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Biomedical subjects

H Rowe

Publications and source records attributed to H Rowe.

At least 19 recordsLinked to original sources
PubMed2003

Treatment of maternal mood disorder and infant behaviour disturbance in an Australian private mothercraft unit: a follow-up study.

Australia has a system of residential parentcraft services which offer brief admissions to mothers experiencing difficulties with infant care and postnatal mood disturbance. Most of these are state-funded public access services. In 1996 a comparable but differentiated service was opened in the private sector. Masada Private Hospital Mother Baby Unit accommodates five mother-infant pairs who are admitted to a five-night structured residential program. Care is provided by a multidisciplinary team comprising a paediatrician, general practitioner, clinical psychologist and specialist nurses. Complex maternal mood disorders as measured on standardised psychometric instruments include depression, anxiety and severe occupational fatigue. Their babies are unsettled, cry for prolonged periods, wake frequently at night and do not sleep well during the day. Many have feeding difficulties. The treatment program comprises both individualised training in infant care and settling strategies and psycho-educational groups offered in a supportive non-judgemental setting. One month post-discharge maternal mood is significantly improved and infant behaviour more manageable compared with functioning on admission.

Adult↗
PubMed1996

Multidisciplinary teamwork--myth or reality?

The provision and delivery of health care has become increasingly complex in recent years due to technological innovation in medicine and increasing client expectations. The challenge for health care workers is to meet the purchasers' demands, one option may be to shift working practices from a functionalist approach to one of multidisciplinary teamwork. This paper explores one example of multidisciplinary teamwork and examines the processes which enhance and those that limit collaboration.

Attitude of Health Personnel↗
PubMed1993

Effect of tibenelast (a phosphodiesterase inhibitor) and theophylline on isoproterenol-stimulated heart rate, cyclic AMP and norepinephrine levels.

The effect of the phosphodiesterase inhibitors (tibenelast, theophylline) and placebo on isoproterenol-induced changes in heart rate, cAMP and norepinephrine levels in normal male volunteers was studied. Heart rates in response to isoproterenol dosing were fitted by linear regression, and horizontal shifts in the regression lines were examined between the three treatments. The shift of the regression line after placebo compared to the preplacebo line was to the right by 2.6 +/- 2.2 ng ISO/kg/min, theophylline pretreatment shifted this line to the left by 2.4 +/- 1.8 ng/kg/min (p < 0.05) and tibenelast by 3.7 +/- 1.9 ng/kg/min (p < 0.02). Both tibenelast and theophylline increased the heart rate response to isoproterenol infusion, whereas norepinephrine and cAMP levels were not different in any treatment.

Adult↗
PubMed1988

Pressor responses to tyramine and norepinephrine after subchronic administration of fluoxetine to man.

The effects of subchronic, oral administration of fluoxetine (60 mg daily for 45 days) were studied in three healthy male volunteers. The pressor responses to intravenous bolus tyramine injections or norepinephrine infusions were assessed during the one-week placebo period, periodically after daily fluoxetine dosing, and then for 11 days post-fluoxetine dosing. The dose-pressor responses, determined from the incremental elevation of systolic blood pressure, were unchanged in each of the three dosing intervals. These results indicate that fluoxetine does not significantly impair the catecholamine uptake mechanism in the peripheral adrenergic neuron on acute or subchronic dosing, nor is any rebound-increased sensitivity evident after subchronic administration. Further, fluoxetine does not appear to demonstrate peripheral alpha-adrenolytic properties in man.

Administration, Oral↗
PubMed1988

The effect of fluoxetine on the pharmacokinetics and psychomotor responses of diazepam.

To determine the effect of fluoxetine on diazepam's pharmacokinetic and psychomotor responses, single oral doses of 10 mg diazepam were administered to six normal subjects on three occasions, either alone or in combination with 60 mg fluoxetine. Diazepam was given alone, after a single dose of fluoxetine, and after eight daily doses of fluoxetine. Psychometric data showed that fluoxetine had no significant effect on the psychomotor responses to diazepam. However, the pharmacokinetic data indicated a change in diazepam disposition after fluoxetine administration. Diazepam AUC was larger, the half-life was longer, and the plasma clearance was lower after fluoxetine administration, suggesting that fluoxetine inhibited the metabolism of diazepam. The reduced formation of an active metabolite, N-desmethyldiazepam, also suggested that fluoxetine inhibited diazepam's metabolism. The clinical implications of this pharmacokinetic drug-drug interaction are minor because psychomotor responses were unaffected and offsetting changes in the kinetics of diazepam and its metabolite occurred. Dosage modification of either fluoxetine or diazepam is unlikely to be necessary.

Adult↗
PubMed1985

Effect of fluoxetine on psychomotor performance, physiologic response, and kinetics of ethanol.

The effects of fluoxetine, a specific serotonin reuptake inhibitor, on the psychomotor performance, physiologic response, and kinetic disposition of ethanol were examined. Fluoxetine (30 or 60 mg) with ethanol (45 ml absolute alcohol per 70 kg body weight) did not alter the plasma or blood concentrations of fluoxetine or ethanol, respectively, when compared with levels after either drug alone. There was no significant effect on standing or recumbent blood pressure or heart rate after single or multiple doses of fluoxetine alone or in the combination. Single or multiple doses of fluoxetine had no effect on the psychomotor activity (stability of stance, motor performance, or manual coordination) or subjective effects of alcohol. Data indicate that fluoxetine does not inhibit ethanol metabolism nor does it have any effects on its psychomotor activity.

Adult↗
PubMed1985

Clinical pharmacology of tomoxetine, a potential antidepressant.

