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PubMedDate not supplied

Examination of iron (III) and hexacyanoferrate (III) ions as reagents for the spectrophotometric determination of promazine and perazine.

Iron (III) chloride and potassium hexacyanoferrate (III) have been tested as reagents for the determination of promazine hydrochloride and perazine. The methods are based on the oxidation of phenothiazines by FeCl3 and K3[Fe(CN)6] in perchloric acid medium. The optimal conditions for the formation of oxidation products of promazine and perazine were examined. The absorption spectra in the UV-VIS region were recorded.

Chlorides↗
PubMedDate not supplied

Analytical studies and application of reaction of promazine and thioridazine hydrochlorides with some oxidants.

The run and analytical application of oxidation reaction of promazine (PM) and thioridazine (TR) hydrochlorides with iron(III) and ferrocyanide(III) are described. The coloured products of oxidation absorb at 512 nm for promazine and 634 nm for thioridazine. This property is a basis of a rapid, accurate and sensitive spectrophotometric method for determination of these phenothiazines. The elaborated methods allow to determine 3-28 microgPM/ml in Fe(III)-PM and 2-11 microgPM/ml in [Fe(CN)6](3-)-PM systems, 2.5-22 microgTR/ml in the Fe(III)-TR and 4-16 microgTR/ml in [Fe(CN)6](3-)-TR systems.

Oxidants↗
PubMed1989

[Provoking effect of promazine on EEG in childhood].

The authors report on the sleep activation of the EEG-recordings by Promazine a Phenothiazine derivative that can be used also in babies and in those elder children who does not tolerate sleep deprivation. The EEG-s are much less altered then by other related compounds or by Barbiturates. The greatest efficacy could be reached in generalized epilepsies, but the method was helpful in other epilepsy forms too. It is emphasized that in no case of acute neurological symptoms of not epileptic origin showed the Promazine induced sleep a convulsive activity.

Adolescent↗
PubMed1984

In vitro cross-linking of bovine lens proteins photosensitized by promazines.

Promazine derivatives induce cross-linking of bovine lens crystallins in vitro by irradiation with near-ultraviolet (UV) light in the presence of O2, as revealed by electrophoresis after denaturation. With the five derivatives tested (promazine [PZ], chlorpromazine [CPZ], triflupromazine [ TFPZ ], methoxypromazine [ MTPZ ], and acepromazine [ ACPZ ] ), single-hit kinetics are observed. Evidence implicating the cation radicals of the PZ derivatives as the causative agent of this in vitro effect is presented. Hydroxyl radicals do not appear to be involved in the photo-cross-linking reaction. Sodium ascorbate protects against damage induced either by PZ derivatives plus light or by PZ cation radicals in the dark. These findings are discussed with respect to development of cataracts induced by these drugs in vivo.

Acepromazine↗
PubMed1978

Short term immobilization in the horse with ketamine CHl and promazine HCl combinations.

Combinations of promaxine HCl and ketamine HCl were used to produce short term dissociative anaesthesia in the horse under normal clinical conditions. Premedication with 1 mg/kg promazine HCl followed 5 min later by a rapid i.v. injection of 2 mg/kg ketamine HCl, induced dissociative anaesthesia of 16 +/- 1 min. When 1 mg/kg promazine HCl and a 2 mg/kg ketamine HCl were given simultaneously by rapid i.v. injection, a state of dissociative anaesthesia was induced with a mean duration of 17.1 +/- 2 min. Both treatments permitted minor surgery in the horse.

Anesthesia↗
PubMed1964

PROMAZINE AND MEPERIDINE (SPARIDOL 50), AN EFFICIENT COMBINATION FOR PREOPERATIVE MEDICATION.

A number of elderly patients undergoing intraocular surgery were premedicated with a combination of promazine 50 mg. and meperidine 50 mg. Superior sedation and a smoother postoperative course were noted as compared to a control group premedicated with the usual high dosages of opiates and barbiturates. The incidence of nausea and vomiting, urinary retention, and postoperative disorientation was less than 20%. Hypotension was not a problem.Promazine was found to potentiate the action of opiates and barbiturates given in smaller dosages, thus permitting surgical procedures to be carried out with safety in an older population prone to the complications of opiate and barbiturate administration. This finding confirms reports noted in the obstetrical literature.

