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Biomedical subjects

O G Cameron

Publications and source records attributed to O G Cameron.

At least 19 recordsLinked to original sources
PubMed1993

Differences between smokers and never-smokers in sensitivity to nicotine: a preliminary report.

Sensitivity to nicotine was explored using test doses administered via intra-nasal aerosol in 10 smokers and 10 never-smokers. Smokers received 1.50 mg nicotine (in 2 sprays, < 5 seconds apart, one spray per nostril); never-smokers received either 0.50 mg (n = 3) or 0.25 mg (n = 7) nicotine. Accumulation of nicotine in plasma, per unit dose administered, was nearly four times greater in never-smokers than in smokers, indicating differences in pharmacokinetic tolerance. To examine sensitivity to nicotine without this confound, peak physiological reactivity (heart rate and blood pressure changes) was divided by peak plasma nicotine increment and the ratio was expressed as a function of cotinine level prior to dosing, thereby relating sensitivity to nicotine to history of exposure. In smokers, functional sensitivity to nicotine was inversely related to customary nicotine intake, replicating previous findings for light and heavy smokers. The observation that never-smokers were not much more sensitive to nicotine than light smokers is notable given the disparity in previous history of exposure.

Administration, Intranasal↗
PubMed1992

Endocrine, cardiovascular, and behavioral responses to clonidine in patients with panic disorder.

We examined adrenergic regulation in patients with panic disorder by challenging 10 patients and 14 age-matched and sex-matched controls with intravenous infusions of clonidine hydrochloride (2 micrograms/kg), an alpha 2-adrenoreceptor agonist. Growth hormone, 3-methoxy-4-hydroxyphenylglycol (MHPG), blood pressure, heart rate, and behavioral (anxiety, sedation) responses were monitored. The data replicated the previously reported finding of blunted growth hormone (GH) responses to clonidine in patients with panic disorder. Reported abnormalities in MHPG, cardiovascular, and behavioral responses of panic patients to clonidine infusion were not replicated. The robustly blunted GH response to clonidine in panic patients supports the adrenergic dysregulation hypothesis of panic disorder, but alternative interpretations of this finding are available and further study is needed.

Adrenergic Fibers↗
PubMed1992

The effects of menstrual phase and nicotine abstinence on nicotine intake and on biochemical and subjective measures in women smokers: a preliminary report.

Nicotine intake, menstrual and smoking withdrawal symptomatology, and baseline cortisol and MHPG were assessed in nine women smokers under conditions of ad lib smoking and overnight abstinence in three menstrual phases (early follicular, mid-to-late follicular, and late luteal). A trend towards higher nicotine intake (p < 0.10) was observed in the mid-to-late follicular phase. Although menstrual symptomatology was not significantly elevated during the smoking abstinence condition overall, abstinence appeared to prevent the normal reduction in symptomatology during the mid-to-late follicular phase that occurred under conditions of ad lib smoking. Menstrual and withdrawal symptoms were highly correlated, and both were most pronounced during the late luteal/abstinence condition. The smoking-specific item "craving" reflected this pattern, though in attenuated form, suggesting that the observed exacerbation of withdrawal symptomatology was not simply due to generalized dysphoria, as queried in both instruments. MHPG was significantly elevated in the late luteal phase, whereas cortisol was significantly higher during ad lib smoking than during abstinence and tended to be highest in the mid-to-late follicular phase. Further investigation will be needed to determine the functional significance of these findings for understanding and treating smoking in women.

Adult↗
PubMed1991

Blunted growth hormone response to clonidine in patients with generalized anxiety disorder.

Patients with panic disorder or depression have abnormal responses to the alpha 2-adrenergic receptor partial agonist clonidine. Evidence linking anxiety to noradrenergic dysfunction and the presence of anxiety symptoms in both depression and panic suggest that abnormal responses to clonidine in these disorders could be due to the anxiety symptoms. To explore a possible link between "nonspecific" anxiety symptoms and abnormal responses to clonidine, patients with DSM-III-defined generalized anxiety disorder were given intravenous infusions of clonidine hydrochloride. Responses of plasma growth hormone, 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, and psychological states were determined in 11 patients with generalized anxiety disorder and 14 healthy subjects. Clonidine produced significantly smaller growth hormone responses in patients than in healthy controls. The two groups did not differ in 3-methoxy-4-hydroxyphenylglycol, heart rate, blood pressure, or psychological responses to clonidine. These results are compared with data from similar studies on patients with panic disorder and depression. The blunting of the growth hormone response to clonidine in all three disorders could be due to the presence of generalized anxiety symptoms. Subsensitivity of postsynaptic alpha 2-adrenoreceptors may be present in all three disorders; however, there are alternative interpretations of growth hormone blunting in response to clonidine. Blunting was observed in DSM-III-defined generalized anxiety disorder, whether or not the DSM-III-R criterion of excessive worry was also present.

