3 inhibitor, on serotonin-induced pulmonary hypertension (PH) and bronchoconstriction. Mongrel dogs were anesthetized with pentobarbital. PH and bronchoconstriction were induced with serotonin: 10 microg/kg + 1 mg x kg(-1) x h(-1), and assessed as % changes in pulmonary vascular resistance and bronchial cross-sectional area (basal = 100%). Initially, the relaxant effects of olprinone (n = 8: 0-1000 microg/kg) and aminophylline (n = 8: 0-100 mg/kg) were compared. Pulmonary vascular resistance and bronchial cross-sectional area were assessed before and 30 min after serotonin infusion began and 5 min after each dose of olprinone or aminophylline. We then determined whether propranolol (0.4 mg/kg) reversed the relaxation induced by olprinone (1000 microg/kg, n = 6) or aminophylline (100 mg/kg, n = 6) compared with saline (n = 6 each). Olprinone and aminophylline dose-dependently attenuated both PH and bronchoconstriction (olprinone > aminophylline: -logED(50)[mean] for PH and bronchoconstriction 5.37+/- 0.35[4.24 microg/kg] vs. 1.60+/-0.23[25.4 mg/kg] and 4.06+/-0.12[87.8 microg/kg] vs. 1.51+/-0.21[30.6 mg/kg], respectively). In addition, olprinone produced more potent pulmonary vasodilation than bronchodilation while aminophylline was equipotent. In addition, there was a significant increase in plasma catecholamines after olprinone (> or =100 microg/kg) and aminophylline (> or =10 mg/kg). With the exception of aminophylline-induced bronchodilation, propranolol did not reverse any of the other effects measured. Therefore, the spasmolytic effects of olprinone are independent of plasma catecholamines, while the bronchodilating effect of aminophylline may partially involve increased levels of circulating catecholamines.

Adrenergic beta-Antagonists↗
PubMed1986

Halothane anesthetic requirements are not affected by aminophylline treatment in rats and dogs.

The authors determined the effects of aminophylline on the anesthetic requirements for halothane in rats and dogs. MAC for halothane was determined in rats (n = 24) before and after aminophylline, 100 mg X kg-1 ip, or an equal volume of saline. Because changes in central noradrenergic neurotransmission have been linked to drug-induced changes in the depth of the anesthetic state, we investigated the effect of aminophylline on the turnover of norepinephrine in discrete brain regions of halothane-anesthetized rats. To facilitate testing at steady-state aminophylline conditions and to permit frequent blood sampling, halothane MAC was determined in dogs (n = 7) before and after a therapeutic level of aminophylline (15 +/- 2 micrograms X ml-1) was obtained. Neither in the rats (1.0 vs. 1.0%) nor in the dogs (1.04 +/- 0.14 vs. 1.01 +/- 0.14%) was halothane MAC affected by aminophylline treatment. Commensurate with the lack of change of anesthetic depth, aminophylline treatment did not affect noradrenergic neurotransmission in the brain of halothane-anesthetized rats. Furthermore, the anticipated increase in circulating catecholamines following aminophylline treatment in dogs did not materialize. The authors conclude that halothane anesthetic requirements are not altered by aminophylline treatment, possibly because of the attenuation of the putative sympathomimetic effects of aminophylline by halothane.

Aminophylline↗
PubMed1995

Effect of aminophylline on high-energy phosphate metabolism and fatigue in the diaphragm.

BACKGROUND: Diaphragmatic fatigue causes respiratory failure, for which aminophylline has been used as therapy. Because the mechanism of action of aminophylline in reversing diaphragmatic fatigue is unclear, we used in vivo 31P magnetic resonance spectroscopy (MRS) to determine the relation between diaphragmatic activation, force output, and aerobic metabolism. METHODS: Bilateral phrenic stimulation was used to pace the diaphragm in pentobarbital-anesthetized piglets (6-10 weeks old; n = 44). Esophageal and abdominal pressures were measured to calculate transdiaphragmatic pressure (Pdi) (Pdi = abdominal pressure-esophageal pressure) as an index of force output. Activation was determined by the amplitude of the compound action potential of the diaphragmatic electromyogram. Aerobic metabolism was assessed with a 31P MRS surface coil on the right hemidiaphragm with the animal in a 4.7-T magnet. The animals were divided into four groups based on aminophylline loading dose: saline, aminophylline 10 mg/kg (A10), aminophylline 20 mg/kg (A20), and aminophylline 40 mg/kg (A40). After aminophylline loading the diaphragm was paced for 25 min followed by a 10-min recovery. RESULTS: Aminophylline concentrations were 12.2 +/- 0.7, 21.9 +/- 2.4, and 44.9 +/- 3.6 mg/l in the A10, A20, and A40 groups, respectively. Compound action potential amplitude decreased in all groups by 30% after 25 min of pacing. Conversely, Pdi remained at 100 +/- 3% of the initial value after 5 min of pacing in the A40 group but decreased to 75 +/- 3% in the saline group. Pdi recovered completely (103 +/- 17%) in the A40 group but remained depressed (72 +/- 6%) in the saline group. Pdi values were intermediate in the A10 and A20 groups. MRS data revealed inadequate energy supply/demand ratio in the saline group such that the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) increased to 1.01 +/- 0.09 after 5 min of pacing. Pi/PCr remained unchanged in the A40 group and was intermediate in the A10 and A20 groups. beta-Adenosine triphosphate and intracellular pH did not differ among groups or as a function of pacing. Diaphragmatic blood flow increased from a resting value of 35-60 to 300-410 ml.min-1 x 100 g-1 during pacing in all groups and was not affected by aminophylline dose. CONCLUSIONS: Aminophylline, in a dose-dependent fashion, delays the onset of fatigue and improves recovery from fatigue. Delayed fatigue is associated with improved aerobic metabolism as reflected in a low Pi/PCr ratio.

Action Potentials↗
PubMedDate not supplied

Influence of chronic aminophylline on the anticonvulsant efficacy of phenobarbital and valproate in mice.

The protective efficacy of phenobarbital (PB, 120 min before testing) and valproate (VPA, 30 min before testing) alone or combined with aminophylline (a single dose of 50 mg/kg, 3-day or 14-day administration twice daily 50 mg/kg at 8.00 a.m. and 8.00 p.m.) was evaluated against maximal electroshock-induced seizures (MES) in male mice. All drugs were given intraperitoneally (i.p.), and the protection provided by PB and VPA was evaluated as the respective ED50 value (in mg/kg). Aminophylline in a single dose of 50 mg/kg (30 min before electroconvulsions) distinctly reduced the protective efficacy of both PB and VPA, reflected by the increase in the respective ED50 values from 22 to 31 mg/kg (p < 0.001) for PB and from 247 to 281 mg/kg (p < 0.001) for VPA. After administration of aminophylline for 3 days (electroshock was performed 30 min after the last aminophylline injection), the respective ED50 values for PB and VPA were 29.5 (p < 0.01) and 269 mg/kg (p < 0.01 vs. saline-treated animals). Chronic treatment with aminophylline (14 days) resulted in further impairment of the protective activity of PB and VPA. Specifically, the ED50 value of PB was 39 mg/kg (p < 0.05 vs. PB+single injection of aminophylline) and that of VPA was 318 mg/kg (p < 0.01 vs VPA+single injection of aminophylline). Plasma levels of both PB and VPA were not affected by chronic aminophylline; moreover, the plasma level of theophylline was even lower after chronic aminophylline as compared with single aminophylline administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminophylline↗
PubMed1995

Bidirectional effects of aminophylline on myocardial ischemia.

