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Biomedical subjects

S A Checkley

Publications and source records attributed to S A Checkley.

At least 55 records · Page 3Linked to original sources
PubMed1986

No effect of naloxone on plasma oxytocin in normal men.

The role of endogenous opiates in the control of the secretion of oxytocin in the basal state in healthy male volunteers was investigated with the opiate antagonist naloxone. There was no change in plasma oxytocin levels, assessed for a 120 min period following the intravenous administration of naloxone (10 mg). Although there was no effect of opiate receptor blockade with naloxone in this basal situation, further studies are needed to evaluate the possible role of opioid regulation of oxytocin during lactation and parturition.

Adult↗
PubMed1985

The effects of alaproclate on the pupillary responses to tyramine, phenylephrine and pilocarpine in depressed patients.

Nine depressed patients were treated with alaproclate, a selective 5-HT uptake inhibitor, for 3 weeks in a dose of 400 mg daily. The pupillary responses to tyramine, phenylephrine, and pilocarpine eye drops were measured on consecutive days before, after 1 week and after 3 weeks of treatment. The tyramine-induced mydriasis was unaffected by alaproclate, suggesting that it does not significantly inhibit the reuptake of noradrenaline. The pilocarpine-induced miosis and the phenylephrine-induced mydriasis were both enhanced after 1 week but not after 3 weeks of treatment. This suggests that alaproclate acutely increases the responsiveness of postsynaptic muscarinic and alpha 1 adrenoceptors.

Alanine↗
PubMed1985

Clinical studies of the effect of (+) and (-)-oxaprotiline upon noradrenaline uptake.

In six normal male subjects the mydriatic effect of tyramine eye drops was inhibited by 1 day's treatment with desipramine and the (+)- but not the (-)-enantiomer of oxaprotiline. In the same experiment, the secretion of melatonin was increased after treatment with (+)- but not with (-)-oxaprotiline. The effects of (+)-oxaprotiline and of desipramine treatment were similar, as were those of (-)-oxaprotiline and placebo. These findings extend to clinical studies the demonstration in animal experiments of stereo-specificity for the effects of (+)- and (-)-oxaprotiline upon noradrenaline uptake. A comparison of the effects of the two enantiomers should provide an ideal strategy for studying effects of noradrenaline uptake blockade in clinical studies.

Anthracenes↗
PubMed1985

Characterization of platelet alpha 2 adrenoceptors and measurement in control and depressed subjects.

The alpha-adrenoceptor on platelets has been characterized using 3H-yohimbine, 3H-dihydroergocriptine, and 3H-clonidine. The receptor, which exhibits the characteristics of an alpha 2-type, has a Bmax for dihydroergocriptine of 330 fmoles/mg protein, for yohimbine of 178 fmoles/mg protein, and for clonidine of 38 fmoles/mg protein. Clonidine, but not yohimbine binding, is decreased by the presence of K+, Na+, or Li+. Adenosine triphosphate (ATP) and the guanosine triphosphate (GTP) analogue, Gpp(NH)p, reduce the affinity of clonidine for its binding site. Acute exercise, such as playing squash, does not apparently alter the Bmax or Kd of 3H-yohimbine binding to platelet membranes, and in vitro studies, with intact platelets or platelet membranes, show that incubation with adrenalin (10 microM) does not induce alterations in Bmax or Kd. In the present study, no correlation was found between age and alpha 2-adrenoceptor numbers. There was no significant difference in the Bmax for 3H-yohimbine binding to platelet membranes from control and depressed subjects, although the mean value for the depressed group was some 10% lower than that for the corresponding control group. There were no overall significant and consistent effects of desipramine (DMI) treatment. After 2-3 days of treatment, the Bmax was reduced by 20%, after 7 days by 14%, and after 21 days it was 8% above the control value. When an additional group of patients on DMI (7 days of treatment) was analyzed using one supramaximal concentration of 3H-yohimbine, there was a significant decrease (25%) in binding.

Adult↗
PubMed1985

Suppression of eating by fenfluramine in patients with bulimia nervosa.

Fifteen patients with bulimia nervosa received fenfluramine (60 mg po) or placebo under double-blind, randomly ordered conditions. Two hours later food was presented. Significantly less food was eaten after fenfluramine and the quantity eaten was inversely correlated with serum fenfluramine levels. Significantly fewer patients reported bulimic symptoms during the test after fenfluramine, but no significant effect was demonstrated after leaving the ward. Fenfluramine caused drowsiness but did not reduce hunger ratings. Similarly, eating failed to reduce hunger ratings normally in the patients. These findings suggest that in patients with bulimia nervosa, hunger is reported abnormally and eating is suppressed by fenfluramine. Bulimic symptoms were probably reduced by fenfluramine, which may prove to be a useful treatment for bulimia nervosa.

Adolescent↗
PubMed1985

The effect of desipramine upon melatonin and cortisol secretion in depressed and normal subjects.

Melatonin and cortisol values in plasma were measured hourly over 24 hours in six depressed patients and six normal volunteers before treatment and after one and three weeks of treatment with desipramine. The normal volunteers were further tested one week after withdrawal of desipramine. The mydriatic effects of tyramine and phenylephrine eye drops were also recorded in the normal volunteers. In neither group of subjects did desipramine treatment reduce melatonin secretion, suggesting that functionally significant down-regulation of beta andrenoceptors was not caused by this treatment. Melatonin secretion was significantly increased after three weeks of treatment in depressed patients. This increase was not found in normal subjects.

Adolescent↗
PubMed1984

Measurement of the GH and other responses to clonidine at different times of the day in normal subjects.

The growth hormone response to clonidine may be impaired in some patients with endogenous depression. To determine whether or not this change is due to a circadian variation in the GH response to clonidine, this measure has been studied in normal subjects at 0900, 1800 and 2100 hr. Similar responses were obtained at 0900 and 1800 hr. The responses at 2100 hr could not be interpreted, as the baseline plasma GH was raised. At no time of day were there impaired GH responses similar to those found in endogenous depression. The effects of clonidine upon blood pressure and alertness were similar at the three times studied, providing no support for any circadian rhythm in the function of the alpha 2-adrenoceptors that mediate these effects of clonidine.

Adult↗
PubMed1984

The GH response to clonidine in endogenous as compared with reactive depression.

The growth hormone (GH) response to clonidine was measured in 10 patients meeting standardized criteria for 'endogenous' depression and in 10 patients individually matched for age and sex but meeting the corresponding criteria for 'reactive' depression. In a paired comparison of patients with reactive and endogenous depression (matched for age and sex), the GH response to clonidine was less in the endogenous member of the pair in 8 out of 10 cases. These findings are interpreted as evidence of a defect at alpha 2 adrenoceptors in neuroendocrine systems in endogenous as compared with reactive depression.

Adjustment Disorders↗
PubMed1984

A neuroendocrine study of stereotactic sub-caudate tractotomy.

The growth hormone and hypotensive responses to clonidine have been measured in six drug free severely depressed patients before, and at two weeks after, the surgical procedure of stereotactic sub-caudate tractotomy. The responses were unaltered two weeks after operation, by which time a small clinical improvement was evident. These findings are discussed in relation to central alpha adrenoceptor functions in depression, and the effect upon this of antidepressant treatment.

Aged↗
PubMed1984

A comparison of the growth hormone responses to clonidine and apomorphine in the same patients with endogenous depression.

The growth hormone responses to clonidine (1.3 micrograms/kgm) and apomorphine (0.005 mg/kgm) have been measured in 8 drug free patients with endogenous depression. In these patients the growth hormone responses to clonidine were significantly smaller than to apomorphine. As these doses of clonidine and apomorphine have previously been reported to cause similar growth hormone responses in normal subjects, these findings support the hypothesis of a defect in the adrenergic but not the dopaminergic regulation of growth hormone in patients with endogenous depression.

Adult↗
PubMed1984

Effects of desipramine treatment upon central adrenoceptor function in normal subjects.

Six normal subjects were given clonidine infusions after 0, 1 and 3 weeks of treatment with desipramine (2 mg/kgm) and at 1 and 3 weeks after withdrawal from desipramine. The sedative and hypotensive effects of clonidine were inhibited after one and three weeks of desipramine treatment, and returned to normal after stopping treatment without any rebound increase. Such a time-course can be explained in terms of the acute effects of the drug, no adaptive changes at receptors need be invoked. By contrast, the growth hormone response to clonidine tended to be increased after one week of desipramine, reduced after three weeks of treatment, and further reduced after discontinuation. Such a time-course is consistent with an adaptive down regulation at alpha 2 adrenoceptors in response to their acute stimulation, due to noradrenaline re-uptake blockade.

Adult↗
PubMed1983

Changes in the sensitivity of the central alpha- and beta-adrenergic systems during desmethylimipramine treatment as assessed by plasma growth hormone response in the baboon.

The tricyclic antidepressant desmethylimipramine (DMI) 2.5 mg/kg IM was administered to adolescent baboons once daily for 21 days, to investigate changes in alpha- and beta-noradrenergic function. Prior to DMI treatment, plasma growth hormone (GH) responses to the intravenous infusion of an alpha 2-adrenergic receptor agonist, clonidine, or a beta 2-adrenergic antagonist, ICI 118,551, were determined. DMI, 2.5 mg/kg, administered acutely did not stimulate the release of GH (up to 4 h post injection). The GH response to clonidine was decreased 4 h after DMI, 2.5 mg/kg. Alterations in plasma GH response to clonidine and ICI 118,551 were evident during and after chronic DMI administration. The GH response to clonidine was significantly diminished after 2 days, and gradually returned to the pretreatment amplitude over 7-21 days of treatment, with an overshoot 2 days after DMI withdrawal. After 21 days of DMI administration the GH response to ICI 118,551 was significantly enhanced, and remained consistently elevated during a withdrawal period of 21 days. These changes in the response to an alpha-adrenergic agonist and a beta-adrenergic antagonist indicate that the long term regulatory changes in receptor sensitivity, occurring between 2 and 21 days of DMI treatment, compensate for the acute effects of DMI on these responses.

Animals↗
PubMed1983

Cushing's syndrome and depression--a prospective study of 26 patients.

Of 26 patients with active Cushing's syndrome assessed before and at three and 12 months after treatment, 21 had pituitary-dependent disease. Median urinary free cortisol values (per 24 hours) were 680, 180 and 200 nmol at zero, three and 12 months (normal less than 270 nmol), with significant improvement (P less than 0.001) at three and 12 months. Depression on the Hamilton rating scale was significantly less at three months (P less than 0.01) and at 12 months (P less than 0.001). We have already demonstrated that some patients with Cushing's syndrome have PSE diagnoses of depression and are more depressed than patients with other pituitary tumours. This is the firmest evidence to date that when Cushing's syndrome occurs it commonly causes depressive illness.

Adolescent↗