[The study of occurrence mechanism in acute and chronic cerebral vasospasm].
Using radioimmunoassay, fluorescence and transmittal++ electronmicroscopy, we studied the of prostaglandin(PG), lipid peroxidation(LPO) and ultrastructure. Fresh arterial blood (imaging acute spasm) produced basilar arterial spasm strongly(+ + +) and vacuole deterioration in vascular walls but there were no changes in 6-keto-PGF1 alpha and TXB2 and PGE2 and LPO. Incubated arterial blood (imaging chronic spasm) produced basilar arterial spasm markedly (+ + +) also. Vacuole deterioration in vascular walls either, and decreased the level of 6-keto-PGF1 alpha apparently (P < 0.01) and elevated the content of LPO significantly (P < 0.01) and there were no changes in the level of TXB2 and PGE alpha. This experiment suggests that the mechanism of acute spasm and chronic spasm is different.
Jiang
K
K
First Affiliated Hospital, Dep. Neurosurgery, Liao Ning.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D001488:Basilar Artery / Q000473:pathology; D005260:Female; D002546:Ischemic Attack, Transient / Q000097:blood / Q000209:etiology* / Q000473:pathology; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D011817:Rabbits; D013345:Subarachnoid Hemorrhage / Q000150:complications; D013929:Thromboxane B2 / Q000097:blood
D008054:Lipid Peroxides; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha