William N. Dawson

The cerebral vasospasm produced by blood, fractions of blood, and blood-borne agents administered intracisternally was studied arteriographically to attain a better understanding of the genesis of vasospasm. The results indicate this phenomenon is multifarious in origin, involving a number of spasmogens. Whole blood, platelets, platelet extracts, some isolated components of platelets, plasma, thrombin, histamine, serotonin and prostaglandins F 1α , E 2 and F 2α produced a significant incidence and duration of spasm. Norepinephrine and prostaglandin E 1 were inactive. Spasm produced by arachidonic acid and red blood cells was of questionable significance. Compared to whole blood, thrombin usually produced spasm which was more delayed in onset while most other active substances produced a shorter-lived spasm. However, among the pure substances tested, serotonin, prostaglandin E 2 and prostaglandin F 2α induced spasm in small doses which most nearly resembled that observed with whole blood. The hypothesis that the course of spasm depends upon synthesis of spasmogens by brain and blood is advanced. Prostaglandin synthesis plays a major role in this concept.