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Biomedical subjects

B Sharp

Publications and source records attributed to B Sharp.

36 records · Page 2Linked to original sources
PubMed1982

beta-Endorphin immunoreactivity and acute behavioral distress in children with leukemia.

Endogenous opiates have been implicated in pain and stress experiences. In order to directly assess the relationship between endorphin activity and acute behavioral distress, beta-endorphin immunoreactivity (beta-EPI) was measured by radioimmunoassay in cerebrospinal fluid of 75 children with acute leukemia undergoing routine lumbar puncture. These data were related to four measures of behavioral distress collected during the procedure. For children 4 years of age and above, beta-EPI correlated inversely with age (r = -.31,p less than or equal to .05). All behavioral measures also inversely correlated with age (r = -.26 to -.67,p less than or equal to .05 to .001). Females had a significantly lower mean beta-EPI than males (p less than or equal to .01), and exhibited greater behavioral distress. beta-EPI and behavioral measures interacted with the use of specific antileukemia agents. L-Asparaginase was associated with lower beta-EPI (p less than or equal to .05), while prednisone was associated with lower behavioral distress on three of the four measures (p less than or equal to .05 to .01). After controlling for age, sex, and chemotherapy, beta-EPI and nurse ratings of anxiety were positively correlated (partial correlation coefficient = .31, p less than or equal to .05). Correlations between beta-EPI and other behavioral measures demonstrated positive trends. Results of this study are interpreted as support for the reactive nature of beta-EPI in cerebrospinal fluid to acute distress, and may help explain documented sex differences in distress behavior. Potential clinical implications and directions for further research are discussed.

Adolescent↗
PubMed1982

Dopamine regulates canine plasma beta-endorphin-immunoreactivity levels.

Intravenous administration of the dopamine antagonists domperidone and metoclopramide elevates canine plasma beta-endorphin immunoreactivity. Pretreatment with dopamine, but not dexamethasone, inhibits this effect. Sephadex G-50 chromatography shows that this response is due to beta-endorphin-like peptides, not beta-lipotropin. These findings indicate that pituitary beta-endorphin secretion is tonically inhibited by dopamine and suggest that the intermediate lobe is the source of this secretion.

Animals↗
PubMed1982

Effect of domperidone, an extracerebral inhibitor of dopamine receptors, on thyrotropin, prolactin, renin, aldosterone, and 18-hydroxycorticosterone secretion in man.

This study investigates the dopaminergic mechanisms involved in the control of corticosteroid secretion in normal subjects. TSH, PRL, PRA, aldosterone, and 18-hydroxycorticosterone (18-OHB) were measured before and after the administration of domperidone (10 mg, iv) to eight healthy males. Domperidone, a selective peripheral dopamine antagonist, stimulated TSH and PRL secretion. Plasma concentrations of aldosterone, 18-OHB, cortisol, and PRA were not altered by domperidone. This is in contrast to previous observations of aldosterone, 18-OHB, and PRA responses to metoclopramide, a dopamine antagonist which readily crosses the blood-brain barrier. Domperidone may fail to stimulate aldosterone, 18-OHB, and renin secretion because it does not cross the blood-brain barrier or does not function as an antagonist for adrenal dopamine receptors modulating 18-OHB and aldosterone secretion.

18-Hydroxycorticosterone↗
PubMed1982

Radioimmunoassay detection of endorphins from long-term culture of human pituitary tumour cells.

Using a sensitive and precise radioimmunoassay for human beta-endorphin, we have demonstrated the sustained secretion of opioid peptides from human pituitary tumour cells. Pituitary tumour tissue obtained from a patient with Nelson's syndrome was maintained in continuous monolayer culture and secreted both beta-lipotropin and beta-endorphin, with predominance of the latter. This is compatible with the idea that the beta-endorphin in normal human serum is secreted as such despite the predominance of beta-lipotropin compared with beta-endorphin in the anterior pituitary.

Cells, Cultured↗
PubMed1981

The role of opiates and endogenous opioid peptides in the regulation of rat TSH secretion.

