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At least 19 recordsLinked to original sources
PubMed1976

Electron-capture GLC determination of phenylpropanolamine as a pentofluorophenyloxazolidine derivative.

A simplified procedure is described for an electron-capture GLC determination of phenylpropanolamine in blood plasma. The method is based on derivatization of phenylpropanolamine with pentafluorobenzaldehyde at room temperature without prior extraction of the drug from plasma. The derivative, pentafluorophenyloxazolidine, is readily extracted from plasma into a small volume of hexane. Samples usually can be injected directly into the gas chromatograph without concentration of the hexane solution. Data are presented to illustrate the suitability of the method for dosage form bioavailability evaluation from plasma phenylpropanolamine levels achieved after acute oral administration of a typical dosage form.

Chromatography, Gas↗
PubMed1978

Simultaneous GLC determination of phenylpropanolamine and chlorpheniramine in urine using a nitrogen selective detector.

A simple, rapid, and sensitive simultaneous quantitative determination of phenylpropanolamine and chlorpheniramine in human urine by GLC, using a nitrogen specific detector, is described. After alkaline extraction from urine, phenylpropanolamine and chlorpheniramine are analyzed directly by GLC, without a derivatization step. Promethazine was used as the internal standard. The total assay time is less than 30 min. The method is useful in studies of pharmacokinetic and pharmacological interactions of drug combinations.

Chlorpheniramine↗
PubMed1979

Severe hypertension after ingestion of an appetite suppressant (phenylpropanolamine) with indomethacin.

Severe systemic hypertension developed in a patient who took indomethacin shortly after ingesting an appetite suppressant ('Trimolets') containing phenylpropanolamine. The hypertension was attributed to a drug interaction whereby the inhibition of prostaglandin synthesis by indomethacin exacerbated the sympathomimetic effects of phenylpropanolamine. It is suggested that withdrawal of preparations containing phenylpropranolamine from general use should be considered in view of their potential for adverse reactions with other commonly used drugs and their doubtful therapeutic value.

Administration, Oral↗
PubMed1976

Simultaneous quantitative GLC determination of chlorpheniramine maleate and phenylpropanolamine hydrochloride in a cold tablet preparation.

A GLC method was developed for the simultaneous determinations of chlorpheniramine maleate and phenylpropanolamine hydrocholride in a cold tablet preparation containing a large amount of aspirin. The method utilizes a solid sampling device to eliminate interference from solvent, and it is rapid and precise. The total analysis time is less than 1.5 hr, thereby permitting its use for quality control purposes.

Aspirin↗
PubMed1977

Quantitative determinations of codeine phosphate, guaifenesin, pheniramine maleate, phenylpropanolamine hydrochloride, and pyrilamine maleate in an expectorant by high-pressure liquid chromatography.

The quantitative determinations of codeine phosphate, guaifenesin, pheniramine maleate, phenylpropanolamine hydrochloride, and pyrilamine maleate in a liquid dosage form are described. All active and inactive ingredients (sodium benzoate and FD&C Yellow No. 5 dye) can be separated with high-pressure liquid chromatography except the two antihistamines, pheniramine maleate and pyrilamine maleate. Pheniramine maleate is determined colorimetrically, and pyrilamine maleate is determined either by difference or spectrophotometrically. The methods are simple short, accurate, and precise. The standard deviations are reported.

Chromatography, High Pressure Liquid↗
PubMed1992

Drug discrimination studies in rats with caffeine and phenylpropanolamine administered separately and as mixtures.

The discriminative stimulus effects of mixtures of caffeine and phenylpropanolamine (PPA) have been investigated because these drugs have been abused together. Rats were trained to discriminate caffeine (20 mg/kg), PPA (20 mg/kg), or a mixture of both drugs, from saline in a two-bar operant conditioning procedure with food reinforcers presented on a tandem VI-FR schedule. Discriminations of mixture, caffeine alone and PPA alone were 90% accurate after 40 sessions. Generalisation to both PPA and caffeine was weak (25-47%) at the doses used in the training mixture, although there was almost complete generalisation to larger doses of PPA. Under these conditions, there was a possible synergistic interaction between caffeine and PPA because the discriminative effect of the mixture could not be fully explained by the combined effects of its component drugs. However, in rats trained on caffeine, PPA had no effect on the dose-response relationship for caffeine; similarly, in rats trained on PPA, caffeine had no effect on the dose-response relationship for PPA (no synergism or antagonism). Generalisation to (+)-amphetamine and cocaine was weakest in rats trained on caffeine, was partial in rats trained on the mixture, and was complete in rats trained on PPA; thus, the mixture of caffeine and PPA was not more like cocaine or amphetamine than PPA alone. The results are in agreement with reports that caffeine and PPA may interact in a complex manner, but do not support the view that the interaction enhances their resemblance to highly abused stimulants such as amphetamine and cocaine.

