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At least 19 recordsLinked to original sources
PubMed2000

An evaluation of l-ephedrine neurotoxicity with respect to hyperthermia and caudate/putamen microdialysate levels of ephedrine, dopamine, serotonin, and glutamate.

l-Ephedrine is an active ingredient in several herbal formulations with a mechanism of action similar to amphetamine and methamphetamine. However, its potential to damage dopaminergic terminals in the caudate/putamen (CPu) has yet to be fully evaluated. The studies here used in vivo brain microdialysis experiments to determine the systemic doses and extracellular brain levels of l-ephedrine necessary to produce similar increases in CPu extracellular dopamine and marked hyperthermia that were previously shown necessary for amphetamine-induced neurotoxicity in male Sprague-Dawley rats. At an environmental temperature of 23 degrees C, a single 40 mg/kg intraperitoneal (ip) dose of l-ephedrine produced marked hyperthermia (>/= 40 degrees C), peak microdialysate ephedrine levels of 7.3 +/- 1.2 microM, and a 20-fold increase in microdialysate dopamine levels. Twenty-five mg/kg produced a lesser degree of hyperthermia, peak microdialysate ephedrine levels of 2.6 +/- 0.4 microM, and a 10-fold increase in dopamine levels. Three doses of 40 mg/kg given at 3-h intervals or 4 doses of 25 mg/kg l-ephedrine given at 2-h intervals were compared with 4 doses of 5 mg/kg d-amphetamine given at 2-h intervals. Multiple doses of either ephedrine or amphetamine caused severe hyperthermia (>/= 41.3 degrees C) but striatal tissue levels of dopamine 7 days after dosing were reduced only 25% or less by ephedrine compared to the 75% reductions produced by amphetamine. The increases in CPu microdialysate levels of serotonin produced by either 4 x 25 mg/kg l-ephedrine or 4 x 5 mg/kg d-amphetamine did not significantly differ, but elevation of dopamine levels by d-amphetamine were over 2-fold times the level caused by l-ephedrine. Microdialysate glutamate levels were elevated to the same extent by either 25 mg/kg l-ephedrine or 4 x 5 mg/kg d-amphetamine. l-Ephedrine may not be as neurotoxic to dopaminergic terminals as d-amphetamine, because non-lethal doses of l-ephedrine do not sufficiently increase the CPu dopamine levels within nerve terminals or the extracellular space to those necessary for a more pronounced long-term dopamine depletion.

Animals↗
PubMedDate not supplied

Biotransformation of D(-)-ephedrine and L(+)-ephedrine in the rabbit, in vivo and in vitro.

Investigations were carried out with radiolabeled D(-)-ephedrine and L(+)-ephedrine to establish whether differences exist in their metabolic fate in the rabbit, in vivo and in vitro. In liver microsomal preparations, a) D(-)-ephedrine was metabolized at a faster rate than L(+)-ephedrine, b) benzoic acid was formed from D(-)ephedrine at a rate about three times greater than from the L(+)-isomer, and c) the relative amounts of norephedrine and 1-phenyl-1,2-propranediol formed from both ephedrine isomers were nearly identical throughout the entire incubation period. In vivo, both ephedrine isomers were extensively metabolized and the majority of total radioactivity (71-91%) was excreted within 24 hr. A greater 14C-excretion rate was observed for L(+)-ephedrine. From an analysis of 0- to 24-hr urine, it was found that a) 47-50% of the urinary 14C was attributable to acidic metabolites (hippuric acid and benzoic acid) from L(+)- and D(-)-ephedrine, b) from 4 to 16% of the total 14C obtained with both isomers was accountable as 1-phenyl-1,2-propanediol, either free or as a glucuronide conjugate, c) no appreciable quantities of sulfate or glucuronide conjugates of p-hydroxylated metabolites of ephedrine or norephedrine was detectable, and d) small amounts (less than 4% of metabolites corresponding to unchanged ephedrine, norephedrine, or 1-hydroxy-1-phenyl-2-propanone were found in urine of animals given either isomer. These experiments indicate that the major pathway for the biotransformation of D(-)-ephedrine and L(+)-ephedrine involves N-demethylation and oxidative deamination of the side chain.

Animals↗
PubMed2002

Terlipressin-ephedrine versus ephedrine to treat hypotension at the induction of anesthesia in patients chronically treated with angiotensin converting-enzyme inhibitors: a prospective, randomized, double-blinded, crossover study.

