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Biomedical subjects

C R Lake

Publications and source records attributed to C R Lake.

At least 109 records · Page 6Linked to original sources
PubMed1982

High plasma norepinephrine levels in patients with major affective disorder.

The authors found that patients with major affective disorder had higher levels of plasma norepinephrine and higher pulse rates (tachycardia) than healthy control subjects, but their blood pressures were normal. These measurements were similar in all three subgroups of patients with affective disorder--manic, bipolar depressed, and unipolar. Because norepinephrine is the primary neurotransmitter of the sympathetic nervous system, these data suggest sympathetic hyperactivity in the major affective disorders. This conclusion is compatible with recent speculation based on the effect of antidepressants on noradrenergic receptors and a failure of alpha-receptors to downregulate normally in patients with major affective disorder.

Adult↗
PubMed1982

Increased cerebrospinal fluid norepinephrine in essential hypertension.

Studies in man and animals suggest increased central noradrenergic activity in hypertension. We can now measure norepinephrine (NE) in cerebrospinal fluid (CSF) accurately and this should provide an index of central noradrenergic activity. NE in CSF is very labile and altered by anxiety, stress, drugs, sodium balance and other factors. When these factors are controlled, NE in CSF appears elevated in essential hypertensives, particularly among young patients. Neurologic diseases that alter NE in CSF cause parallel alterations in blood pressure. Increased central noradrenergic activity is reflected in CSF NE levels and may cause some forms of hypertension.

Age Factors↗
PubMed1982

Segregation and linkage studies of plasma dopamine-beta-hydroxylase (DBH), erythrocyte catechol-O-methyltransferase (COMT), and platelet monoamine oxidase (MAO): possible linkage between the ABO locus and a gene controlling DBH activity.

Measurements of dopamine-beta-hydroxylase (DBH), catechol-O-methyltransferase (COMT), and monoamine oxidase (MAO) along with 27 polymorphic marker phenotypes were available for 162 patients with major affective disorders and 1,125 of their relatives. Levels of enzymes were previously found not to be associated with illness. Pedigree analysis methods for quantitative traits are used to test single-gene hypotheses for segregation of DBH in 32 families with 411 individuals. COMT in 30 families with 351 individuals, and MAO in 50 families with 309 individuals. The familial distribution of both DBH and COMT are consistent with two codominant alleles at the same locus that account for 56% and 59% of the total variance, respectively. MAO activity cannot be shown to be segregating as a single major gene, but a purely nongenetic hypothesis is also rejected. A possible linkage of a locus for DBH to the ABO locus is indicated by a maximum lod score of 1.82 at 0% and 10% recombination fractions for males and females, respectively. A lod score of 0.61 at 0% recombination for a similar analysis in a single large pedigree was reported by Elston et al., making the combined lod score for the two studies equal to 2.32 at 0% recombination.

Adult↗
PubMed1982

Hypokalemia stimulates plasma epinephrine and norepinephrine in the rat.

We examined the effect of dietary potassium depletion on plasma and urinary catecholamines in the rat. Ingestion of a potassium deficient diet for 45 days increased plasma norepinephrine by 80% and plasma epinephrine by 270%. Urinary excretion of epinephrine, norepinephrine and dopamine were not significantly affected by hypokalemia. The results suggest that the increase in plasma catecholamines may be mediated "reflexly" by an accompanying increase in vasodilator agents or may represent a direct "stress" effect of hypokalemia on the release of epinephrine and norepinephrine.

Animals↗
PubMed1981

Essential hypertension: central and peripheral norepinephrine.

The concentration of norepinephrine in cerebrospinal fluid from patients with essential hypertension is higher than that from healthy normal volunteers, but the concentrations of norepinephrine in plasma from these groups are similar. This finding indicates that central nervous system noradrenergic hyperactivity occurs in essential hypertension but apparently is not reflected in abnormal function of the peripheral sympathetic nervous system in these patients.

Adult↗
PubMed1981

CSF levels of norepinephrine during alcohol withdrawal.

Cerebrospinal fluid norepinephrine (NE) levels were determined by radioenzymatic assay in 21 patients with a variety of neurological diseases and 49 patients in acute alcohol withdrawal. A second determination was made in 19 patients who had recovered from the alcohol withdrawal syndrome. Cerebrospinal fluid NE concentration was higher in the patients during alcohol withdrawal (192.3 plus or minus 22.3 pg/mL) and decreased during recovery to 137.8 plus or minus 15.9 pg/mL. The CSF NE level was higher in both groups than in patients with other neurological disorders. This may help explain the adrenergic signs observed during alcohol withdrawal.

Adult↗
PubMed1981

Tyramine infusions and selective monoamine oxidase inhibitor treatment. II. Interrelationships among pressor sensitivity changes, platelet MAO inhibition, and plasma MHPG reduction.

The relationship between changes in IV tyramine pressor sensitivity accompanying selective monoamine oxidase (MAO) inhibitor treatment and estimates of MAO-A and MAO-B inhibition in vivo were studied. Reductions in platelet MAO activity provided an index of MAO-B inhibition, while changes in plasma 3-methoxy-4-hydroxyphenethylene glycol (MHPG) were used as an hypothesized reflection of MAO-A inhibition. Chronic treatment with the MAO-A inhibitor clorgyline and the MAO-B inhibitor pargyline showed significant inhibition of the alternate MAO enzyme as well, although this crossover effect was greater for pargyline than clorgyline. The MAO-B inhibitor deprenyl appeared to maintain the greatest degree of MAO inhibition selectivity in vivo. Tyramine pressor sensitivity changes accompanying administration of the MAO inhibitors were highly correlated with decreases in plasma MHPG (r = 0.92), supporting our previous data indicating the rank order of clorgyline greater than pargyline greater than deprenyl for enhancement of tyramine pressor sensitivity and, thus, suggesting that tyramine potentiation is primarily a function of MAO-A rather than MAO-B inhibition. Changes in plasma MHPG are suggested to provide a potentially useful clinical index of in vivo MAO-A inhibition.

