Search PubMed⌕ Search

Biomedical subjects

R I Wang

Publications and source records attributed to R I Wang.

At least 19 recordsLinked to original sources
PubMed1989

Choice of rating form for evaluating anxiolytics.

The HAM-A has been a popular tool for assessing the anxiety status of patients. However, when studying anxiolytics, HAM-A presents problems. It includes 89 signs and symptoms grouped under 14 major items. Redundant symptoms appear in several items, and different symptoms under the same item may have variable severity, resulting in inconsistent ratings. In addition, evaluation of all 89 symptoms is time consuming and cumbersome, especially when frequent ratings are required in studying patient response to pharmacotherapy. The WARS was specifically designed to quantify symptoms of anxiety for the study of anxiolytics. It contains 12 one-word items, expressing all the relevant and commonly occurring psychic and somatic symptomatology relevant to anxiety. Symptomatology due to medication is rated separately on a side-effect scale. The WARS is thus more sensitive in detecting therapeutic changes. Because of its simplicity and lack of ambiguity, the WARS can be accurately and effortlessly completed in studying anxiolytics.

Anti-Anxiety Agents↗
PubMed1987

Hydrogen peroxide-induced glutathione depletion and aldehyde dehydrogenase inhibition in erythrocytes.

To study relationships between lipid peroxidation and aldehyde dehydrogenase (ALDH) inhibition, the Stocks and Dormandy model of H2O2-induced lipid peroxidation in erythrocytes was employed. Hydrogen peroxide treatment of erythrocytes and erythrocyte lysates caused a dose-dependent inhibition and depletion of ALDH and reduced glutathione (GSH) respectively. Complete ALDH inhibition and glutathione depletion occurred before significant lipid peroxidation was detected by HPLC analysis of malondialdehyde-thiobarbituric acid adducts. Hydroxyl radical scavengers did not antagonize the hydrogen peroxide-induced enzyme inhibition. Studies with the iron chelator desferrioxamine suggested that the hydrogen peroxide-induced ALDH inhibition was mediated by iron in erythrocyte lysates but not in semi-purified (and Chelex-treated) ALDH preparations. Glutathione peroxidase reduction of H2O2 exhibited an anomalous GSH dependence which was not in agreement with the accepted reaction mechanism. Reduced glutathione also antagonized the hydrogen peroxide-induced ALDH inhibition by possible complex formation with the enzyme. A hypothetical model is presented which accounts for the observed responses to hydrogen peroxide.

Aldehyde Dehydrogenase↗
PubMed1986

Erythrocyte aldehyde dehydrogenase: assay of a potential biochemical marker of alcohol abuse.

Erythrocyte aldehyde dehydrogenase (ALDH; EC 1.2.1.3) may be a new biochemical indicator of alcohol abuse. An improved assay for it is described and characterized. We found that expression of erythrocyte ALDH activity in terms of hemoglobin was valid, and preferable to expression in terms of erythrocyte volume. A normal reference interval was determined from results for 375 healthy subjects (236 men, 139 women). We compared these data with results for 109 men admitted to our alcohol detoxification program. The mean erythrocyte ALDH of the alcohol abusers was 30% lower than our mean value for men (p less than 0.001). Values did not change between the time the patient presented for admission and greater than 48 h later (when blood-ethanol concentration was zero). Other variables that affect erythrocyte ALDH activities--changes in pH, temperature, other assay conditions, and drug treatments such as disulfiram and nitrate anti-anginals--are discussed.

Alcoholism↗
PubMed1985

Enhanced development of dispositional tolerance to methadone by desipramine given together with methadone.

Rats given 2-day oral administration of methadone (15 mg/kg, twice on day 1 and once on day 2) by gastric tube developed dispositional tolerance to methadone analgesia as demonstrated by a decrease in analgesic response and by an increase in methadone metabolism. The increased metabolism of methadone was evidenced by a decrease in brain concentration of 14C-methadone and increases in the percentages of total 14C in liver or urine as 14C-water-soluble metabolites (14C-WSM) after the rats were challenged with a test dose of 14C-methadone. Two-day pretreatment with a combination of desipramine (DMI) (10 mg/kg, ip) and methadone (15 mg/kg, po) enhanced the development of dispositional tolerance to methadone analgesia which was evidenced by a greater decrease in the brain concentration of methadone and a greater increase in methadone metabolism as compared to those changes in rats pretreated with only methadone. Repeated treatment with DMI alone neither decreased the analgesic effect of methadone nor stimulated methadone metabolism. It is suggested that DMI given together with methadone promoted the induction of methadone metabolism in the liver by prolonging the enzyme-stimulating state of methadone, thus enhancing the development of dispositional tolerance to methadone.

Analgesia↗
PubMed1985

Effects of acute and chronic morphine treatment on methadone analgesia and metabolism.

