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At least 19 recordsLinked to original sources

PubMed1975

The action of aminophylline on the acutely transplanted dog heart: effect of alpha- and beta-adrenoceptor blockade.

1 Aminophylline inhibits the coronary vasodilator actions of adenosine. Our previous studies suggested that low dose infusions of aminophylline reduce coronary blood flow in the isolated heart. In the present study we investigated the actions of aminophylline on coronary blood flow and myocardial contractility in a transplanted heart model. Drugs were given by close coronary arterial infusion. 2 Aminophylline in low doses (200 mug/min) reduced coronary blood flow by 21 plus or minus 2% (mean plus or minus s.e. mean) but did not alter myocardial contractility or heart rate. Higher doses (500 and 1000 mug/min) increased coronary blood flow and myocardial contractility without changing heart rate. 3 Alpha-adrenoceptor blockade with phenoxybenzamine did not affect the response to a low dose of aminophylline (200 mug/min). 4 Propranolol in doses of 10 and 30mug/min blocked beta-adrenoceptors but did not change coronary blood flow. The higher dose reduced myocardial contractility. 5 The effects of a high dose of aminophylline (1000 mug/min) on coronary blood flow were not changed by either alpha- or beta-adrenoceptor blockade, although propranolol (30 mug/min) reduced the augmentation in myocardial contractility. 6 The results show that when given in doses which do not alter myocardial contractility, aminophylline reduces coronary blood flow in the isolated heart and that this is not mediated through an alpha-adrenoceptor mechanism. They also show that the increases in coronary blood flow and positive inotropic effects obtained with higher doses of aminophylline are not mediated through catecholamines and suggest that higher doses of aminophylline have a small direct coronary vasodilator action. The low dose vasoconstrictor response may be produced by inhibition of the coronary vasodilator action of locally produced adenosine.

Adrenergic alpha-Antagonists↗

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↗

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↗

PubMed1976

Effect of aminophylline on tryptophan and other aromatic amino acids in plasma, brain and other tissues and on brain 5-hydroxytryptamine metabolism.

1 Aminophylline and other methylxanthines increase brain tryptophan and hence 5-hydroxytryptamine turnover. The mechanism of this effect of aminophylline was investigated. 2 At lower doses (greater than 100 mg/kg i.p.) the brain tryptophan increase could be explained by the lipolytic action of the drug, i.e. increased plasma unesterified fatty acid freeing plasma tryptophan from protein binding so that it became available to the brain. 3 Plasma unesterified fatty acid did not increase when aminophylline (109 mg/kg i.p.) was given to nicotinamide-treated rats but as both plasma total and free tryptophan rose, a tryptophan increase in the brain still occurred. 4 The rise in brain tryptophan concentration following the injection of a higher dose of the drug (150 mg/kg i.p.) could no longer be explained by a rise of plasma free tryptophan as the ratio of brain tryptophan to plasma free tryptophan rose considerably. Plasma total tryptophan fell and the plasma insulin concentration rose. 5 The increase of brain tryptophan concentration after injection of 150 mg/kg aminophylline appeared specific for this amino acid as brain tyrosine and phenyllanine did not increase. However as their plasma concentrations fell the brain/plasma ratio for all three amino acids rose. 6 The higher dose of aminophylline increased the muscle concentration of tryptophan but that of tyrosine fell and that of phenylalanine remained unaltered. The liver concentrations were not affected. 7 The aminophylline-induced increase of the ratio of brain tryptophan of plasma free tryptophan no longer occurred when the drug was given to animals injected with the beta-adrenoreceptor blocking agent propranolol or the diabetogenic agent streptozotocin. 8 The changes in brain tryptophan upon aminophylline injection may be explained by (a) increased availability of plasma tryptophan to the brain due to increased lipolysis and (b) increased effectiveness of uptake of tryptophan by the brain due to increased insulin secretion.

Amino Acids↗

PubMed1975

Potentation of the cardiac response to aminophylline by oxyfedrine.

