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Biomedical subjects

H C Stancer

Publications and source records attributed to H C Stancer.

At least 55 records · Page 3Linked to original sources
PubMed1977

The effect of a peripheral decarboxylase inhibitor (carbidopa) on monoamine and neuroendocrine function in man.

Carbidopa, a selective extracerebral decarboxylase inhibitor, was given to 10 normal volunteers to determine its effects on endogenous catecholamine, indoleamine, and endocrine function. Tryptamine, which is largely extracerebral in origin, was inhibited markedly (80 percent) by the carbidopa; 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenolglycol (MHPG) excretion also were inhibited by the drug but not to the same degree as tryptamine. These differential results may be due partly to the higher central nervous system origin of the 5-HIAA and MHPG but also to a peripheral "stores" effect. In addition, carbidopa resulted in significant increases in plasma prolactin and a small but significant decrease in plasma glucagon.

Adult↗
PubMed1976

Total and free plasma tryptophan levels in patients with affective disorders: effects of a peripheral decarboxylase inhibitor.

Previous reports of decreased cerebrospinal fluid tryptophan levels and decreased free plasma tryptophan levels, as well as a reduction in the volume of distribution of tryptophan, suggest that alterations in the disposition of plasma tryptophan may occur in depressives. We examined the disposition of plasma tryptophan in ten normal controls and ten depressed patients. These measures were made on two drug-free baseline days and on two days when the subjects had been receiving the peripheral decarboxylase inhibitor, carbidopa, which inhibits tryptophan metabolism via extracerebral indoleamine pathways.

Adolescent↗
PubMed1976

Urinary cyclic AMP in relation to lithium treatment in manic-depressive illness.

Urnary cyclic AMP was measured longitudinally in six patients with bipolar affective disorder. The values varied from 3.55 to 19.0 mugmol/24 hours with considerable variation between subjects. Three of these patients improved with administration of lithium carbonate. This improvement was not correlated with a change in cyclic AMP excretion. Five normal male volunteers were studied over a 5-day period. The urinary excretion for this group showed the same large intersubject variability but smaller intrasubject variation as was found for the patient group. It is suggested that erroneous results may be obtained for urinary cyclic AMP excretion if mean group values are used from patients not studied longitudinally.

Adult↗
PubMed1976

Gonadal effects of pinealectomy and immunization against N-acetylindolealkylamines in the hamster.

In order to determine whether circulating melatonin (MEL) is necessary for the gonadal regression seen in hamsters exposed to a short photoperiod, animals were immunized with N-acetylserotonin (NAS) conjugated to protein. Antibodies formed against this conjugate bind MEL and NAS equally. When exposed to a short photoperiod (L:D, 1:23), a dramatic regression was seen in gonadal weight with no effect on body, Harderian gland or adrenal weight. Plasma testosterone levels also dropped. Immunization against NAS did not modify these effects, suggesting that circulating MEL does not mediate the antigonadal effect of the short photoperiod.

Animals↗
PubMed1976

Effect of carbidopa on prolactin, growth hormone and cortisol secretion in man.

Serum prolactin, growth hormone and cortisol levels were examined in normal volunteers following administration of carbidopa, a peripheral decarboxylase inhibitor. 24-hour urinary tryptamine levels dropped markedly indicating that inhibition of decarboxylase was effective. Prolactin levels rose while growth hormone and cortisol remained unchanged. Since the tuberoinfundibular dopamine nerve terminals lie outside the blood brain barrier, this study suggests that these neurons are involved in prolactin but not in growth hormone or cortisol regulation. Findings are compatible with two alternate hypotheses--either that dopamine is a physiologic prolactin inhibiting factor (PIF) or that tuberoinfundibular dopamine neurons regulate the release of PIF.

Adult↗
PubMed1976

Brain and peripheral metabolism of 5-hydroxytryptophan-14C following peripheral decarboxylase inhibition.