UNLABELLED: In patients chronically treated with angiotensin converting-enzyme inhibitors (ACEI), typically selected doses of ephedrine do not always restore arterial blood pressure when anesthesia-induced hypotension occurs. We postulated that the administration of terlipressin, an agonist of the vasopressin system, with ephedrine more effectively restores pressure in this setting than the administration of ephedrine alone. This prospective, randomized, cross-over, double-blinded study compared terlipressin combined with ephedrine (n = 19) with ephedrine alone (n = 21) in treating hypotension at the induction of anesthesia in 40 ACEI-treated patients undergoing hypotension (mean arterial blood pressure [MAP] <65 mm Hg or <30% of baseline value) after standardized anesthetic protocol (target-controlled IV anesthesia with propofol). Data are mean +/- SD. Patient characteristics, MAP, and heart rate before and after the induction of anesthesia during hypotensive episodes were not significantly different between the two groups. After the first bolus, MAP was significantly greater in the Terlipressin-Ephedrine group (72 +/- 12 mm Hg versus 65 +/- 8 mm Hg, P < 0.05). The occurrence of a second hypotensive episode (5% versus 71%, P < 0.001), the duration (2 +/- 1 min versus 3 +/- 1 min, P < 0.01) of hypotensive episodes, and the median dose of ephedrine (3 versus 6 mg, P < 0.05) were significantly less in the Terlipressin-Ephedrine group. In conclusion, terlipressin combined with ephedrine is more effective than ephedrine alone for treating anesthesia-induced hypotension in ACEI-treated patients. We conclude that this patient population with a partially blocked endogenous response to hypotension may be good candidates for successful use of a vasopressin analog to counteract intraoperative refractory hypotension. IMPLICATIONS: Vascular surgical patients chronically treated with drugs that inhibit the functioning of the renin-angiotensin system may experience hypotension unresponsive to conventional therapy. This double-blinded, cross-over study demonstrated that in these patients the use of a vasopressin analog, terlipressin given with ephedrine, was effective in reversing intraoperative systemic hypotension refractory to ephedrine.

Aged↗
PubMed1983

Stereospecific radioimmunoassays for l-ephedrine and d-ephedrine in human plasma.

Haptens were prepared by the reaction of d-ephedrine or l-ephedrine with methyl acrylate and subsequent alkaline hydrolysis of the methyl ester groups. The haptens were coupled to bovine serum albumin by a mixed anhydride method, and the resulting drug-protein conjugates were used to immunize rabbits. Antisera raised to these conjugates were highly stereospecific. Neither antiserum cross-reacted with the optical antipode of its substrate nor with racemic pseudoephedrine. Separate radioimmunoassays (RIAs), developed for d-ephedrine and l-ephedrine, were used to measure the concentrations of the enantiomers of ephedrine in the blood of two volunteers dosed with racemic ephedrine. The RIAs were validated by comparing the sum of the concentrations of the enantiomers, determined by RIA, with total ephedrine concentrations determined by a nonstereoselective GLC-ECD method.

Animals↗
PubMedDate not supplied

Degradation of (-)-ephedrine by Pseudomonas putida. Detection of (-)-ephedrine: NAD+-oxidoreductase from Arthrobacter globiformis.

A bacterium utilizing the alkaloid (-)-ephedrine as its sole source of carbon was isolated by an enrichment-culture technique from soil supplemented with 4-benzoyl-1,3-oxazolidinon-(2). The bacterium was indentified as Pseudomonas putida by morphological and physiological studies. The following metabolites were isolated from the culture fluid: methylamine, formaldehyde, methylbenzoylcarbinol (2-hydroxy-1-oxo-1 phenylpropane), benzoid acid, pyrocatechol and cis, cis-muconic acid. A pathway for the degradation of (-)-ephedrine by Pseudomonas putida is proposed and compared with the degradative pathway in Arthrobacter globiformis. The enzyme, which is responsible for the first step in the catabolism of (-)-ephedrine could be demonstrated in extracts from Arthrobacter globiformis. This enzyme catalyses the dehydrogenation of (-)-ephedrine yielding phenylacetylcarbinol/methylbenzoylcarbinol and methylamine. It requires NAD+ as cofactor and exhibits optimal activity at pH 11 in 0.1 M glycine/NaOH buffer. The Km value for (-)-ephedrine is 0.02 mM and for NAD+ 0.11 mM, respectively. No remarkable loss of activity is observed following treatment with EDTA. The enzyme has been shown to react with a wide range of ethanolamines. A slight enrichment was obtained by ammonium sulphate precipitation. The name (-)-ephedrine: NAD+-oxidoreductase (deaminating) is proposed.

Arthrobacter↗