[Prolactin, gonadotropic hormone and estradiol secretion in the hyperprolactinemia syndrome].
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Biomedical subjects
Publications and source records attributed to T O Chernova.
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It was established that early degeneration of motor fibers of the sciatic nerve of rats (24 and 48 hours after division) is marked by diminished activity of the antioxidant enzymes superoxide dismutase and glutathione reductase and activation of lipid peroxidation leading to increased accumulation of malonic dialdehyde. alpha-tocopherol acetate prevents activation of lipid peroxidation and partly suppresses the development of functional signs of degeneration (lowered amplitude of the M-response, slow restoration of the neuromuscular synapse, and decrement reaction to rhythm stimulation). OBQ2 oxidant (derivative of 4-anilino-5-methoxy-1,2-benzoquinone) had no effect on the rate of degeneration development, which is evidence of insufficiency of radical protection for realization of the anti-degeneration effect.
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It was previously proposed that hyperprolactinemia in primary hypothyroidism is caused by enhanced release of hypothalamic TRH leading to elevation of both TSH and prolactin levels. Since the dopaminergic system is involved in regulation of prolactin and TSH secretion, we attempted to evaluate the origin of hyperprolactinemia in patients with primary hypothyroidism using tests with metoclopramide, a dopaminergic blocker (10 mg, i.v.) and TRH. Two groups of patients were examined: 20 women with primary hypothyroidism and normal prolactin levels (group A) and 10 women with primary hypothyroidism and hyperprolactinemia (mean basal prolactin level 1514.8 +/- 300.8 mIU/ml). Prolactin reaction in metoclopramide test in group A was markedly increased vs. control group (1131 and 776%, respectively). In group B prolactin reaction in metoclopramide test was blurred (299%), similarly as in patients with microprolactinomas. We came to a conclusion that hyperprolactinemia in patients with primary hypothyroidism is unlikely to be caused by excessive TRH release, but possibly by the presence of subclinical microadenoma which manifests by the hypothyroid state or, possibly, by disturbed dopaminergic regulation of prolactin and TSH secretion in patients with primary hypothyroidism.
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