BACKGROUND: Aminophylline blocks adenosine receptors and increases levels of plasma catecholamines. We investigated the effect of aminophylline on myocardial ischemia by varying its severity and attempted to identify the mechanism by which aminophylline modulates myocardial ischemia in the canine model. METHODS AND RESULTS: In 41 open-chest dogs, the left anterior descending coronary artery was cannulated and perfused with blood through a bypass tube from the left carotid artery. When coronary blood flow (CBF) was reduced to 80% of the control, aminophylline increased fractional shortening (FS) from 11.0 +/- 0.4% to 18.5 +/- 1.7% (P < .05) and lactate extraction ratio (LER) from 7.5 +/- 0.1% to 13.6 +/- 1.0% (P < .01). The endocardial to epicardial flow ratio (Endo/Epi ratio) of regional myocardium was also increased. Release of adenosine was increased compared with the nonischemic condition (7 +/- 3 versus 28 +/- 5 pmol/mL). Prazosin, an alpha 1-adrenoceptor antagonist, blunted the aminophylline-induced improvement in contractile and metabolic function. Administration of 8-phenyltheophylline, a selective antagonist of adenosine receptors, did not increase FS, LER, or the Endo/Epi ratio when CBF was reduced to 80% of control. When CBF was reduced to 60% of control, aminophylline did not change the metabolic and contractile function. In contrast, when CBF was reduced to 33% of control, release of adenosine was increased markedly (243 +/- 19 pmol/mL) and aminophylline induced decreases in FS, LER, and Endo/Epi ratio similar to those observed with 8-phenyltheophylline. CONCLUSIONS: Aminophylline had opposite effects on the ischemic myocardium depending on the severity of ischemia. It improved mild ischemia but worsened severe ischemia. The beneficial effect of aminophylline was attributable to alpha 1-adrenoceptor stimulation, which improves endomyocardial flow in the ischemic myocardium. The deleterious effect was attributable to the aminophylline-induced blockade of adenosine receptors.

Adenosine↗
PubMed1983

Increased ventilation caused by improved diaphragmatic efficiency during aminophylline infusion.

The mechanism underlying the increase in ventilation (VE) observed during aminophylline infusion was investigated in 12 anesthetized spontaneously breathing dogs. Progressive doses of aminophylline were infused every 30 min, leading to plasmatic levels of 10 to 20, 20 to 30, 30 to 50 mg/L. The increase in VE observed while increasing aminophylline plasmatic concentration ranged from 4.2 +/- 6 to 9.5 +/- 1.2 L/min. Concomitantly to VE, we measured an index of the inspiratory neuromuscular output of the diaphragm, the transdiaphragmatic pressure generated at FRC 0.1 s after the onset of a spontaneous inspiration developed against closed airways (Pdi0.1). For each plasmatic level of aminophylline, Pdi0.1 increased as VE (117 +/- 4, 126 +/- 2, 140 +/- 6% of control values for 10 to 20, 20 to 30, 30 to 50 mg/L, respectively). To establish the role played by an improvement in diaphragmatic contractility in the increase in Pdi0.1 with aminophylline, we measured for each plasmatic level of aminophylline the transdiaphragmatic pressure generated at FRC against closed airways during supramaximal stimulation at 10, 20, 50, and 100 Hz of the 2 phrenic nerves (Pdi). Pdi increased while increasing aminophylline plasmatic level for all the frequencies of stimulation. A relationship was found between Pdi and Pdi0.1 at any aminophylline plasmatic level as well as with VE. No change in the mechanical properties of the respiratory system occurred with aminophylline. We conclude that the increase in VE observed after aminophylline administration in our animal model is essentially due to an improvement in diaphragmatic contractility rather than an increase in the central nervous system output.

Aminophylline↗
PubMed1983

Action of intravenously administered aminophylline on normal airways.

The changes in airway caliber and plasma cyclic-AMP levels after intravenously administered aminophylline, and the effect of DL- and D-propranolol on these responses have been investigated in a double-blind manner in normal subjects. Aminophylline 5.6 mg/kg was given intravenously over a 10-min period and the airway response was measured as change in specific airway conductance (delta SGaw) in the body plethysmograph. In the initial study in 6 subjects, orally administered placebo or propranolol was followed 2 h later by intravenously administered aminophylline. Neither placebo nor propranolol alone caused any change in SGaw at 2 h. After placebo, intravenously injected aminophylline produced a 30% increase in SGaw, reaching a peak 5 min after injection. This response was equivalent to 77% of the maximal response to 400 micrograms inhaled albuterol in the same subjects. After propranolol, the airway response to aminophylline was attenuated, with a 53% reduction in delta SGaw at the time of peak response. In a further study on 6 subjects, intravenously given aminophylline produced a 25% increase in SGaw and a 51% increase in plasma cyclic-AMP levels after placebo tablets. Pretreatment with 40 and 80 mg DL-propranolol caused a dose-dependent reduction of both the airway and plasma cyclic-AMP response to aminophylline. The airway response to aminophylline was not attenuated by D-propranolol so the effect of DL-propranolol is thought to be due to beta-adrenoceptor blockade. The absence of any detectable change in SGaw after DL-propranolol suggests there is little resting sympathetic tone to the airways in normal subjects. In the absence of sympathetic stimulation, the rapid response to aminophylline is unlikely to be due to phosphodiesterase inhibition. The attenuation of the airway and cyclic-AMP response by propranolol suggests that part of the action of aminophylline may be due to beta-agonist activity.

