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Biomedical subjects

I M McIntyre

Publications and source records attributed to I M McIntyre.

At least 55 records · Page 3Linked to original sources
PubMed1988

Melatonin plasma response to MAO inhibitor: influence on human pineal activity?

Strong negative correlation has been observed between nighttime (physiological) elevation of plasma melatonin and plasma melatonin increase induced by a single dose of MAO inhibitor, tranylcypromine. The possible use of acute plasma melatonin response to MAO inhibitor as a functional test for the evaluation of human pineal activity is discussed.

Circadian Rhythm↗
PubMed1988

Platelet serotonin uptake in panic disorder: comparison with normal controls and the effect of treatment.

Platelet serotonin uptake was measured in 59 patients with panic attacks and compared to 26 controls. Scatchard analysis of the data showed that the maximal rate of uptake (Vmax) of serotonin was significantly higher in patients than controls. The affinity constant (Km) was not different. In a sub-group of 24 patients, benzodiazepine treatment did not alter the kinetics of platelet serotonin uptake. These findings suggest an abnormality in serotonergic function in patients with panic attacks. Insofar as the platelet is a model of central neuronal function they support serotonergic hyperactivity as a biochemical basis of panic attacks.

Adolescent↗
PubMed1988

Clinical effects of serotonin reuptake inhibitors in the treatment of depressive illness.

The serotonergic hypothesis of depression has stimulated the development of a range of chemically diverse compounds that have an exclusive effect on this neurotransmitter for potential use as antidepressant drugs. The group of serotonin reuptake inhibitors are at various stages of clinical development. The authors review the efficacy, side effect profiles, and toxicity of zimelidine, fluvoxamine, and citalopram in detail and ifoxetine, fluoxetine, indalpine, paroxetine, and sertraline in brief. Evidence suggests that, compared with tricyclic antidepressants, these drugs may cause fewer anticholinergic effects and lower cardiotoxicity in the treatment of major depressive disorders. These advantages need to be weighed against an emerging pattern of gastrointestinal complaints, insomnia, and akathisia. The place of serotonin reuptake inhibitors in therapy can be fully evaluated only after further studies, particularly those involving long-term use. The adverse experience associated with zimelidine suggests that caution and vigilance should be exercised in future studies of agents in this class. These drugs will undoubtedly provide important insights into depressive illness and some anxiety disorders and may fulfill their initial promise.

Clinical Trials as Topic↗
PubMed1987

Platelet 3H-rauwolscine binding in patients with panic attacks.

Platelet alpha 2 binding was measured in 14 patients with panic attacks and 21 controls using the antagonist 3H-rauwolscine as radioligand. The mean (+/- SD) Bmax values of patients (116 +/- 45 fmoles/mg protein) and controls (106 +/- 32 fmoles/mg protein) was not significantly different (p greater than 0.05, Mann-Whitney U test). There was a nonsignificant trend for the Kd of patients (1.25 +/- 0.67 nM) to be higher than that of controls (0.96 +/- 0.32 nM). The results do not support an adrenergic abnormality in panic patients.

Adolescent↗
PubMed1987

The dexamethasone suppression test in panic disorder.

The dexamethasone suppression test (DST) was performed in 35 patients with panic disorder and 21 normal control subjects. Non-suppression of plasma cortisol was determined as 4 micrograms/dl and using this figure 29% of panic patients and 9.5% of controls were non-suppressors. There was no significant difference in the number of suppressors and non-suppressors between patient and control groups (chi 2 = 1.81; P greater than 0.05). Both pre- and postdexamethasone cortisol concentrations were significantly different between the two groups possible indicating a cortisol hypersecretion in some panic patients.

Adolescent↗
PubMed1987

Melatonin rhythm in human plasma and saliva.

Human plasma and saliva were collected at frequent intervals throughout the night and after a nocturnal challenge by exposure to 3,000 lx of light for 1 h in the middle of the night. Melatonin, as measured by radioimmunoassay, was found to correlate highly in plasma and saliva, described by a linear regression equation: y = 55x-2.6 (r = 0.90). The nocturnal melatonin rhythm in saliva was parallel to that observed in plasma. A good correlation was also observed between plasma and salivary melatonin on exposure to light. Melatonin in both fluids showed a significant fall during light exposure. Levels returned to normal nocturnal values within 2 h after returning to darkness. These results indicate that salivary melatonin, although lower than plasma melatonin, may be used as an index of pineal gland release of melatonin. It is suggested that saliva may be useful as a non-invasive technique for obtaining data on melatonin profiles, especially in pilot-test and screening situations.

Adult↗
PubMed1986

Possible melatonin involvement in the hypotensive effect of MAO inhibitors.

Effect of selective inhibitors of MAO-A and B isoenzymes on pineal melatonin (and related indoles), arterial blood pressure and brain MAO-A and B activities has been evaluated in intact, pinealectomized and sham-operated rats. Selective inhibition of MAO-A but not MAO-B activity stimulated pineal melatonin synthesis and decreased arterial blood pressure in intact and sham-operated animals. Pinealectomy attenuated the hypotensive effect of MAO-A inhibition. The possible melatonin contribution to both antidepressive and hypotensive effects of MAO inhibitors is discussed.

Animals↗
PubMed1986

Plasma melatonin concentrations in depression.

The pineal hormone melatonin was measured in midnight plasma samples from 11 depressed patients and 18 control subjects. Plasma melatonin concentrations were significantly lower in the depressed patients. The implication of these findings for beta-adrenoceptor subsensitivity in depression is discussed.

Depressive Disorder↗
PubMed1985

Stress-induced synthesis of melatonin: possible involvement of the endogenous monoamine oxidase inhibitor (tribulin).

Cold-restrained stress increased rat pineal melatonin and N-acetylserotonin content. This effect was partially prevented by lorazepam. Serotonergic turnover (ratio of 5-hydroxyindole acetic acid to serotonin) was significantly decreased in stressed but not in stressed rats pretreated with lorazepam, suggesting stress-induced inhibition of monoamine oxidase (MAO). Literature data indicate that the same type of stress increases the production of the endogenous MAO inhibitor. The implication of stress-induced MAO inhibition on melatonin synthesis in anxiety and drug withdrawal is discussed.

Animals↗
PubMed1985

Selective inhibition of MAO-A but not MAO-B activity increases rat pineal melatonin.

Clorgyline, a selective MAO-A inhibitor, increased (5 times) rat pineal melatonin and N-acetyl-serotonin (NAS) content, and decreased 5-HIAA level by 80%. Deprenyl, a selective MAO-B inhibitor, did not change melatonin or other pineal indoles content. The data obtained show that inhibition of MAO-A but not B enzyme is responsible for pineal melatonin increase caused by MAO inhibitors. It is suggested that the stimulation of melatonin synthesis caused by MAO inhibitors may contribute to their antidepressive effect.

Animals↗