The administration of morphine to rats at room temperature is reported to suppress serum thyrotropin (TSH) levels by a hypothalamic mechanism. However, it is unknown whether endogenous opioid peptides (EOP) are involved in the control of TSH secretion. The present studies show that naloxone (10 mg/kg, i.p.) an opiate-receptor antagonist, prevented the decline in rat serum TSH which occurs with heat exposure. Morphine sulfate (20 mg/kg, i.p.) treatment prevented the cold-induced elevation in serum TSH and pretreatment with haloperidol (0.3 mg/kg, i.p.) eliminated morphine's influence. Medial-basal hypothalamic thyrotropin-releasing hormone (TRH) content, measured by RIA, increased in the morphine-treated rats which were exposed to 4 degrees C. A submaximal intravenous dose of TRH (300 ng/100 g) was given to determine whether morphine suppresses serum TSH through the release of hypothalamic thyrotropic inhibitors. Morphine pretreatment did not alter TSH stimulation by TRH. Morphine alone or combined with TRH did not alter basal or stimulated TSH secretion in vitro. These studies strongly suggest that, in rats, the EOP modulate TSH secretion under conditions such as acute heat exposure which was associated with a decline in serum TSH. Under specific circumstances, the suppression of serum TSH by morphine may be dopamine-dependent.

Animals↗
PubMed1981

Neurotransmitter control of hypothalamic-pituitary-thyroid function in rats.

The possible roles of monoamine neurotransmitters in the regulation of the hypothalamic-pituitary-thyroid axis were examined in the rat. Rats were treated acutely and repeatedly with drugs which are presumed to alter neurotransmitter functional activity. These drugs include neurotransmitter precursors (tryptophan and L-DOPA), synthesis inhibitors (p-chlorophenylalanine and alpha-methyltyrosine), uptake inhibitors (desipramine and zimelidine) and lithium carbonate. The hormone levels measured were hypothalamic TRH and SLI content and serum TSH, T4 and T3. We conclude that augmented serotonergic or dopaminergic activity may inhibit TRH release, but that release from these inhibitions is not sufficient to stimulate TRH release. The release of TRH seems to be mediated by norepinephrine. Lithium treatment results in increased hypothalamic TRH.

Animals↗
PubMed1981

Morphine and naloxone: effects on beta-endorphin immunoreactivity in canine plasma and secretions from rat pituitaries.

Morphine and naloxone were administered to five dogs to assess their effects on endogenous opioid release. Morphine (3 mg/20 kg) produced a significant (P less than 0.05) increase in plasma beta-endorphin immunoreactivity(beta EI) compared to saline control. The peak stimulation [19.2 +/- 4.97 baseline to 48.1 +/- 6.82 (SEM) pg/ml] occurred at +10 min and rapidly returned to preinjection levels at +60. At a dose 10 times equipotent to circulating basal beta EI, morphine (4-6 micrograms) failed to affect beta EI release. Naloxone, surprisingly, also caused a significant (P less than 0.025) release of beta EI. After naloxone, beta EI rose from a preinjection baseline of 36.4 +/- 5.82 pg/ml to a peak of 172 +/- 44.1 pg/ml at 45 min post injection. Naloxone pretreatment also obscured the effect of subsequently injected morphine (3 mg/20 kg). In three naloxone-treated dogs, gel chromatography of pooled basal and peak plasma revealed a preponderance of beta-lipotropin compared to beta-endorphin. To determine the site of stimulation of beta EI by opiates and opioids, a series of rat anterior pituitary incubations were performed. Neither morphine (10(-6) M) nor D-Ala2-methionine enkephalinamide (10(-6) M) nor naloxone (10(-6) M) had an effect significantly different from control medium on the release of beta EI from the pituitaries. In a second set of experiments we compared the effect on beta EI release of hypothalamic median eminence extract alone or with morphine. Hypothalamic median eminence extract at two concentrations produced significant release of beta EI, which was unaffected by the addition of morphine. These results suggest that stimulation of release of endogenous opioid peptides by opiates occurs at a suprapituitary level.

Animals↗
PubMed1981

beta-Endorphin 61-91 and other beta-endorphin-immunoreactive peptides in human semen.

Human semen contains large amounts of authentic beta-endorphin and other beta-endorphin immunoreactive peptides. To eliminate the non-specific effects of semen in the beta-endorphin RIA, the beta-endorphin immunoreactive peptides were extracted with octadecylsilane-C18 reverse phase beads. beta-Endorphin immunoreactivity was parallel to the RIA standard curve. Sephadex G-50 gel chromatography showed that 93% of the immunoreactive material coeluted with beta-endorphin. Reversed phase high pressure liquid chromatography of semen extract demonstrated several peaks of beta-endorphin immunoreactivity; one of these was coincident with synthetic h-beta-endorphin61-91.

Chromatography, Gel↗
PubMed1981

Treatment of hyperthyroidism with sodium ipodate (oragrafin) in addition to propylthiouracil and propranolol.