The influence of oxyfedrine on the cardiostimulatory effects of aminophylline was studied in the isolated perfused guinea-pig heart. It was found that oxyfedrine potentiated the stimulatory effects of aminophylline on isometric contraction, dF/dt, coronary flow and heart rate. This potentation was abolished after pretreatment with propranolol. Histamine, though to a lesser extent, also potentiated the effects of aminophylline. When oxyfedrine and histamine were infused simultaneously in the presence of propranolol, the response of the heart to aminophylline was also potentiated; the magnitude of this potentiation was comparable to that obtained with histamine alone, indicating that propranolol abolished only the action of oxyfedrine but not that of histamine. The mechanical effects of aminophylline were accompanied by a slight (15 per cent) but significant inhibition of phosphodiesterase, which was not further augmented by oxyfedrine. The results suggest that the potentiating effects of oxyfedrine or histamine on the cardiostimulatory actions of aminophylline are elicited by their stimulatory actions on adenylate cyclase activity.

Aminophylline↗

PubMed1975

Effect of tolbutamide on aminophylline-, 3,5-AMP-dibutyrate- or glucagon-induced insulin release from pancreatic islets after impairment of pyridine nucleotide metabolism caused by 6-aminonicotinamide (6-AN).

The effect of tolbutamide on pyridine nucleotides and insulin secretion stimulated by aminophylline, 3,5-AMP-dibutyrate or glucagon was studied in pancreatic islets of rats previously treated with 6-aminonicotinamide (6-AN), an inhibitor of pyridine nucleotide synthesis. After being incubated for 60 min in a Krebs-Ringer-Bicarbonate-Buffer in the absence of glucose, pancreatic islets of rats i.p. injected with 35 mg/kg of 6-AN 6 hrs before pancreas removal contained about 30% less NADP and NADPH than did islets of control rats. No changes of NDA or NADH were observed in islets of 6-AN-treated animals. Addition of 16.5 mM glucose led to an increase of NADH, NADPH and a decrease of NADP in islets of both groups of animals; NAD levels remained unchanged. In vitro addition of tolbutamide to islets of control rats did not affect the levels of NADPH or NADP in the presence of 5.5 mM glucose. When 16.5 mM glucose were present, a decrease of NADPH and an increase of NADP was obvious. No effect of tolbutamide on insular NADPH or NADP was observed in islets of rats previously treated with 6-AN be it in the presence of 5.5 or 16.5 mM glucose. In islets of 6-AN-treated rats insulin release in response to aminophylline or 3,5-AMP-dibutyrate in the presence of 5.5 mM glucose was significantly depressed, when compared to islets of untreated controls. Addition of tolbutamide increased insulin release due to aminophylline, 3,5-AMP-dibutyrate or glucagon islets of controls. Tolbutamide alone was without effect. In islets of 6-AN-treated rats aminophylline, 3,5-AMP-dibutyrate or glucagon stimulated insulin release only when tolbutamide was present. Our data suggest that there is no direct interference of tolbutamide with pyridine nucleotides of pancreatic islets, and that tolbutamide increases the secretory response of the beta-cell to aminophylline, 3,5-AMP-dibutyrate or glucagon when insulin release due to these agents is inhibited during decrease of insular NADP and NADPH, caused by 6-AN.

6-Aminonicotinamide↗

PubMed1978

Comparative toxicity of caffeine and aminophylline (theophylline ethylenediamine) in young and adult rats.

The toxicity of aminophylline and caffeine was studied in adult and 2-day-old rats following a single subcutaneous injection of the respective drug. Following the injection of high doses of either methylxanthine, adult rats developed convulsions, tremors, lethargy and licking of lips. In adult rats, the LD50 of caffeine and aminophylline was the same after 24 h and after 1 week of observation: caffeine 265 mg/kg, and aminophylline 202 mg/kg (theophylline base 172 mg/kg). In young rats, the LD50 was greater when the observation was carried out for 1 week than at 24 h after the injection; at 24 h: caffeine 220 mg/kg, and aminophylline 169 mg/kg (theophylline base 144 mg/kg); at 1 week: caffeine 155 mg/kg, and aminophylline 140 mg/kg (theophylline base 119 mg/kg). Young rats failed to gain weight at a normal rate after administration of either methylxanthine. The greater toxicity of both methylxanthines in newborn animals may be at least partly due to the extremely slow elimination of theophylline and caffeine in the neonate.

