Arterial Wall Changes in Cerebral Vasospasm

Abstract

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… 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 vasoconstruction, is associated with degenerative ultrastructural changes in the endothelium and vascular smooth muscle cells which may denote a temporarily irreversible state.

Intracranial Vessel Wall MRI: Principles and Expert Consensus Recommendations of the American Society of Neuroradiology

“…In vasospastic arteries, smoothmuscle cells shorten in length with increased overlap among cells, resulting in nearly a 500% increase in wall thickness for a 60% luminal narrowing. 32,34 Lack of arterial wall enhancement is concordant with the limited histopathologic data in RCVS, showing an absence of arterial wall inflammation. 32,35,36 We have seen some individual cases that appear to be RCVS with more than minimal wall enhancement, so we recommend caution in relying strongly on VW-MR imaging discrimination between RCVS and vasculitis until this approach is validated in a larger study.…”

Subarachnoid haemorrhage induces an inflammatory response followed by a delayed persisting increase in asymmetric dimethylarginine

“…The clinical implication of this chronic elevation of ADMA is unclear. However, after SAH, ultrastructural changes has been found in cerebral arteries [25] and increased carotid-artery intima-media thickness has been linked to increased ADMA concentrations [25,26] . Whether ADMA is directly involved in these processes is unknown, but elevated ADMA have been linked to numerous cardiovascular diseases [4,8].…”

Comparison of three rat models of cerebral vasospasm

“…A substantial number of studies on subarachnoid hemorrhage-induced cerebral vasospasm have been conducted. They used various species and various methods of inducing experimental subarachnoid hemorrhage such as intracisternal administration of blood (12,19,30,38,39,(43)(44)(45)(46), endovascularly (5,11,22,28,38,44,47) or extravascularly (4,20) puncturing the artery, and blood clot placement around the artery (15). It can be said that existing subarachnoid hemorrhage models of large animals, such as primates and canines, are the preferred models for cerebral vasospasm (31); however, these preferred models are high in cost and often limited in availability due to the difficulties involved in extensive surgery and handling of the subjects when inducing subarachnoid hemorrhage.…”