Morphine sulfate (5 mg/kg s.c.) given 30 min prior to administration of methadone prolonged methadone analgesia and increased the brain level of methadone measured 60, 120 and 180 min after administration of methadone. Rats rendered tolerant to morphine analgesia by subcutaneous implantation of two pellets, each containing 75 mg of morphine base, for 1-3 days showed cross-tolerance to methadone analgesia regardless of the presence or absence of morphine pellets. Decreases in the brain concentrations of methadone measured at 60 and 120 min time points accompanied the decreased analgesia. Neither acute nor chronic morphine pretreatment affects the biotransformation of methadone. The results suggest that the cross-tolerance to methadone analgesia seen in chronic morphine-implanted rats was partly associated with a decrease in the brain concentration of methadone occurring by a mechanism not directly related to a change in the biotransformation of methadone. In view of the known inhibitory effect of chronic morphine pretreatment on drug metabolism, our findings might demonstrate a unique phenomenon between morphine and methadone.

Analgesics↗
PubMed1983

Further efficacy evaluation of doxpicomine for postoperative pain.

In this single-dose, double-blind study, the analgesic activity of 400 and 200 mg doxpicomine was compared with 100 and 50 mg meperidine and placebo when given intramuscularly in 102 subject patients experiencing severe postoperative pain. Results indicate that 400 mg doxicomine is similar to 100 mg meperidine in analgesic activity, onset, and duration of action. Side effects were of the same order as those produced by other centrally acting analgesics.

Adolescent↗
PubMed1982

Clinical comparison of propoxyphene napsylate and methadone in the treatment of opiate dependence.

In this double-blind comparison of propoxyphene napsylate (PN) 800 mg in two divided doses versus methadone 20 mg, methadone 10 mg or placebo methadone, it was found that PN: 1) did not alleviate withdrawal symptoms in patients previously maintained on methadone 20 mg; 2) produced a slightly overmedicated effect in the detoxified group of exmethadone patients; and 3) compared favorably to methadone 10 mg in suppressing withdrawal symptoms without producing evidence of overmedication in those patients previously stabilized on a methadone maintenance dose of 10 mg.

Adult↗
PubMed1981

Propoxyphene napsylate compared to methadone for opiate dependence.

When high single doses of propoxyphene napsylate (PN) were given to patients on a methadone maintenance program, results indicated that, to avoid undesirable side effects, the dose should not exceed 600 mg. However, when PN was given in divided doses (800 mg/day in two equal doses), no significant adverse reactions were noted. In the double-blind comparison of 800 mg PN in two divided doses versus 20 mg methadone, 10 mg methadone, or placebo methadone, it was found that PN (1) did not alleviate withdrawal symptoms in patients previously maintained on 20 mg methadone, (2) produced a slightly overmedicated effect in the detoxified group of ex-methadone patients, and (3) compared favorably to 10 mg methadone in suppressing withdrawal symptoms without producing evidence of overmedication in those patients previously stabilized on a methadone maintenance dose of 10 mg. It is concluded that on a mg for mg basis, PN at a dose of 80-times that of methadone will relieve withdrawal symptoms in the treatment of mildly addicted patients requiring 10 mg methadone or less per day.

Adult↗
PubMed1981

Effect of intraventricular beta-endorphin and morphine on hypothalamic-pituitary-adrenal activity and the release of pituitary beta-endorphin.

The effects of intraventricular (i.v.t.) morphine sulfate (MS) and beta-endorphin (beta-EP) on pituitary-adrenal activity and the release of pituitary beta-EP were studied in rats. Pituitary-adrenal activity was monitored by measuring plasma corticosterone (CS) levels. 45 min after i.v.t. injection, both MS and beta-EP caused dose-related increases in plasma CS, with beta-EP being approximately ten times more potent on a molar basis. MS injected i.v.t. at 0.3, 1.0, 3.0 and 10.0 microgram did not cause a significant reduction in pituitary immunoreactive (i.r.) beta-EP, but did cause an increase in plasma i.r. beta-EP at 3 microgram of MS. beta-EP injected i.v.t. at 1.5 microgram caused a reduction of pituitary i.r. beta-EP. Since i.v.t.-injected beta-EP may have contributed to the measured plasma i.r. beta-EP, a nonimmunoreactive analog (Des-Asn20-beta c-EP) was used to assess the change in plasma i.r. beta-EP. 5 microgram of DES-Asn20-beta c-EP injected i.v.t. caused increases in plasma i.r. beta-EP and CS, as well as a 40% reduction in pituitary i.r. beta-EP. The concomitant intraperitoneal (i.p.) injection of naloxone HCl (10 mg/kg) significantly blocked the increase in plasma CS induced by 5 microgram of beta-EP. When naloxone HCl, 10 mg/kg was injected alone, a significant increase in plasma CS was found. The results indicate that i.v.t. beta-EP is more potent than MS in causing the release of pituitary ACTH and beta-EP. These findings are consistent with a role for brain endorphins in the regulation of CRF release.

Animals↗
PubMed1979

The clinical analgesic efficacy of oral nefopam hydrochloride.

The analgesic efficacy of 60 and 120 mg nefopam hydrochloride was compared to 650 mg aspirin and placebo in a double-blind single-dose study. Oral doses were administered to 120 patients suffering from acute postsurgical or fracture pain. All active medications demonstrated analgesic activity in comparison to placebo. Patients on 120 mg nefopam obtained the greatest degree of analgesia. Side effects were minor and did not interfere with the course of therapy. The incidence of side effects (sweating, nausea, and lightheadedness) was greater on 120 mg nefopam than on 650 mg aspirin).

Adult↗