Ten patients with hyperthyroidism due to Graves' disease were treated with sodium ipodate (1 g daily) in addition to propranolol (P) plus propylthiouracil (PTU; 100 mg every 8 h) and were compared with a control group of 8 patients treated with P and PTU. Patients on P and PTU had a mean (+/- SEM) basal free T3 index of 387 +/- 59 (normal, 70--160) compared with that of 409 +/- 47 (P greater than 0.05) in the sodium ipodate group. The respective basal free T4 index values (normal, 4.5-10.9) were 21.3 +/- 2.8 for the controls and 25.9 +/- 2.8 for the ipodate group (P greater than 0.5), and the basal rT3 values were 192 +/- 49 and 210 +/- 41 (normal, 16--50 ng/dl; P greater than 0.05). The average percent changes in each thyroid index and rT3 were calculated. The first 3 days on P and PTU served as the basal period for the control group, and comparisons were made to the following 9 days. The ipodate group received P and PTU for 2.7 +/- 3.0 days, and comparisons were made with the interval on ipodate, P, and PTU (mean, 9.1 +/- 0.9 days). For the free T3 index, the control group showed a mean decrement of 20.5 +/- 4.4% compared with 50.2 +/- 3.1% for the ipodate group (P less than 0.001). The respective free T4 index decrements were 14.5 +/- 4.4% and 18.5 +/- 2.7% (P greater than 0.05). The respective changes in rT3 were -13.4 +/- 7.6% and +140 +/- 26.9% (P less than 0.001). In patients with hyperthyroidism, short term daily therapy with sodium ipodate plus P and PTU produces a greater reduction of free T3 index values than that caused by P and PTU alone.

Female↗
PubMed1980

Immunological and biological studies on cholecystokinin in rat brain.

Cholecystokinin-like immunoreactivity (CCK-LI) was demonstrated by radioimmunoassay in aqueous (n = 3) and acid (n = 10) extracts of cortex (42 +/- 9 pmol/g; 4.0 +/- 1.8 pmol/g), thalamus (4.1 +/- 1.1 pmol/g; 1.0 +/- 0.2 pmol/g), and hypothalamus (58 +/- 14 pmol/g; 6.3 +/- 0.7 pmol/g). Sephadex chromatography revealed that more than 95% of the immunoreactivity in acid extracts coeluted with CCK33 standard. In aqueous extracts more than 80% of immunoreactivity coeluted with CCK8 standard. Both the CCK33- and CCK8-like materials induced contraction of guinea pig gallbladder in vitro. L-Tryptophan (200 mg/kg) and high-dose morphine (20 mg/kg) decreased CCK33-LI concentrations in hypothalamus and thalamus. Low-dose morphine (5 mg/kg) decreased CCK33-LI in hypothalamus. We conclude that 1) CCK-LI is present in cortex, thalamus, and hypothalamus of the rat brain, 2) CCK-LI exists in two predominant molecular forms coeluting with CCK33 and CCK8, 3) both molecular forms are biologically active, and 4) concentrations of rat brain CCK33-LI are modulated by serotonergic and opiate mechanisms.

Animals↗
PubMedDate not supplied

High concentrations of p-Glu-His-Pro-NH2 (thyrotropin-releasing hormone) occur in rat prostate.

Thyrotropin-releasing hormone (TRH) immunoreactivity occurs in high concentration within the rat prostate. Previous studies have shown that the immunoreactive species consists of more than one TRH-like tripeptide which cross-reacts in the TRH radioimmunoassay. The component which was highly retained during cation exchange chromatography was subjected to a preparative scale isolation, purification and structural analysis. The methods used included methanol extraction, water-ethyl ether partitioning, cation exchange chromatography, affinity chromatography, high pressure liquid chromatography, TRH radioimmunoassay, in vitro pituitary bioassay, TRH receptor assay, and amino acid analysis. The mean concentration of the predominant amino acids (Glu, His, Pro), 344 pmoles/ml, and the TRH concentration measured by TRH radioimmunoassay prior to acid hydrolysis, 372 pmoles/ml, were nearly identical. Because the material analyzed cochromatographed with synthetic TRH in several chromatographic systems, had a radioreceptor potency which was indistinguishable from that for synthetic TRH, and released TSH and prolactin but not growth hormone from rat pituitaries in vitro, it is concluded that pGlu-His-Pro-NH2 is one of the TRH-like peptides in the rat vental prostate.

Amino Acids↗