Key result
SAH vasospasm cuts vessel caliber ~57% and triggers unique degenerative arterial changes.
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A right-sided subarachnoid hemorrhage (SAH) was created in 12 monkeys. Only the right (clot-side) cerebral arteries developed angiographic vasospasm (VSP), which was maximal 7 days after SAH. Eight animals were killed at this time and the remainder at 14 days. At the time of killing the middle cerebral arteries (MCAs) were harvested, and four normal, left (non-clot-side) MCAs were vasoconstricted in vitro with prostaglandin F2 alpha. All MCAs were studied with scanning and transmission electron microscopy. Right MCAs in maximal VSP 7 days from SAH were undistinguishable on scanning electron microscopy from normal arteries vasoconstricted in vitro: both groups demonstrated a mean 57% reduction in vessel caliber and a 5-fold increase in vessel wall thickness compared to normal, nonvasoconstricted left MCAs. On transmission electron microscopy, however, arteries in SAH-induced VSP showed degenerative changes in the tunica intima and media. These changes were still evident at 14 days, despite considerable resolution of VSP. These findings, as well as those from other pathological studies of animal and human cerebral arteries in VSP, suggest that the arterial narrowing and vessel wall thickening seen within several weeks of SAH is due primarily to medial contraction, but unlike simple vasoconstriction, is associated with degenerative ultrastructural changes in the endothelium and vascular smooth muscle cells which may denote a temporarily irreversible state.
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Findlay et al. (1989) studied Cerebral vasospasm following experimental right-sided subarachnoid hemorrhage (n=12). Experimental right-sided subarachnoid hemorrhage-induced vasospasm vs. Normal left middle cerebral arteries (with 4 vasoconstricted in vitro with prostaglandin F2 alpha) was evaluated on Reduction in vessel caliber, increase in vessel wall thickness, and ultrastructural changes in middle cerebral arteries on scanning and transmission electron microscopy. SAH-induced vasospasm and in vitro prostaglandin F2 alpha vasoconstriction both reduced vessel caliber by 57% and increased wall thickness 5-fold, with SAH uniquely causing degenerative changes.
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