Blood Platelets↗
PubMed1981

The hyperactive child syndrome: peripheral sympathetic nervous system function and the effect of d-amphetamine.

We evaluated sympathetic nervous system function in medication-free hyperactive children by measuring plasma levels of norepinephrine (NE) and dopamine-beta-hydroxylase and then comparing the effects of two therapeutics doses of d-amphetamine to placebo in these patients. The medication-free hyperactive patients and controls had similar plasma NE levels and blood pressures while recumbent, and a similar increase in NE on standing, but the patients had a larger pressor response on standing. In the hyperactive patients d-amphetamine significantly increased blood pressure, pulse rate, and NE levels. The change in NE levels correlated with the change in amphetamine levels. The medication-free patients, when more anxious, had higher plasma NE levels.

Attention Deficit Disorder with Hyperactivity↗
PubMed1981

Mania associated with LSD ingestion.

The authors report a patient who suffered a full-blown manic attack after ingesting LSD or an LSD analogue. The patient experienced acute symptoms of LSD intoxication, which resolved but were followed in about 3 weeks by a typical manic episode of psychotic magnitude. The mania cleared with lithium therapy.

Adult↗
PubMed1981

The effect of pimozide on CSF norepinephrine in schizophrenia.

The authors measured CSF norepinephrine concentrations in drug-free schizophrenic patients with and without probenecid administration and in drug-free normal control subjects. Schizophrenic patients had significantly higher baseline norepinephrine values. The dopamine metabolite homovanillic acid correlated significantly with norepinephrine. During chronic treatment with the neuroleptic pimozide, patients' norepinephrine levels were significantly decreased. The pimozide-induced decrease in norepinephrine, as well as the percent decrease, correlated significantly with the patients' decrease in global psychosis. These data are consistent with recent reports of elevated concentrations of norepinephrine in specific brain areas of schizophrenic patients, and they support a role for norepinephrine metabolism in the pharmacological effects of antipsychotic drugs.

Adolescent↗
PubMed1981

Deprenyl in Parkinson disease.

(-)Deprenyl, a specific monoamine oxidase subtype B inhibitor (MAOI-B), has been reported to be a safe and valuable adjunct to conventional treatment of parkinsonism. A double-blind, clinical comparison of (-)deprenyl with placebo was undertaken in 11 parkinsonian patients; the efficacy of 10 mg daily was studied over 4 weeks. In four cases the clinical score for parkinsonian deficits improved during deprenyl therapy, and in five it deteriorated; there was no change in one patient. Two subjects failed to complete the study. (-)Deprenyl induced euphoria and insomnia. It was concluded that any advantages deriving from the use of (-)deprenyl in parkinsonism are limited, and probably dominated by its elevation of mood. Biochemical analysis failed to reveal any significant increase in platelet or plasma catecholamine concentrations during deprenyl therapy. There was, however, a significant decrease in plasma epinephrine (p < 0.05) and platelet MAO activity (p < 0.005).

Adult↗
PubMed1981

Adrenocortical function and plasma norepinephrine in normal human subjects.

Abnormal adrenocortical regulation has been reported in patients with endogenous depression, including excessive cortisol production with loss of circadian periodicity and decreased suppression by dexamethasone. The inhibitory effect of the neurotransmitter norepinephrine (NE) on the hypothalamic-pituitary adrenal (HPA) axis through the regulation of corticotropin-releasing factor has been suggested by animal in vitro studies. In this study of six normal human subjects we have examined the relationship of basal cortisol activity and its sensitivity to dexamethasone suppression, measured by 24-hr urinary free cortisol, with basal noradrenergic activity, diurnal variation, and response to postural stimulation, measured by plasma NE. Base-line cortisol and the degree of dexamethasone suppression were significantly inversely correlated with all base-line measures of NE response to stimulation. NE response to stimulation on the morning after dexamethasone was also inversely correlated with the degree of cortisol suppression. The increase in the morning NE response to stimulation after dexamethasone was inversely correlated with both base-line and suppressed cortisol levels. There is significant diurnal variation in stimulated NE activity after dexamethasone. There results are consistent with an inhibitory role for NE in the regulation of HPA system and a reciprocal effect for cortisol on noradrenergic activity. The implication of this relationship for the understanding of adrenocortical regulation in depression is discussed.

Adult↗
PubMed1980

Schizophrenia: elevated cerebrospinal fluid norepinephrine.

Concentrations of norepinephrine in cerebrospinal fluid are higher in schizophrenic patients, particularly in those with paranoid features, than in normal volunteer subjects of the same age. This observation supports recent reports of elevated concentrations of norepinephrine in specific brain areas adjacent to the cerebral ventricles of paranoid schizophrenic patients. Overflow of the amine from periventricular regions into the cerebrospinal fluid may reflect abnormally high release or diminished enzymatic destruction of norepinephrine in patients with schizophrenia.

Adult↗