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I M McIntyre

Publications and source records attributed to I M McIntyre.

81 records · Page 5Linked to original sources

Platelet serotonin uptake in panic disorder.

Platelet serotonin uptake was measured in 45 patients (12 males, 33 females) with panic attacks and 21 controls (9 males, 12 females). Higher Vmax values were obtained in the patient group than in the controls (100.2 +/- 11.5 vs. 34.9 +/- 3.8 pmol/10(8) platelets/min; P less than 0.0005) while the affinity constant Km was not significantly different (2.28 +/- 0.3 vs. 1.71 +/- 0.18 microM). A value of Vmax in excess of 60 pmol/10(8) platelets/min was observed in 60% of patients and in only 5% of controls. The results point to a specific abnormality of platelet serotonin uptake in patients with panic attacks.

Adult↗

The pineal hormone melatonin in panic disorder.

The nocturnal synthesis of the pineal hormone melatonin was examined from 8 p.m. to midnight in 11 patients with panic disorder and eight control subjects. Patient concentrations of melatonin were significantly lower than controls at 10 p.m. (P less than 0.05; Kruskal-Wallis one-way ANOVA) and midnight (P less than 0.01). At 9 p.m. and 11 p.m., patient concentrations were also lower than controls, but were not statistically significantly different (P = 0.09). From these data, it is postulated that some patients with panic disorder exhibit a generalised defect in sensitivity of beta-adrenergic receptors or of sympathetic transmission.

Adult↗

Plasma immunoreactive beta-endorphin in dexamethasone suppressors and non-suppressors of cortisol.

Immunoreactive plasma beta-endorphin level was assayed in 33 patients with major affective disorder and in 16 psychiatrically normal controls before and after dexamethasone (1 mg) administration at 23.00 h. There were 18 cortisol suppressors and 15 non-suppressors among the patient group. All controls suppressed cortisol. Plasma beta-endorphin before dexamethasone was significantly different between suppressors, non-suppressors and controls (P less than 0.05, ANOVA). Concentrations of beta-endorphin were 4.7 +/- 0.7, 3.1 +/- 0.3 and 2.8 +/- 0.3 pmol/l for non-suppressors, suppressors and controls respectively. Following dexamethasone, beta-endorphin concentrations were again significantly different between groups (P less than 0.005, ANOVA). Concentrations were 4.6 +/- 0.7, 2.3 +/- 0.2 and 1.6 +/- 0.2 pmol/l for non-suppressors, suppressors and controls respectively. The implications of these findings are discussed.

Adrenocorticotropic Hormone↗

A kinetic analysis of platelet monoamine oxidase activity in patients with panic attacks.

A kinetic analysis of platelet monoamine oxidase (MAO) was performed in 22 patients with panic disorder and 14 normal controls, using tyramine as a substrate. Patients and controls did not differ significantly for either Km or Vmax, when same sex contrasts were carried out. The results do not support some studies that have shown elevated MAO activity in patients with panic attacks. The reasons for the discrepancies between previous studies and the present one are explored.

Adult↗

Platelet serotonin uptake and 3H-imipramine binding in panic disorder.

Platelet serotonin uptake and 3H-imipramine binding were measured in eight patients with panic disorders and nine controls. The Vmax of serotonin uptake was significantly elevated in patients compared to controls (77 +/- 14 vs. 50 +/- 4 pmol/10(8) platelets/min; P less than 0.05) while Km values were not different (1.46 +/- 0.41 vs. 1.24 +/- 0.20 microM). 3H-Imipramine binding to ruptured platelet membranes was not significantly different between patients and controls for either Bmax (395 +/- 71 vs. 412 +/- 107 fmol/mg protein) or Kd (0.90 +/- 0.18 vs. 1.09 +/- 0.30 nM). The implications for a serotonergic dysfunction in panic disorders are discussed.

Adult↗

Melatonin, cortisol and prolactin response to acute nocturnal light exposure in healthy volunteers.

An investigation of the cortisol and prolactin responses accompanying acute melatonin suppression by light (600 lux) in humans is described. Light given from midnight to 0300h suppressed nocturnal plasma melatonin concentrations by 65%. Despite this significant suppression of melatonin, no significant effect on plasma cortisol or prolactin concentrations was observed. These data support recent studies which argue that, if there is a relationship between melatonin, the hypothalamo-pituitary, and the hypothalamo-pituitary-adrenal axis in humans, it is neither direct nor simple.

Adult↗

Simultaneous HPLC gradient analysis of 15 benzodiazepines and selected metabolites in postmortem blood.

The simultaneous identification and quantitation of 15 benzodiazepines and selected metabolites in postmortem blood, serum, or liver homogenate is described. The assay involves extraction with diethylether, followed by an acid clean-up step of the ether. Chromatographic separation was achieved on a Nova-Pak phenyl 18 column using ultraviolet detection at 240 nm. A gradient HPLC system was developed to improve separation of nitro-reduction metabolites from the solvent front and endogenous peaks. The mobile phases consisted of a gradient from 15 to 28% acetonitrile in 40 mM potassium phosphate buffer. Within-run and day-to-day precision were generally 10-15%. The method described is sensitive and reproducible for the analysis of benzodiazepine concentrations in postmortem tissues.

Benzodiazepines↗

A class-independent drug screen in forensic toxicology using a photodiode array detector.

A class-independent drug screen, that is suitable for use in clinical and forensic toxicology and uses gradient-elution high-performance liquid chromatography and photodiode array detection, is presented. The assay is capable of detecting and identifying therapeutic and toxic amounts of barbiturates, anti-convulsants, diuretics, non-steroidal anti-inflammatory drugs, sulfonylurea anti-diabetic drugs, theophylline, and analgesic drugs. The assay has been successfully used to screen over 1000 postmortem blood specimens.

Chromatography, High Pressure Liquid↗

Simultaneous determination of morphine and codeine in blood and bile using dual ultraviolet and fluorescence high-performance liquid chromatography.

The separation and identification of morphine and codeine from postmortem blood and bile was accomplished using a liquid-phase extraction method followed by reversed-phase high-performance liquid chromatography with combined UV and fluorescence detection. Identification of morphine and codeine was based on relative retention time matching with calibration standards, together with their fluorescence-to-UV response ratios. Linear calibration curves for morphine and codeine ranged from 0.10 to 3.0 mg/L for blood and 5.0 to 100 mg/L for bile. Morphine concentrations (in autopsy cases), where the intravenous use of heroin or morphine was suspected as the cause of death, were 0.10-0.89 mg/L (mean, 0.29 mg/L) for blood and 3.3-112 mg/L (mean, 38 mg/L) for bile. Codeine concentrations, where therapeutic use or overdosage of codeine occurred, were 0.06-6.4 mg/L (mean, 1.5 mg/L) in blood and 0.22-89 mg/L (mean, 24 mg/L) in bile. This method allowed simultaneous detection of morphine and codeine from blood and bile with little interference from extraneous peaks. The procedure described provides a selective, sensitive, accurate, and reliable method suitable for both clinical and forensic toxicology.

Bile↗