Age Factors↗

PubMed1978

Effect of aminophylline on ventilatory responses in normal man.

The bronchodilator effects of aminophylline have been well documented but its effect on ventilatory drives has not been systematically evaluated. Accordingly, the ventilatory responses to hypoxia and to hypercapnia were measured before and after the intravenous administration of 5 mg of aminophylline per kg of body weight to 6 normal subjects. Hypoxic ventilatory response, as measured by an index of the relation between ventilation and hypoxia (parameter A) increased from a mean +/- SE control value of 146 +/- 25 to 254 +/- 35 75 min after the infusion (P less than 0.05). Significant increases in A were also noticed immediately after and 35 and 50 min after the aminophylline infusion. Oxygen consumption increased from a control value of 235 +/- 21 to 263 +/- 21 ml per min STPD (P less than 0.03), and CO2 production increased from 184 +/- 12 to 202 +/- 13 ml per min STPD (P less than 0.01) after aminophylline. Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercapnia, was not altered after the aminophylline. Thus, in addition to bronchodilation, the augmentation of the ventilatory response to hypoxia may be a useful factor when this drug is used in acute respiratory failure secondary to airway obstruction.

Adult↗

PubMed1978

Effects of cortisol and aminophylline upon survival, pulmonary mechanics, and secreted phosphatidyl choline of prematurely delivered rabbits.

Rabbits delivered at 27.0 days of gestation were studied after administration of cortisol (2 mg/kg/day), aminophylline (6.25 mg/kg/day), or sterile saline to the does on days 24-26 of gestation. Survival at 60 min was 52.9% in the aminophylline-treated group and 22.2% in the control and cortisol-treated groups with all animals being in a warm, oxygen-enriched environment and receiving frequent tactile stimulation. Lung volume at 30 cm H2O was lower in the cortisol-treated group than in the controls or aminophylline-treated group in animals surviving for 60 min (Table 2). The aminophylline-treated group retained significantly more gas at low pressures on the deflation curve (Table 2) and had significantly more phosphatidylcholine recovered in lung lavage fluid (Table 3) than the other groups. Aminophylline appears to have enhanced lung maturation better than cortisol in this experimental model.

Adenosine Monophosphate↗

PubMed1978

Effect of aminophyllin and dexamethasone on secretion of pulmonary surfactant in fetal rabbits.

Aminophyllin, dexamethasone, or saline was injected into 27.5-day fetal rabbits 2.5 hr before sacrifice, after which static pressure-volume curves with air were performed. In further similar experiments the lungs were lavaged with physiologic saline which was analysed for total phospholipid content. There were no changes in total lung capacity (TLC) induced with either aminophyllin or dexamethasone. The lungs of fetal rabbits injected with saline retained 44% TLC (+/-3 SE) after deflation to 10 cm H2O trans-pulmonary pressure compared with 48% TLC (+/-3 SE) in those injected with dexamethasone, a difference which was not statistically significant. In contrast, the lungs of fetal rabbits injected with aminophyllin retained 53% TLC (+/-2 SE) after deflation to 10 cm H2O pressure, a significant increase when compared with saline controls (P less than 0.01). There were no changes in lung weight or lung water. These results were interpreted to mean that aminophyllin decreased surface tension and augmented secretion of pulmonary surfactant. This was supported by finding significantly increased total phospholipid recovered in the lung lavage fluid of fetal rabbits injected with aminophyllin, 62 microgram/g dry lung weight (+/-6 SE) compared with 32 microgram/g dry lung weight (+/-3 SE) in saline controls (P less than 0.05). Phospholipid recovered from dexamethasone-injected fetal rabbits was not significantly increased, 38 microgram/g dry lung weight (+/-4 SE).

Aminophylline↗

PubMed1979

Influence of aminophylline and cyclic AMP on glycogen metabolism in fetal rat lung in organ culture.

The glycogen content of fetal rat lung declines coincident with increased pulmonary phospholipid synthesis. Aminophylline, a methylxanthine cyclic adenosine 3',5' monophosphate (AMP) phosphodiesterase inhibitor, and cyclic AMP augment fetal lung phospholipid synthesis. Because lung glycogen breakdown may contribute to pulmonary phospholipid synthesis, the effects of aminophylline and cyclic AMP on glycogen metabolism were studied in explants of 19 day fetal rat lung in organ culture. Treatment with aminophylline or dibutyryl cyclic AMP for 24 hr, resulted in a 25% (P less than 0.025) and 75% (P less than 0.001) decrease, respectively, in the glycogen content of the explants. Glycogen synthase I activity was reduced by 32% in aminophylline treated cultures (P less than 0.025) and 25% in cyclic AMP treated cultures (P less than 0.025). The percent of total synthase in the active form was significantly reduced in all treated cultures. Neither aminophylline nor cyclic AMP treatment resulted in significant changes in glycogen phosphorylase a or total phosphorylase activity.

Aminophylline↗

PubMed1976

A controlled trial of intravenous salbutamol and aminophylline in acute asthma.

In a randomized double-blind trial an intravenous injection of salbutamol (100mug) was compared with an intravenous injection of aminophylline (250mg) in 23 patients with acute exacerbations of asthma. Salbutamol (11 cases) and aminophylline (12) produced a mean proportionate increase in FEV of 26% and 23% respectively. Blood gas pressures showed a trend to improvement with a mean rise in oxygen tension of 2mm Hg(0-2kPa) in the aminophylline group and of 6mm Hg (0-8kPa) in the salbutamol group. Electrocardiogram patterns also showed overall improvement, and mean decreases in pulse rate of 8 beats per minute and 2 beats per minute were noted in the aminophylline and salbutamol groups respectively. Differences in results did not reach conventional levels of significance and no serious side effects were noted. It was concluded that in the doses and routes of administration compared, salbutamol was as effective as aminophylline.

Acute Disease↗

PubMed1977

Reversal of ethanol intoxication in humans: an assessment of the efficacy of L-dopa, aminophylline, and ephedrine.

The effect of postethanol treatment with L-Dopa, aminophylline and/or ephedrine was investigated. In one experiment, healthy, male, moderate drinkers ingested ethanol (0.8 g/kg) and then either L-Dopa (1.5 g), or placebo. In a second experiment, subjects ingested ethanol followed by aminophylline (200 mg), ephedrine (50 mg), aminophylline (200 mg) plus ephedrine (50 mg), or placebo. Double-blind, within-subjects, crossover designs were employed. Treatment with L-Dopa significantly reduced ethanol's effect on the electroencephalogram, motor coordination, and divided attention performance (t-test for paired data). Treatment with aminophylline and/or ephedrine also significantly reduced ethanol's effects on the electroencephalogram and motor coordination. The ethanol-antagonism may result from central noradrenergic stimulation.

Adult↗

PubMed1975

Effects of aminophylline on the threshold for initiating ventricular fibrillation during respiratory failure.

Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.

Acid-Base Equilibrium↗

PubMed1978

Potentiation of isoprenaline-induced plasma cyclic AMP response by aminophylline in normal and asthmatic subjects.