Tomoxetine (LY139603) selectively inhibits norepinephrine uptake in animals and has activity in animal models of depression. Tomoxetine was administered in single oral doses up to 90 mg to healthy normal volunteers. In addition, normal human subjects received either 20 or 40 mg of tomoxetine b.i.d. for 1 week to evaluate the safety and pharmacologic activity of the compound in humans. At these doses, no serious drug-related adverse effects were encountered. Activity of the compound at the lower dose (20 mg b.i.d.) was evaluated by examining changes in the pressor responses to infused norepinephrine and tyramine and by determining [3H]serotonin uptake in platelets harvested from subjects receiving the compound. Pressor sensitivity to norepinephrine was increased by 261 +/- 69% of control, and pressor sensitivity to tyramine was decreased by 51 +/- 6% of control during treatment. Changes in the pressor sensitivity to norepinephrine in individual subjects were positively correlated with drug levels. There were no statistically significant changes in platelet [3H]serotonin uptake. These results indicate that tomoxetine selectively inhibits norepinephrine uptake in humans at doses which are clinically well tolerated and suggest that tomoxetine has potential clinical use as an antidepressant.

Adult↗
PubMed1978

Pharmacologic effects in man of a specific serotonin-reuptake inhibitor.

Fluoxetine (Li-ly 110140) caused a 63 percent inhibition of [3H]serotonin uptake into platelets obtained from normal volunteers to whom the drug was administered daily for 7 days. This dose had no effect on the usual pressor response produced by injections of norepinephrine or tyramine.

Behavior↗
PubMed1978

Physiologic disposition of lergotrile.

Lergotrile, an ergot alkaloid, has been shown to be effective in treating disorders associated with elevated serum prolactin levels (e.g., galactorrhea-amenorrhea). Lergotrile has also been found to be a potent dopaminergic agonist and thus to be effective in Parkinson's disease. This study describes the physiologic disposition of lergotrile after administration to human volunteers. N-14CH3-lergotrile was rapidly absorbed from the gastrointestinal tract. Lergotrile was detected at low concentrations in plasma when subjects received large doses over extended periods of time. The major portion of radioactivity in plasma was attributed to the presence of circulating metabolites of lergotrile. Lergotrile metabolities were eliminated in the feces (ca. 60%), urine (ca. 20%), and breath (ca. 7% as 14CO2). A metabolite in feces was identified as 13-OH-lergotrile (up to 30% of the dose). A metabolite in urine was formed by conversion of the C8-acetonitrile group of lergotrile to a carboxyl group (about 10% of the dose). The presence of 14CO2 in the expired air after administering N-14C-methyl-lergotrile indicated that the drug was N-demethylated to form norlergotrile.

Acetonitriles↗
PubMed1977

Physiologic disposition of nabilone, a cannabinol derivative, in man.

Nabilone is a cannabinoid that is being evaluated in man as a potentially useful psychoactive drug. We found that nabilone was readily absorbed from the human gastrointestinal tract when administered orally as a coprecipitate with polyvinyl-pyrrolidone. The absorbed drug disappeared from plasma rather rapidly (half-life, approximately 2 hr), evidently due to extensive tissue distribution and rapid metabolism. The metabolites of nabilone persist in plasma for extended periods (half-life of total radioactivity exceeds 20 hr). Circulating metabolites include isomeric carbinols formed by reduction of the ketone in the 9-position of nabilone. Nabilone is eliminated in feces (about 65% of dose) and urine (20%). The excretory products in urine have not been identified, but metabolites that are labile to hydrolysis by beta-glucuronidase or sulfatase do not appear to be formed in significant amounts. A metabolite of nabilone in feces has been identified as a diol formed by reduction of the 9-keto group plus oxidation at the penultimate carbon of the dimethylheptyl side chain. The long duration of action of nabilone in the face of rapid and extensive metabolic elimination suggests that the pharmacologic effects, at least in part, may be exerted by one or more active metabolites.

Administration, Oral↗
PubMed1976

The effect of nisoxetine (Lilly compound 94939), a potential antidepressant, on biogenic amine uptake in man.

Preclinical studies with nisoxetine (Compound 94939) (3-[o-Methoxyphenoxy]-N-methyl-3-phenylpropylamine HCl) had shown it to have antidepressant properties and to be almost devoid of anticholinergic activity and depressant effects on cardiac conduction (in contrast to the commonly used tricyclic antidepressants from which nisoxetine significantly differs in structure). Placebo and nisoxetine (10-20 mg b.d. for 7 days) were administered to normal volunteers in a single-bind crossover study. Adverse side effects were minimal. There were no significant changes in heart rate or blood pressure seen when no other drugs were given. The effect of nisoxetine on uptake of biogenic amines was utilized to study its mechanism of action. The transient rise in blood pressure seen after an intravenous bolus of tyramine decreased by one-half to two-thirds while the rise in blood pressure upon continuous noradrenaline infusion was enhanced some two-to eight-fold. Both effects occurred after on dose and were greater with larger doses and chronic administration. In vitro, nisoxetine inhibits 5-HT uptake into platelets. However, platelets harvested from subjects receiving chronic nisoxetine administration did accumulate 5-HT. Plasma concentration of nisoxetine in these individuals was shown to be lower than that needed to block 5-HT uptake. We concluded that nisoxetine, in safe doses, specifically increased the sensitivity of noradrenaline and decreased tyramine responsiveness, presumably by blocking uptake at the axonal membrane. In contrast, in these clinical doses it had virtually no effect on 5-HT uptake into platelets.

Adult↗