Analgesics, Opioid↗
PubMed1978

Kinetics and mechanism of oxidation of promazine and promethazine by ferric perchlorate.

The equilibrium constants, kinetics, and mechanism of promazine and promethazine oxidation by ferric perchlorate were investigated at different temperatures and acidities using a stopped-flow spectrophotometric technique. The overall reaction can be represented as follows: (formula: see text) where P+ represents the radical cation corresponding to the phenothiazine derivative. The equilibrium quotients were evaluated at 1.00 M HClO4, 25.0 degrees, and ionic strength 1.0 M. The kinetics of reaction follow the equation: -d[P] divided by dt = k1[Fe3+][P]-k-1[Fe2+][P+] The rate constants k1 and k-1 are independent of acidity and are related to the corresponding equilibrium quotients.

Chemical Phenomena↗
PubMed1983

Lack of singlet oxygen formation by photoexcited promazine derivatives in aqueous and ethanolic solutions.

The EPR detection of nitroxide formation and the observation by thin layer chromatography of the specific 1O2 oxidation product of cholesterol, have been used to appreciate singlet oxygen production by promazine and four of its derivatives during irradiation with near-UV light of ethanolic and aqueous solutions. Within the range of sensitivity of the methods, no 1O2 had been detected.

Acepromazine↗
PubMed1987

Alkaline labilization of DNA photosensitized by promazine derivatives.

Superhelical pBR322 DNA has been photosensitized in the presence of various promazine derivatives. Agarose gel electrophoresis of the photosensitized DNA reveals that true single-strand breaks are induced during irradiation. Alkaline treatment of the photosensitized DNA with a subsequent alkaline agarose gel electrophoresis demonstrates that in addition to true single-strand breaks, these drugs can induce alkali-labile lesions. Although true single-strand breaks are induced randomly into a 5'-[32P]-end labeled pBR322 DNA fragments, the alkaline-labile alterations are located specifically at the level of guanine residues. A strong correlation seems to exist between the visualization of this labilization and the induction of a covalent photoadduct on guanine by the photosensitization mediated by PZ.

Alkalies↗
PubMed1992

Inhibition and induction of cytochrome P450 2B1 in rat liver by promazine and chlorpromazine.

Phenothiazine tranquilizers have been associated with pharmacokinetic drug interactions in man. In this study the in vivo and in vitro effects of the clinically important phenothiazines promazine (PZ) and chlorpromazine (CPZ) on drug oxidations catalysed by specific cytochrome P450 (P450) enzymes were investigated in the rat. In vitro, the two drugs were relatively ineffective inhibitors of constitutive P450 activities, but were inhibitory toward the principal phenobarbital-inducible P450 2B1 and, to a lesser extent, P450 1A1. Administration of PZ and CPZ to male rats did not markedly influence the total microsomal P450 content of the liver. However, the quantitatively important male-specific P450 2C11 was down-regulated by CPZ and concomitant induction of P450 2B1 and associated 7-pentylresorufin O-depentylase activity were noted. A small increase in the activity of microsomal 7-ethylresorufin O-deethylase was also observed following administration of both drugs to rats, suggesting induction of P450 1A1/2. Considered together, it is apparent that the two phenothiazines are preferential inhibitors and inducers of P450 2B1 in rat liver. Drug interactions in humans involving phenothiazines may reflect a combined effect of induction and inhibition processes as well as down-regulation of other P450s, such as that produced by CPZ on P450 2C11.

Animals↗
PubMed1976

Stimulation of food intake in horses by diazepam and promazine.

In two adult horses doses of 0.02-0.03 mg/kg diazepam, intravenously, increased 1 hr intake 54-75% above control levels. Intake was stimulated when the diet was a high grain, calorically dense one and also when the diet was a high fiber, calorically dilute one. Two young rapidly growing weanling horses showed an even more pronounced stimulation of intake. Following diazepam 1 hr intake was increased 105-240% above control lelvels. Promazine at a dose of 0.5 mg/kg also stimulated intake in adult horses, but not as markedly as did diazepam. A transquilizer and a neuroleptic appear to have a stimulatory eff upon short-term intake in horses.

