Does cerebral vasospasm result from denervation supersensitivity?
This study examined the role of denervation supersensitivity in the development of cerebral vasospasm. Adrenergic denervation of cat basilar artery was accomplished by resection of the superior cervical ganglia or by injection of 6-hydroxydopamine into the cisterna magna. In vivo dose-response characteristics were determined for normal and for denervated arteries, and no significant differences were found between topical applications of serotonin, norepinephrine, epinephrine, fresh blood, or incubated blood. In addition, analysis of cat blood incubated in vitro revealed that the levels of serotonin, norepinephrine, and epinephrine diminished over time, whereas levels of hemoglobin and methemoglobin increased up to Day 14. The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.
D000818:Animals; D001488:Basilar Artery / Q000294:innervation* / Q000648:ultrastructure; D002415:Cats; D003714:Denervation / Q000009:adverse effects*; D004305:Dose-Response Relationship, Drug; D004837:Epinephrine / Q000097:blood / Q000494:pharmacology; D006454:Hemoglobins / Q000032:analysis; D002546:Ischemic Attack, Transient / Q000097:blood / Q000209:etiology*; D008706:Methemoglobin / Q000032:analysis; D008854:Microscopy, Electron; D009638:Norepinephrine / Q000097:blood / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology
D006454:Hemoglobins; D012701:Serotonin; D008706:Methemoglobin; D009638:Norepinephrine; D004837:Epinephrine