Adult↗
PubMed1990

Adrenergic status in anxiety disorders: platelet alpha 2-adrenergic receptor binding, blood pressure, pulse, and plasma catecholamines in panic and generalized anxiety disorder patients and in normal subjects.

In order to evaluate adrenergic function in anxiety disorders, platelet alpha 2-adrenergic binding parameters and supine and standing blood pressure, pulse, and venous plasma epinephrine and norepinephrine were determined in patients with panic attacks or generalized anxiety disorder and in normal subjects. The maximum number of binding sites (Bmax) for the partial agonist tritiated clonidine was significantly lower for both patient groups than for normal subjects, and the Bmax for the antagonist tritiated yohimbine was significantly lower for panic patients. There were no other substantive differences across groups. Prior exposure to psychotropic drugs might account for the results for clonidine binding, but not for yohimbine. The Bmax for clonidine was correlated with norepinephrine increases upon standing and, for panic patients, with the severity of full unexpected panic attacks. These data provide further evidence of adrenergic receptor abnormalities in people with anxiety disorders.

Adult↗
PubMed1990

Alpha 2-adrenoreceptor status in obsessive-compulsive disorder.

Ten patients with obsessive-compulsive disorder (OCD) and 13 normal control subjects received intravenous infusions of 2 X 10(-6) g/kg of clonidine and normal saline on separate days. Responses to the drug relating to plasma growth hormone (GH), 3-methoxy-4-hydroxyphenylglycol (MHPG), heart rate, blood pressure, and several symptoms were determined. Additionally, platelet alpha 2-adrenoreceptor binding was measured in most of the subjects. GH, MHPG, blood pressure, and heart rate responses to clonidine did not differ between groups. As expected, patients reported more symptoms than normal subjects, and clonidine was sedating for both groups. Patients did not differ from normal subjects in the symptom response to clonidine. The maximum number of binding sites (Bmax) for tritiated clonidine was significantly greater in OCD patients than in normals. This pattern of alpha 2-adrenoreceptor status is different than the patterns in major depression and panic anxiety.

Adult↗
PubMed1990

Caffeine and human cerebral blood flow: a positron emission tomography study.

Positron emission tomography (PET) was used to quantify the effect of caffeine on whole brain and regional cerebral blood flow (CBF) in humans. A mean dose of 250 mg of caffeine produced approximately a 30% decrease in whole brain CBF; regional differences in caffeine effect were not observed. Pre-caffeine CBF strongly influenced the magnitude of the caffeine-induced decrease. Caffeine decreased paCO2 and increased systolic blood pressure significantly; the change in paCO2 did not account for the change in CBF. Smaller increases in diastolic blood pressure, heart rate, plasma epinephrine and norepinephrine, and subjectively reported anxiety were also observed.

Administration, Oral↗
PubMed1990

Changes in sensory-cognitive input: effects on cerebral blood flow.

Eight healthy right-handed young men were subjected to local CBF measurement by [15O]water and positron emission tomography during partial sensory deprivation and during sensory-cognitive activation; physiological, hormonal, and subjective stress measurements were also performed. Results indicated that (a) "whole-brain" CBF increased during activation; (b) the greatest increase in CBF was in the primary visual cortex; (c) differences between hemispheres were not observed, but CBF was greater anteriorly than posteriorly in the deprivation condition only; (d) within-subject variability of CBF was not influenced by the sensory-cognitive condition; and (e) the procedure was not stressful.

Adult↗
PubMed1990

Aerobic physical training and alterations in pressor response during norepinephrine infusion: a controlled single-subject experiment.

