Histamine content in the brain can be increased by thioperamide, a selective histamine H3 receptor antagonist. It can also improve brain edema in adult hypoxic rats. Brain edema is precisely considered as the important pathological change of neonatal hypoxic-ischemic encephalopathy.
As a study reported in the Neural Regeneration Research
(Vol. 8, No. 19, 2013), thioperamide was used to increase histamine content in the brain, and then the mechanism of action of thioperamide during brain edema in a rat model of neonatal hypoxic-ischemic encephalopathy was examined. Results showed that thioperamide significantly decreased brain water content and malondialdehyde levels, while significantly increased histamine levels and su-peroxide dismutase activity in the hippocampus. This evidence demonstrates that thioperamide could prevent oxidative damage and attenuate brain edema following neonatal hypoxic-ischemic encephalopathy.
The researchers further found that the H1 receptor antagonist, pyrilamine, reversed the effects of thioperamide; however, the H2 receptor antagonist, cimetidine, had no significant influence on the effects of thioperamide. The researchers suggest that thioperamide can increase brain histamine content and attenuate brain edema and oxidative damage by acting in combination with postsynaptic H1 receptors in a rat model of neonatal hypoxic-ischemic encephalopathy.