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Morphine-induced TSH release in normal and hypothyroid subjects
Neuroendocrinology
|April 1, 1985
Summary
Morphine, an opioid agonist, significantly increases thyroid-stimulating hormone (TSH) and prolactin (PRL) serum levels in both healthy and hypothyroid individuals. An opioid antagonist, naloxone, blocks these morphine-induced hormonal changes.
Area of Science:
- Endocrinology
- Neuropharmacology
Background:
- Opioid agonists like morphine can influence endocrine function.
- Thyroid-stimulating hormone (TSH) and prolactin (PRL) are key pituitary hormones with complex regulatory pathways.
Purpose of the Study:
- To investigate the effects of morphine and naloxone on serum TSH and PRL levels.
- To compare these effects in hypothyroid patients and normal volunteers.
Main Methods:
- Administered intravenous morphine (10 mg) and naloxone (10 mg) to hypothyroid patients and normal volunteers.
- Measured serum TSH and PRL levels before and after drug administration.
- Evaluated the impact of naloxone pretreatment on morphine's effects.
- Assessed morphine's effect on TRH-stimulated TSH and PRL release in euthyroid volunteers.
Main Results:
- Morphine administration caused a significant increase in serum TSH and PRL in all subjects.
- The increase in PRL was similar between hypothyroid and normal groups; TSH increase was more pronounced in hypothyroid subjects.
- Naloxone pretreatment completely blocked morphine's stimulatory effects on TSH and PRL.
- Naloxone alone did not significantly alter TSH or PRL secretion.
- Morphine enhanced TSH and PRL responses to TRH stimulation.
Conclusions:
- Morphine exerts a direct stimulatory effect on TSH and PRL secretion.
- Opioid receptors appear to play a role in the regulation of TSH and PRL release.
- These findings highlight the neuroendocrine impact of opioid agonists.