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Biomedical subjects

S Schanberg

Publications and source records attributed to S Schanberg.

27 records · Page 2Linked to original sources

Intrahepatic glucose: a requirement for neonatal ODC induction by specific hormones.

We have shown previously that short-term nutritional deprivation causes a tissue-specific loss of liver ornithine decarboxylase (ODC) induction after isoproterenol, phenylephrine, or glucagon administration in rat pups. To examine the role of nutrition in the regulation of hepatic ODC, we tested the ability of intragastric nutrient administration to reverse nutritionally related deficits in the ODC response to hormonal challenge. Intragastric whole milk was effective in restoring ODC induction and accumulation of its immediate product, putrescine, in response to isoproterenol administration. Glucose was shown to mediate this effect by the ability of intragastric skimmed milk, lactose, galactose, or D-glucose to return ODC induction, and the inability of casein, sucrose, fructose, L-glucose, or pyruvate plus lactate to do so. D-Glucose also reestablished ODC induction by phenylephrine and glucagon. Parenteral administration of D-glucose produced results comparable to those obtained after intragastric administration. Isoproterenol induction of ODC was prevented when hepatic glucose uptake was blocked by phlorizin but not by blockade of central nervous system glucose uptake with 2-deoxyglucose. We conclude that intrahepatic glucose is an absolute requirement for hepatic ODC induction by isoproterenol, phenylephrine, or glucagon in preweanling rats.

Animals↗

Neuroendocrine response to cold in Raynaud's syndrome.

Eleven patients with Raynaud's syndrome accompanied by monospecific IgG ANA, nine patients with Raynaud's syndrome in the absence of ANA, and nine normal volunteers were exposed to an ambient cold challenge during which time venous blood was continuously sampled. ANA negative patients were shown to have significantly higher levels of cortisol during a cold challenge than either ANA positive patients or normal controls, and exhibited significantly lower levels of plasma norepinephrine compared with normal controls. ANA positive patients did not differ significantly from normals in their neuroendocrine response to cold. It is suggested that the high plasma cortisol found in Raynaud's syndrome in the absence of ANA may be responsible for the vasospasticity in this group of patients.

Antibodies, Antinuclear↗

Involvement of alpha noradrenergic receptors in mediation of brain polyphosphoinositides metabolism in vivo.

The acute effects of norepinephrine (NE) on polyphosphoinositide (PPI) metabolism were examined in regions of rat brain in vivo with the techniques of intracisternal injection and microwave irradiation fixation. NE (80 nmol/g of brain) increased PPI incorporation of both [32P] orthophosphate and [3H] inositol by 50 to 100% within 5 min of the simultaneous intracisternal administration of both drug and radiolabel. These effects of NE were more pronounced in the brainstem and cerebellum than in the cerebral cortex, and were greater for triphosphoinositide than for diphosphoinositide. The increases were blocked by phentolamine and phenoxybenzamine but not by propranolol or atropine, suggesting that alpha noradrenergic receptors mediated the effect. Similar metabolic responses were observed with PPI precursors, phosphatidic acid and monophosphoinositide. However, no other phospholipid was altered in response to the agents administered in these studies (data not shown). Increased incorporation of radiolabels into PPI was never accompanied by detectable increases in endogenous PPI concentrations, suggesting that head group turnover was stimulated rather than whole molecule synthesis. Also, the increase in PPI phosphate radiolabel incorporation was not due to NE effects on the specific activity of phosphate donor precursors (nucleotides). The present data suggest that the PPI may be involved in the membrane processes that result from stimulation of alpha noradrenergic receptors in brain.

Animals↗

Platelet monoamine oxidase and serum dopamine-beta-hydroxylase activity in chronic alcoholics.

Previous independent reports suggest that low platelet monoamine oxidase (MAO) activity and high serum dopamine-beta-hydroxylase (DBH) activity may be associated with alcoholism or vulnerability toward alcoholism. However, there are also contradictory reports in the literature with regard to each of these two enzymes. We measured both platelet MAO and serum DBH activity in alcoholics followed up at periodic intervals for 12 months after hospitalization for acute alcoholism. Platelet MAO activity in the alcoholics was significantly lower compared to that of nonpsychiatric controls throughout the 12-month period, whereas serum DBH activity in the alcoholics was essentially the same as control values. Thus, low platelet MAO activity, previously reported in a spectrum of clinical psychiatric disorders, appears to be a relatively stable phenomenon in chronic alcoholics irrespective of acute intoxication or pathophysiological factors associated with acute decompensation in individuals vulnerable to alcoholism.

Acute Disease↗

Serum dopamine-beta-hydroxylase in chronic alcoholism.

Previous reports suggest that high serum dopamine-beta-hydroxylase (DBH) activity may be associated with vulnerability to alcoholism. However, there are also contradictory studies in the literature. Therefore we measured serum DBH in chronic alcoholics followed for 12 months in a treatment programme after psychiatric hospitalization for acute alcoholism. Mean serum DBH activity in the alcoholics was unchanged from controls at 3 months, 6 months and 12 months following hospital discharge. These data imply that serum DBH activity does not provide a useful metabolic screen for vulnerability to chronic alcoholism. However, prospective studies of patients at high risk to develop alcoholism will be helpful in further clarification of this issue.

Adult↗

Burn injuries benefit from massage therapy.

Twenty-eight adult patients with burns were randomly assigned before debridement to either a massage therapy group or a standard treatment control group. State anxiety and cortisol levels decreased, and behavior ratings of state, activity, vocalizations, and anxiety improved after the massage therapy sessions on the first and last days of treatment. Longer-term effects were also significantly better for the massage therapy group including decreases in depression and anger, and decreased pain on the McGill Pain Questionnaire, Present Pain Intensity scale, and Visual Analogue Scale. Although the underlying mechanisms are not known, these data suggest that debridement sessions were less painful after the massage therapy sessions due to a reduction in anxiety, and that the clinical course was probably enhanced as the result of a reduction in pain, anger, and depression.

Adult↗

The relationship between hostility and beta-adrenergic receptor physiology in health young males.

OBJECTIVE: We examined the relationship between hostility and mononuclear leukocyte (MNL) beta-adrenergic receptor function in a sample of young healthy males. METHOD: Thirty subjects were selected for having scored above 20 (N = 11) and below 14 (N = 19) on the Cook-Medley Hostility (Ho) scale. MNL beta-adrenergic receptor function was characterized in terms of receptor density (Bmax) and ligand-binding affinity (Kd) in homogenized cells, and intracellular cyclic adenosine monophosphate (cAMP) responses to saline, isoproterenol, and forskolin in whole cells. Subjects also completed the Multidimensional Anger Inventory (MAI), which assesses dimensions of anger. RESULTS: Relative to men with low Ho scores, men with Ho scores above 20 showed lower receptor number and greater forskolin-stimulated cAMP. Moreover, high hostile men reported a greater frequency of anger, longer duration of anger, more frequent brooding, and a hostile outlook. CONCLUSIONS: These data indicate that adrenergic receptor down-regulation is associated with hostility. This association may be linked to hostile persons' propensity for excessive and prolonged neuroendocrine responses to either psychological stressors or the experience of chronic stress associated with frequent and prolonged bouts of anger.

Adolescent↗