Abstract
Summary
1) Serotonin, administered into brain-tissue via an extravascular route, induces edema, possibly due to its musculotropic property. 2) Serotonin was confirmed to have a neurotropic action which appeared to be responsible for the reversible hemiplegic symptoms. 3) The neurotropic effect of serotonin is biphasic, i.e. when administered in low dosage via internal-carotid artery, it causes transient spastic paralyses. In high dosage, it causes flaccid paralyses without inducing cerebral edema. 4) Chlorpromazine and reserpine both block the edemainducing action of serotonin. Reserpine is, however, effective in a much lower dosage. 5) Chlorpromazine potentiates the neurotropic depressant effect of serotonin, but apparently does not alter its stimulating action. 6) Reserpine inhibits the neurotropic effect of serotonin. This holds true for the spastic as well as for the flaccid symptoms. 7) Therapeutic considerations suggest that reserpine may be specifically indicated in prophylactic treatment of apoplexy.
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