The action of ergotamine on the intracranial venous pressure and on the cerebral venous outflow of the dog.

The effect of ergotamine and dihydroergotamine on the cerebral circulation was studied in the dog, anaesthetized with chloralose, by recording the intracranial venous pressure and the venous outflow from the superior cerebral vein. Under optimal experimental conditions, ergotamine (5 to 10 mug./kg.) and dihydroergotamine (100 mug./kg.) gave a marked and long-lasting cerebral vasoconstriction accompanied by a slight hypertension. The cerebral vasoconstriction provoked by ergotamine may be very small and was sometimes absent when the cerebral blood-flow was low. This vasoconstrictor effect is more pronounced the higher the initial intracranial venous pressure and hence the cerebral blood-flow. After the induction of a cerebral vasodilatation by 48/80 or strychnine, the vasoconstrictor action of ergotamine was more pronounced. The effect was not observed when CO(2) was employed to modify the intracranial venous pressure. Simultaneous registration of the cerebral, nasal cavity, and kidney vascular responses demonstrated the relative specificity of the action of ergotamine on the cerebral vessels. The small doses of ergotamine used may weaken or abolish the vasoconstrictor action of adrenaline on cerebral vessels. The modification of the responses of the cerebral circulation which such factors as anaesthesia, respiratory acidosis, and operative trauma can produce have been confirmed and emphasized. The results support the view that the vasoconstrictor action of ergotamine on the cerebral vessels might account for the therapeutic value of this drug in migraine.