Animals↗
PubMed1992

Effects of adrenalectomy and deprivation condition on food intake after phenylpropanolamine or clonidine.

alpha-Adrenergic receptors within the paraventricular hypothalamus (PVN) modulate feeding such that activation of alpha 2-adrenoceptors by drugs such as clonidine (CLON) increase feeding; whereas activation of alpha 1-adrenoceptors by drugs such as phenylpropanolamine (PPA) suppress feeding. Prior studies suggest that the feeding-stimulatory effect of alpha 2-adrenergic activation is a function of drug dose as well as the deprivation condition and adrenal status of the animal. Specifically, CLON's effects on feeding are greatest at low doses in food-satiated adrenally intact rats. Whether a similar profile is produced by alpha 1-adrenoceptor agonists such as PPA has not previously been explored. Thus, the present study provides a comparison of the effects on food intake of drug dose, deprivation condition, and adrenalectomy induced by these alpha 2- and alpha 1-adrenergic drugs. Accordingly, both adrenalectomized (ADX) as well as sham-control (SHAM) adult male rats underwent a series of 1-h feeding tests following administration of PPA (5, 10, 20 mg/kg, IP) as well as CLON (0.0125, 0.025, 0.05, 0.1 mg/kg, IP) under both deprived and nondeprived testing conditions. The results suggest that the deprivation condition, but not the surgical condition (ADX vs. SHAM), exerts the greatest overall effect on food intake following administration of alpha-adrenergic drugs.

Adrenalectomy↗
PubMed1992

Reversal of cirazoline- and phenylpropanolamine-induced anorexia by the alpha 1-receptor antagonist prazosin.

Phenylpropanolamine (PPA) is a phenethylamine anorectic drug that exerts direct agonist effects predominantly on alpha 1-adrenoceptors, with some alpha 2-adrenergic activity. Microinjections of PPA, as well as the alpha 1-adrenergic receptor agonists cirazoline, methoxamine, and 1-phenylephrine, into rat paraventricular nucleus (PVN) suppress feeding. The present study further evaluates the alpha 1-adrenergic basis of PPA-induced anorexia by examining the effects of systemic injections of the alpha 1-adrenergic antagonist prazosin (PRAZ, 2 and 5 mg/kg, IP) on the anorexia induced by systemic injections of PPA (5, 10, and 20 mg/kg, IP), as well as cirazoline (0.05, 0.1, and 0.2 mg/kg, IP). Although neither PRAZ dose alone altered food intake in the present study, 2 mg/kg PRAZ effectively reversed the feeding-suppressive effects of both PPA and cirazoline. These results strongly support the hypothesis that alpha 1-adrenoceptor stimulation mediates the anorexia induced by drugs such as PPA and cirazoline.

Adrenergic alpha-Agonists↗
PubMed1975

Phenylpropanolamine inhibits feeding, but not drinking, induced by hypothalamic stimulation.

In rats bearing lateral hypothalamic electrodes that elicited both feeding and drinking, intraperitoneal injection of the appetite suppressant drug phenylpropanolamine (Propadrine) inhibited only feeding. This occurred whether feeding and drinking were tested simultaneously or separately. Selective inhibition of lateral hypothalamic feeding also followed injection of this drug through lateral, but not medial, hypothalamic electrode cannulas. We conclude that hypothalamically induced feeding is under some of the same pharmacological controls as spontaneous feeding, that this control may be exerted, in part, in or near the lateral hypothalamus, and that the neural systems which induce feeding and drinking during hypothalamic stimulation can be pharmacologically separated.

Animals↗
PubMed1978

Effect of the anorectic drug, phenylpropanolamine, on blood glucose in rats.

Phenylpropanolamine hydrochloride (PPA) is a widely used decongestant and anorectic drug. The present study investigated the hypoglycemic effects of intraperitoneal PPA on rats to test the possibility that it might derive some of its anorectic properties through effects on glucostatic mechanisms. PPA tended to lower blood glucose levels in normal rats; the glycemia reducing effect was larger and statistically significant in rats made hyperglycemic by prior treatment with streptozocin to cause diabetes. This is the first evidence that PPA migh possibly reduce feeding by increasing blood sugar utilization.

Animals↗
PubMed1992

Effectiveness of phenylpropanolamine in the management of moderate obesity.

Phenylpropanolamine (PPA), an over-the-counter drug, is used for weight reduction but its effectiveness is controversial. One hundred and one ambulatory subjects (85 female; 16 male), 21-61 years old, 15-45% overweight but otherwise healthy, were studied. The study was divided into two phases: (i) a double blind (DB), placebo-controlled (P) phase in which all subjects took placebo for two weeks and subsequently took PPA, 75 mg sustained release or placebo for six weeks and (ii) an extended double blind phase in which subjects chose to continue up to 20 weeks. All subjects were instructed on a 5023 kJ (1200 kcal) diet. Both groups lost weight at weeks 4, 6 and 8, but the weight loss was greater for the PPA treated (2.59 kg) than for the placebo treated (1.07 kg) subjects (P = 0.01). Dropout was 29.4% for PPA and 44% for placebo treated subjects. In the 36 subjects who chose to continue in the extended double blind study, the difference persisted (PPA 5.1; placebo 0.4 kg) (P = 0.02). No difference between the groups was observed in blood pressure, pulse rate or subjective side effects. In spite of greater weight loss on PPA, patients did not report a greater anorexic effect. We conclude that PPA enhances weight loss in subjects treated with a hypocaloric diet and is free of untoward side effects.

Adult↗
PubMed1992

Relative bioavailability of carbinoxamine and phenylpropanolamine from a retard suspension after single dose administration in healthy subjects.

The plasma pharmacokinetics of carbinoxamine (CA, CAS 486-16-8) and phenylpropanolamine (PP, CAS 14838-15-4) after single dose administration of a retard suspension (Rhinopront), containing a resinate as sustained-release agent, were compared to those of the same active principles given as an aqueous solution. The study was performed in 20 healthy subjects who received the two formulations according to a standard crossover design with a one-week wash-out. Blood samples were obtained up to 24 h post-dose. PP and CA were assayed in the plasma samples by gas chromatography with electron-capture detection and HPLC with coulometric detection, respectively. The pharmacokinetic results indicated sustained release of the two active principles with the retard suspension: CA appeared in plasma at a much slower rate than with the solution, a 30% lower Cmax being reached after 8.0 h instead of 3.0 h post-dose. For PP, Cmax was 23% lower and occurred 3.0 post-dose instead of 1.5 h with the solution. The extent of absorption of the two drugs, as assessed by AUC (0-24 h), was slightly smaller with the retard suspension than with the aqueous solution. However, the test/reference ratio remained within 95% confidence intervals of 80-87% and 88-98% for CA and PP, respectively, indicating bioequivalence of the two formulations. A simulation of the plasma levels during repeated administration indicated that dosing with the retard suspension at 12-h intervals should yield the same steady-state plasma levels as a 5 times daily administration of a divided dose of the aqueous solution, for both drugs.

Adult↗
PubMedDate not supplied

[Evanescent toxic thyroid adenoma. Possible role of phenylpropanolamine].

A patient with a toxic adenoma, already reduced in size by TSH, presented on the third day after treatment of a common cold by phenylpropanolomine, a severe pain in the thyroid gland. 4 weeks later, the nodule, which measured 3 x 4 cm. had clinically disappeared and the scan returned to normal. The disappearance 5 months later of the antithyroid antibodies confirmed the cure. Catecholamines, stimulating the production of thyroid hormone and producing temporary ischemia of the gland, phenylpropanolamine, a sympathomimetic drug, may have caused hemorrhagic necrosis of the adenoma and its disappearance.

Adenoma↗