Age Factors↗
PubMed1977

Effects of d-amphetamine, chlordiazepoxide and promazine on responding of squirrel monkeys maintained under fixed-interval schedules of food presentation and stimulus-shock termination.

Responding of two squirrel monkeys was maintained under a multiple 5-min fixed-interval schedule of food presentation and termination of a stimulus in the presence of which shocks occurred. Under the stimulus-shock termination schedule, shocks occurred independently of responding, on the average of every three minutes; a response after 5 min terminated the prevailing stimulus and shock-presentation schedule. Response rates and patterns of responding under both schedules were comparable although they differed slightly between monkeys. d-Amphetamine increased and promazine decreased responding under both fixed-interval schedules. Chlordiazepoxide increased responding maintained by food presentation but decreased responding maintained by termination of the stimulus-shock complex. Under certain conditions and with certain drugs, the event that maintains responding can determine the effects a drug will have on behavior.

Animals↗
PubMed1998

Validated high-performance liquid chromatographic assay for the determination of promazine in human plasma. Application to pharmacokinetic studies.

A high-performance liquid chromatographic method for the determination of promazine in human plasma is described. The assay involves a single-step liquid-liquid extraction using pentane-2-propanol (98:2, v/v). The analyte of interest and the internal standard chlorpromazine were separated on a Spherisorb CN column using a mobile phase of acetonitrile-50 mM ammonium acetate (9:1, v/v). Electrochemical detection was achieved using an applied potential of +750 mV. The assay was validated according to international requirements prior to application to a pharmacokinetic study and was found to be specific, accurate and precise with a linear range of 0.25-25 ng ml(-1).

Antipsychotic Agents↗
PubMed1992

Haemodynamic responses following meperidine and promazine induced neuroleptanalgesia in calves.

Induction of neuroleptanalgesia in 6 calves by i/v administration of a combination of meperidine (/ 12 mg/kg body weight) and promazine (/ 3 mg/kg body weight) elicited various haemodynamic responses. The MAP and CVP exhibited significant (p less than 0.01) overall variations with fluctuating fall and rise at different observation periods. A significant (p less than 0.01) rise could be observed in HR which manifested a maximum and an abrupt rise (104.31%) at 5 minutes postinjection. Cardiac output, cardiac index, stroke volume, stroke index and total peripheral resistance exhibited significant (p less than 0.01) overall variations with an initial fall in their values as compared to the respective base values. The cardiac output and cardiac index showed an alternate fall and rise from the preceeding value while the stroke volume, stroke index and total peripheral resistance manifested decreased values throughout the observation period as compared to base value. The values of all parameters measured, except heart rate, stroke volume, stroke index and total peripheral resistance, nearly returned to preinjection level by 120 minutes.

Animals↗
PubMed1999

Effects of caffeine and promazine hydrochloride on plasma catecholamines in thoroughbreds at rest and during treadmill exercise.

Our aim was to investigate plasma catecholamine responses to so-called 'doping' drugs and exercise in Thoroughbreds. Plasma adrenaline (Ad) and noradrenaline (NA) were determined after the administration of caffeine and promazine hydrochloride (PRZ) using a high performance liquid chromatographic method. Caffeine or PRZ was administered i.m. to Thoroughbreds and its effects on plasma catecholamines at rest and during exercise were compared with the saline control. The treadmill exercise was performed 1 h after administration. A dose of 5.0 mg/kg bwt caffeine was found to significantly increase both plasma Ad and NA levels but this was not the case for the 2.5 mg/kg bwt dose and their peak levels at 1.5 h were about 3 and 2.5 times as compared with the control values at 1.5 h (Ad: mean +/- s.e. 21.2 +/- 2.8 pg/ml, NA: 55.5 +/- 4.1 pg/ml), respectively. Both 1.0 and 1.5 mg/kg bwt PRZ doses reduced the plasma Ad to below the detection limit (10 pg/ml) and significantly reduced the plasma NA. The 2.5 mg/kg bwt caffeine dose significantly increased plasma Ad and NA during exercise and approximately doubled their maximal values as compared with the saline control (Ad: mean +/- s.e. 12.328 +/- 4.733 ng/ml, NA: 9.997 +/- 4.146 ng/ml). The 1.5 mg/kg bwt PRZ dose decreased the plasma Ad during exercise but the effect was not significant. On the other hand, PRZ significantly increased the plasma NA as compared with the saline control. In conclusion, the present study demonstrates that the plasma catecholamine responses to caffeine and PRZ were modified by exercise. It is probable that the modification may be related to exercise-induced activation of the sympathetico-adrenal axis.