1 The effect of intravenous aminophylline infusion (6 mg-1 kg in 20 min, then 0.9 mg-1 kg-1 h thereafter) and its interaction with inhaled isoprenaline (800 microgram ex inhaler) on plasma cyclic AMP levels was studied in five normal and five asthmatic subjects. 2 Aminophylline infusion alone did not significantly change plasma cyclic AMP levels in either group. 3 In both groups, the plasma cyclic AMP response to isoprenaline aerosol inhalation was enhanced by aminophylline, although to a lesser degree in the asthmatic subjects. 4 The results provide in vivo evidence consistent with the hypothesis that in man, therapeutic doses of aminophylline may exert their clinical effects by inhibition of cyclic AMP phosphodiesterase.

Adult↗

PubMed1977

Potentiation by carbachol and aminophylline of histamine- and db-cAMP-induced parietal cell activity in isolated gastric glands.

The response to combinations of gastric acid secretagogues was studied in isolated glands from the rabbit gastric mucosa in terms of changes in oxygen consumption and accumulation of the weak base aminopyrine (AP). The latter reflects the acid secreting status of the glands. The following secretagogues were investigated: histamine, carbachol, aminophylline and db-cAMP. The histamine respiratory dose-response curve was shifted to the left in the presence of the phosphodiesterase inhibitor aminophylline. Both ED-50 and maximum response were significantly increased. Histamine-induced AP accumulation was also strongly enhanced by aminophylline (5 X 10(-4) M). These results are consistent with the hypothesis that histamine stimulation of acid secretion is mediated by cyclic AMP. Carbachol-stimulated oxygen consumption could not be potentiated by aminophylline and the combined effect was only additive. The response to a combination of histamine and carbachol was a significant increase in oxygen consumption above what could be expected from an additive effect alone. Carbachol addition to glands prestimulated with histamine gave a rapid increase in the respiratory rate resulting in a new steady state level within 10-15 min, as compared with a time constant of about 40 min when both drugs were added simultaneously. Likewise AP accumulation increased more rapidly and reached a higher value after addition of histamine + carbachol as compared with histamine alone. The db-cAMP-stimulated oxygen consumption was in all respects equally affected by carbachol as was histamine stimulation. This indicates that the well known cholinergic potentiation of histamine stimulation is not due to an increased sensitivity of the histamine receptor but is of a more general nature. A mechanism involving intracellular availability of Ca2+ is proposed as one possible explanation of this potentiation.

Aminophylline↗

PubMed1979

Isoproterenol and aminophylline reduce lung capillary filtration during high permeability.

Pseudomonas bacteremia in sheep causes a prolonged increase in lung vascular permeability to protein. Isoproterenol and aminophylline could effect lung fluid balance after Pseudomonas by reducing vascular pressures or by blocking release of permeability mediators. We measured vascular pressures, lung lymph flow, and lymph and plasma protein concentrations in unanesthetized sheep under baseline conditions and during steady-state increased permeability after Pseudomonas. Pseudomonas caused pulmonary vascular pressures to rise and lung lymph flow to increase fivefold, but lymph/plasma protein concentration did not change. Pulmonary vascular pressures and lung lymph flow decreased during intravenous infusion of isoproterenol and aminophylline. The decrease in lymph flow after isoproterenol and isoproterenol plus aminophylline was linearly related to the decrease in microvascular pressure (r = 0.71). Lymph/plasma total protein concentration ratios and lymph clearance of proteins with molecular radii 36--96 A remained high during isoproterenol and aminophylline. These drugs can substantially reduce transvascular filtration primarily because they reduce lung vascular pressures.

Aminophylline↗

PubMed1979

Antisecretory actions of aminophylline in the rat and dog.

The effect of aminophylline on gastric acid secretion has been studied in the rat and dog. Aminophylline was shown to possess antisecretory activity when given either by oral or parenteral administration in an acute gastric fistula rat preparation. In the chronic gastric fistula dog aminophylline at 50 mg/kg intragastrically induced a small but significant stimulation of basal acid secretion. This dose of aminophylline also significantly inhibited acid secretion induced by gastrin tetrapeptide, and 2-deoxy-D-glucose but did not block acid secretion induced by histamine.

Aminophylline↗