Following selective peripheral decarboxylase inhibition, a greater fraction of peripherally measured monoamine metabolites should derive from central nervous system monoamine metabolism. In rats pretreated with the peripheral decarboxylase inhibitor L-alpha-(3,4-dihydroxybenzyl)-alpha-hydrazinopropionic acid (MK-486) (50 mg/kg i.p. or i.v.), the peripheral formation of 5-hydroxytryptamine-14C (5-HT-14C) from the precursor DL-5-hydroxytryptophan-14C (5-HTP-14C) was reduced by 82 to 100% over a 4-hour interval. There was a marked increase in the penetration of 5-HTP-14C into brain and in the appearance in brain of 5-HT-14C and 5-hydroxyindoleacetic acid-14C (5-HIAA-14C). The cerebral metabolism of 5-HTP-14C in vehicle-pretreated animals appeared to occur mainly in the brain vascular compartment. Following MK-486 pretreatment, the in vivo metabolism of 14C-5-hydroxyindoles in the extracerebral compartment obeys linear kinetics as does the uptake and decarboxylation of 5-HTP-14C in brains. The cerebral turnover of 5-HT-14C appeared to increase as a function of the dose of 5-HTP injected. This phenomenon may be a result of either saturation of brain 5-HT storage sites or nonspecific metabolism of 5-HTP in brain catecholamine neurons. A highly signigificant correlation was found between the brain and blood 5-HIAA-14C levels following MK-486. The adrenal formation of 5-HT, which was not inhibited by MK-486, did not appear to contribute significantly to the blood 5-HIAA-14c levels. These results suggest the possibility that following peripheral decarboxylase inhibition a larger fraction of peripherally measured 5-HIAA may derive from central nervous system 5-HT metabolism.

5-Hydroxytryptophan↗
PubMed1975

Hypothalamic-pituitary function in anorexia nervosa.

We studied nine patients with anorexia nervosa: five were "undernourished" and four were "well-nourished". The undernourished patients had significantly higher plasma growth hormone (GH) levels in a fasting state and higher GH rebounds following glucose administration. In four of these patients, GH levels decreased to normal after weight restoration. Decreased urinary follicle stimulating hormone (FSH) in three and plasma luteinizing hormone in six patients were not related to nutritional status; however, positive correlation was found between duration of illness and urinary FSH. Other results included decreased plasma testosterone in the one male, elevated plasma cortisol in five, and decreased 17-ketosteroid excretion in five patients. The results support elevated GH as secondary to starvation of anorexia nervosa and not an independent hypothalamic-pituitary disturbance. Other endocrine findings indicate hypothalamic-pituitary malfunction is not confined to GH.

Adolescent↗
PubMed1975

The origin of blood k-hydroxyindoleacetic acid following L-hydrazino-alpha-methyldopa (MK-486).

Blood 5-HIAA-14C levels derived from exogenous D,L-5-HTP-14C were investigated in normal, sham-operated and nephrectomized rats pretreated with MK-486 and probenecid (200 mg/kg i.p.). Blood 5-HIAA-14C levels decreased in nephrectomized rats following probenecid. Peripheral decarboxylase inhibition by MK-486 was enhanced by both probenecid and nephrectomy. Increased penetration of 5-HTP into brain occurred following probenecid. The results indicate that following MK-486 about 20% of the blood 5-HIAA-14C derived from 5-HTP-14C in rats originates in the CNS.

5-Hydroxytryptophan↗
PubMed1975

The origin of blood 5-hydroxyindoleacetic acid following L-hydrazine-alpha-methyldopa (MK-486).

Blood 5-HIAA-14C levels derived from exogenous D,L-5-HTP-14C were investigated in normal, sham-operated and nephrectomized rats pretreated with MK-486 and probenecid (200 mg/kg i.p.). Blood 5-HIAA-14C levels decreased in nephrectomized rats following probenecid. Peripheral decarboxylase inhibition by MK-486 was enhanced by both probenecid and nephrectomy. Increased penetration of 5-HTP into brain occurred following probenecid. Thr results indicate that the following MK-486 about 20% of the blood 5-HIAA-14C derived from 5-HTP-14C in rats originates in the CNS.

5-Hydroxytryptophan↗