Experimental cerebral vasospasm after subarachnoid hemorrhage. Participation of adrenergic nerves in cerebral vessel wall

S Endo, J Suzuki
1979 Stroke  
= 2 ^mol/min/g Total brain glucose = 6 X 0.37 = 2.22 jimol/g Correcting for cerebrospinal fluid and blood glucose contamination (see Footnote 1) to obtain net tissue glucose content: net tissue content = (2.22) -(6 X 0.105) = 1.59 E = 2 jimol/min per g -r-1.59 jimol/g = 1.26 min 1 Table 2 predicts that the integral of brain glucose specific activity is about 95% that of the plasma integral at 10 min. If greater accuracy is required or if a shorter time were necessary, brain glucose specific
more » ... vity could be calculated as a function of time and used in equation 6 instead of plasma values. This latter approach would be analogous to that developed by Sokoloff and co-workers for "Cdeoxyglucose. 23 SUMMARY Distribution and morphology of nerves in basilar-artery-induced vasospasm were investigated electronmicroscopically. Small cored vesicles were transformed, decreased and disappeared gradually after development of vasospasm induced by blood-CSF mixture incubated 5-10 days. These changes were not induced by fresh arterial blood, lysed platelets in saline and mechanical stimulation. In the portion with severe vasospasm induced by incubated blood-CSF mixture, nerve distribution was rich and uniform in all portions of the adventitia. In the portion with slight vasospasm, nerves were extremely scanty in the innermost area of the adventitia, within 10fi from the outer edge of the media. The severity of experimental vasospasm became definitely lighter and the duration shorter after bilateral cervical sympathectomy. These findings indicate that nerves, especially the adrenergic axon in the innermost area of the adventitia, may play an important role on the genesis of late vasospasm. The difference in nerve distribution may be a factor influencing individual differences in frequency or severity of vasospasm. Stroke Vol 10, No 6, 1979 VASOSPASM associated with subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysm plays an important role in determining prognosis, but the nature and cause of vasospasm are unclear. We report the results of our studies of neurogenic participation in the genesis of vasospasm by investigating nerves in a vessel wall after induced vasospasm, electronmicroscopically and after surgical sympathectomy. Method Adult cats weighing 2.5-5.0 kg, were anesthetized with intramuscular pentobarbital, and placed on an electric temperature controlled surgical table. Tracheostomies were performed and spontaneous respiration permitted. Body temperature, femoral arterial pressure, respiratory rate and acid-base balance were measured. By the transclival approach, a bone window of about 2 X 2 cm was made in the clivus, and the dura was opened at the midline. About 2/3 of the proximal portion of the basilar artery was exposed. To induce vasospasm the following were used: fresh blood (10 cats), lysed platelets in saline with 1.2 Mg/ m ' serotonin on the average (5 cats), and autogenous blood and CSF mixture incubated at 37°C for 5 days (10 cats), 7 days (17 cats), and 10 days (3 cats). In 5 cats the basilar artery was rubbed through the arachnoid membrane to induce vasoconstriction by mechanical stimulation. The sequential caliber change of the basilar artery was measured using photographs taken before and after spasm was induced. The severity of induced vasospasm was classified according to the degree of constriction as follows: Grade I, constriction less than 10%, Grade II, greater than 10 but less than 30%, Grade III, more than 30 but less than 50%, and Grade IV, more than 50%. In the 5 control cats, a mock operation exposing the basilar artery was performed and the sequential changes of caliber measured. After the varying periods, these basilar arteries were fixed and removed for electronmicroscopic examination. In order to fix the basilar artery in situ with vasospasm, fixatives were injected through the right axial artery and applied on the arachnoid surface simultaneously. The aorta was cut off to stop the heart abruptly. In the 5 additional control cats without operation the brain was immediately removed and the basilar artery excised after anesthesia. The removed arterial segments were fixed in ice-cold 2% by guest on July 22, 2018 http://stroke.ahajournals.org/ Downloaded from
doi:10.1161/01.str.10.6.703 pmid:524411 fatcat:pl27zhba2jgghgyidwl5sknqnu