Adult↗
PubMed2001

Comparative effect of theophylline and aminophylline on theophylline blood concentrations and peripheral blood eosinophils in patients with asthma.

The comparative effects of a new theophylline preparation (Theodrip) and aminophylline on blood concentrations of theophylline were examined in 74 patients with asthma. Subjects were intravenously administered 200 mg of Theodrip or 250 mg of aminophylline for 1 h. The mean increases in blood theophylline concentration after Theodrip or aminophylline administration were 8.80 +/- 1.80 mg/l and 8.81 +/- 2.15 mg/l, respectively. In addition, these patients were divided into four groups based on baseline theophylline concentrations before infusion of Theodrip or aminophylline: i) naïve patients (not administered theophylline); ii) those with a baseline theophylline concentration of 0-5 mg/l; iii) those with a baseline theophylline concentration of 5-10 mg/l; iv) those with a baseline theophylline concentration of 10-15 mg/l. Mean increases in blood theophylline concentration after administration of Theodrip in each group were similar to those after aminophylline administration. We found no significant differences between Theodrip and aminophylline. However, when the comparative effects of Theodrip and aminophylline on peripheral blood eosinophil counts were examined, Theodrip, but not aminophylline, reduced blood eosinophil counts. With acute exacerbations of bronchial asthma, it is expected that Theodrip, but not aminophylline, may have an antiinflammatory effect. In conclusion, it is suggested that Theodrip is a more useful drug than aminophylline in patients with acute exacerbations of bronchial asthma.

Adult↗
PubMed1983

Enflurane, halothane, and aminophylline--uptake and pharmacokinetics.

This study was designed to evaluate the effects of induction of enflurane or halothane anesthesia on the distribution and elimination of previously administered intravenous aminophylline, and to evaluate the effect of previously administered intravenous aminophylline on the uptake of enflurane or halothane. Fifty-four dogs were studied: 6 received no anesthetic, 24 received enflurane, and 24 halothane. The six animals receiving no anesthetic were given 10 mg/kg of aminophylline. In each of the two groups of 24 animals, six animals served as controls and received no aminophylline. Of the other 18 animals in each group, six received 10 mg/kg of aminophylline, six received 25 mg/kg of aminophylline, and six received 50 mg/kg of aminophylline intravenously before induction of enflurane or halothane anesthesia. The redistribution (alpha) phase of theophylline was similar when anesthesia was induced with either enflurane or halothane and slightly more rapid when no anesthetic was given following aminophylline administration. The elimination (beta) phase of theophylline in the presence of either anesthetic was not significantly different than when no anesthetic was administered. The uptake of enflurane or halothane was unaffected by prior administration of aminophylline. Differences in arrhythmogenicity between enflurane and halothane after aminophylline administration are not related to alterations in theophylline pharmacokinetics or anesthetic uptake.

Aminophylline↗
PubMed1992

Anticonvulsant activity of carbamazepine and diphenylhydantoin against maximal electroshock in mice chronically treated with aminophylline.

The anticonvulsant activities of both carbamazepine and diphenylhydantoin alone (after a single intraperitoneal administration) or combined with aminophylline were studied against maximal electroshock-induced convulsions in male mice. Aminophylline (injected acutely at 50 mg/kg) significantly increased the ED50 values of both antiepileptics. Given for three days, aminophylline (50 mg/kg, twice daily) still impaired the potency of both antiepileptics and after chronic aminophylline administration a further decrease in the protective activity of carbamazepine and diphenylhydantoin was found. Specifically, after 14 days of aminophylline treatment, ED50s for carbamazepine and diphenylhydantoin were 26 and 19 mg/kg, respectively. These ED50s were significantly elevated compared to values determined after acute aminophylline treatment (21.2 and 14.9 mg/kg, respectively). Plasma levels of both antiepileptics were unaffected by chronic aminophylline which seems to exclude a pharmacokinetic interaction in terms of total plasma levels at least. The present results clearly indicate that the aminophylline-induced impairment of the anticonvulsant activity of carbamazepine and diphenylhydantoin is enhanced over time. This may render aminophylline a hazardous drug to epileptic patients who are prescribed this smooth muscle relaxant.

Aminophylline↗
PubMed1986

Effect of aminophylline on amygdaloid-kindled postictal inhibition.

Previous studies have shown that methylxanthines such as aminophylline increase the clinical severity and length of electrically elicited limbic afterdischarges in naive and kindled rats without lowering seizure threshold. When fully amygdaloid-kindled rats are electrically stimulated at intertrial stimulation intervals of less than 60 minutes, significant residual inhibition can be demonstrated. The present study examines the effect of three doses of aminophylline (25, 50 and 100 mg/kg) on repeated daily stimulations of fully amygdaloid-kindled rats. After 100 mg/kg aminophylline, the first elicited amygdaloid-kindled seizure afterdischarge was doubled in length compared to saline controls. The second elicited seizure 15 minutes later resulted in status epilepticus and hindlimb extension in the majority of the aminophylline-treated animals with death occurring in 28%. When 25 or 50 mg/kg of aminophylline was given daily for five days before the first of five daily stimulation trials, each separated by 15 minutes, no significant reduction in postictal inhibition was demonstrated compared to saline controls. The 50 mg/kg aminophylline dose consistently and significantly lengthened only the first afterdischarge of each day without affecting the postictal inhibition seen with repeated stimulations. The neural substrate that governs immediate postictal inhibition of amygdaloid-kindled seizures appears to be resistant to modification by aminophylline at low doses. At high doses of aminophylline (100 mg/kg), sustained epileptical activity occurred. The sustained seizure activity seen at the high dose of aminophylline may be secondary to blockade of the processes which normally terminate seizure activity, or it may represent actual inhibition of the immediate postictal inhibitory processes.

Adenosine↗
PubMed2003

Bronchodilator effects of intravenous olprinone, a phosphodiesterase 3 inhibitor, with and without aminophylline in asthmatic patients.

AIMS: There is no evidence demonstrating the clinical usefulness of phosphodiesterase (PDE) inhibitors in the treatment of asthma, although PDE3 and 4 inhibitors have received much attention for the treatment of bronchial asthma. We compared the bronchodilator effects of intravenously administered olprinone, a selective PDE3 inhibitor, and aminophylline, a nonselective PDE inhibitor, both alone and concomitantly. METHODS: In 12 patients with mild stable asthma, we compared the acute bronchodilator effects of the following two drugs, alone and together using a double-blind crossover design: intravenous administration of olprinone, 30 micro g min-1; aminophylline, 2.25 mg min-1; and olprinone plus aminophylline over a total period of 150 min. RESULTS: Mean maximal increase (95% confidence interval) in the FEV1 was 7.8% (2.4, 13.2), 17.1% (10.0, 24.2), 16.6% (11.2, 22.0), and 1.0% (-1.1, 3.1) during infusion of aminophylline, olprinone, aminophylline and olprinone, and saline, respectively. The magnitude of bronchodilatation produced by olprinone was greater than that by aminophylline. The combination of aminophylline and olprinone did not produce any greater bronchodilatation than olprinone alone. Olprinone alone or in combination with aminophylline lowered diastolic blood pressure, and increased heart rate. CONCLUSIONS: These results suggest that the intravenous administration of PDE3 inhibitors exhibits a bronchodilatory effect. There are no additive or synergistic effects of administration of olprinone and aminophylline at the same time.

3',5'-Cyclic-AMP Phosphodiesterases↗