Animals↗
PubMed1986

Toxicity of promazine and chlorpromazine to isolated rat hepatocytes and its modification by liposome entrapment.

Isolated rat hepatocytes were used to determine the relationship between magnitude of uptake by cells and cytotoxic effects of chlorpromazine (CPZ) and promazine (PZ). Cell injury was evaluated by the extent of leakage of cytoplasmic and lysosomal enzymes from cells to surrounding medium and by cytopathic changes seen under surface scanning electron microscopy, after drug exposure. The drug uptake was time- and dose-dependent; cell preparations exposed to equal concentrations of either drug in the medium contained a twice greater concentration of CPZ than of PZ. Cytoplasmic and lysosomal enzyme leakage from cells exposed to 200 and 500 microM of CPZ showed significantly greater toxicity than control cells or those exposed to PZ at the same concentration. Surface activity of drugs was determined to calculate their surface excess. The surface pressure of CPZ is about twice that of PZ at equimolar concentration and correlated with extent of drug uptake and toxicity, suggesting that the surfactibility could play a role in bioavailability and toxicity of these drugs to liver cell membranes. Cytotoxicity was decreased by entrapment of CPZ inside liposomes; up to 40% for lactate dehydrogenase leakage and 47% of beta-glucuronidase, presenting further evidence for the potential use of liposomes.

Animals↗
PubMed1981

A comparison of the in vivo metabolism of phenothiazine and promazine in the neonatal guinea pig.

The in vivo metabolism of promazine and phenothiazine was studied in neonatal guinea pigs aged 1-21 days. Urinary metabolites were estimated for both compounds; marked fluctuations with age were noted, some values being greater than those found for adult animals. Unconjugated phenol (C-oxidation products) levels were very low, although glucuronide excretion was always present; glucuronyl transferase activity did not appear to be limiting, and was present as early as 1 day after birth. Peak sulphoxide excretion showed no correlation with output of other metabolites, suggesting that S- and C-oxidation are not directly linked.

Aging↗
PubMed2005

Relation of postmortem blood alcohol and drug concentrations in fatal poisonings involving amitriptyline, propoxyphene and promazine.

Drugs and alcohol often occur together in fatal poisonings, complicating the process of determining the cause of death. Especially when found in concentrations generally regarded as toxic but not lethal, the question arises whether the combination of sublethal amounts was the likely cause of death. In this study, we examined poisoning deaths involving amitriptyline, propoxyphene and promazine, which are, after benzodiazepines, the most frequently occurring drugs in Finnish alcohol-related poisonings. From the forensic toxicology database, covering the years 1995-2002, we extracted 332 fatal poisonings, calculated median blood alcohol and drug concentrations, constructed concentration-concentration and concentration-response curves and evaluated the significance of the presence of therapeutic amounts of benzodiazepines. Median amitriptyline and propoxyphene concentrations were lower in alcohol-related cases than in clean drug poisonings. Correspondingly, the median blood alcohol concentrations in all drug-related poisonings were 1.5-2.2 mg/g lower than that found in clean alcohol poisonings. Alcohol concentration proved to be a more sensitive indicator of alcohol-drug interaction than drug concentration. This result suggests that when alcohol is present, relatively small overdoses of the studied drugs may result in fatal poisoning. In this context, fatal drug and alcohol concentrations and the issue of determining the most important agent in fatal drug-alcohol intoxications are discussed.

Amitriptyline↗