To test the influence of aerobic physical training on pressor response to infused norepinephrine, the present study utilized a single subject A-B-A-B withdrawal design consisting of 9-week alternating sedentary and aerobic phases (S1, A1, S2, A2). During each 9-week phase the subject underwent infusions every 3 weeks, consisting of saline, low-dose and high-dose norepinephrine (Low-NE, High-NE). Heart rate and mean arterial blood pressure were monitored continuously; resting platelet and plasma catecholamines were also measured. Infusions were conducted 48 h from the most recent exercise bout to minimize residual effects of acute exercise. Fitness level was confirmed by VO2max during graded exercise testing at the conclusion of each 9-week phase. Blood pressure during saline did not differ between aerobic and sedentary phases. However, in all but one comparison, aerobic fitness was associated with a highly significant reduction in pressor response during Low-NE as well as High-NE. Plasma norepinephrine was higher during the two aerobic phases; platelet catecholamines and plasma epinephrine showed no reliable association with fitness. Results for this subject support an attenuation of pressor response associated with aerobic conditioning.

Adult↗
PubMed1990

Guidelines for diagnosis and treatment of depression in patients with medical illness.

Many medically ill people report depressed mood. Differentiating a true depressive syndrome from the expectable mood change due to the presence of the medical illness is problematic. The author describes criteria potentially useful in making this diagnostic differentiation and reviews predictors of treatment response in primary depression, with the implication that use of these criteria is clinically appropriate until more data on secondary depression are available. It is often necessary to formulate treatment for medically ill depressed patients on the basis of empirical observations, that is, to use a treatment trial for diagnostic as well as therapeutic purposes. In such treatment circumstances, it is imperative to use unambiguous criteria to define a therapeutic response and to stop or change treatment if these criteria are not met.

Depressive Disorder↗
PubMed1989

Simple phobia: evidence for heterogeneity.

Although simple phobia is a residual category in DSM-III, clinical experience suggests at least four subtypes of this group. To test the validity of the subtypes, the authors compared patients with one of four simple phobias subtypes (n: animal-insect = 25, blood-injury = 9, situational = 46, choking-vomit = 8). Significant sex differences were observed; all animal and insect phobics and seven of eight choking-vomit phobics were female, while the other two groups showed approximately equal numbers of males and females. Mean age of onset was significantly older for situational phobics than animal-insect or blood-injury phobics; choking-vomit probands were intermediate. Frequency of situational phobias differed significantly among relatives of the four proband groups, with highest frequency being found among situational probands. Thus, these clinical and epidemiological variables support the separation of simple phobia into at least these four diagnostic groups.

Adult↗
PubMed1989

Women and anxiety.

Some, but not all, of the DSM-III-R defined anxiety disorders are more frequent in women than in men; social phobia and obsessive-compulsive disorder are most equal in sex ratio. Clinical and community-epidemiologic samples tend to agree, and family studies indicate that the higher frequency of anxiety in women may represent one clinical presentation of a familial affective disorder/substance abuse-sociopathy "spectrum" disorder. Developmental studies suggest that gender differences relevant to the expression of anxiety symptoms may start quite early in life; psychodynamic theories would also tend to implicate early learning and experience. Women may be more responsive to life stresses, which might influence the occurrence of anxiety symptoms; however, the actual role and source of these stresses is not yet fully understood. Physiologic differences in brain structure between men and women are undoubtedly important in the gender differences in symptoms observed. Clinical management can be affected by these differences.

Anxiety Disorders↗
PubMed1989

Free 3-methoxy-4-hydroxyphenylglycol determined in plasma by liquid chromatography with coulometric detection.

We describe a simple "high-performance" liquid-chromatographic method for determining free 3-methoxy-4-hydroxyphenylglycol (MHPG) in plasma, with coulometric detection and with 4-methoxy-3-hydroxyphenylglycol (iso-MHPG) as the internal standard. MHPG and iso-MHPG are extracted from plasma into ethyl acetate and the extract is washed with a sodium bicarbonate solution, evaporated, reconstituted, and injected into a 25 x 0.4 cm column packed with 3-micron particles of C18 material. We used a mobile phase of acetate buffer (100 mmol/L, pH 5.0) and methanol (92:8 by vol) and an oxidation voltage of 0.5 V. The detection limit of the assay is 0.1 micrograms/L. The interassay CV for a sample with a mean MHPG concentration of 3.84 micrograms/L was 5.2%. The average absolute recovery for the method was 37%.

Adult↗