Cerebral arterial constriction after experimental subarachnoid hemorrhage is associated with blood components within the arterial wall

Abstract

Sequential cisternal blood injections in dogs reproduce some of the morphological and physiological features seen in man after subarachnoid hemorrhage-induced vasospasm. This study reports the morphological features observed in cerebral vessels in areas exposed to subarachnoid blood. Subarachnoid hemorrhage was produced in dogs by two cisternal injections of non-heparinized autologous blood 48 hours apart. Dogs were sacrificed 48 hours after the second injection. Angiographic narrowing of the basilar artery was routinely present 48 hours after the second injection, and there was a good correlation between angiographic vasospasm and a narrowed arterial lumen at postmortem examination. All basilar arteries showed structural changes with electron microscopic examination; these included endothelial cell vacuoles, early smooth-muscle cell necrosis, intimal changes, and adventitial erythrocytes, leukocytes, and mast cells. The finding that accompanied vessel constriction most uniformly was packing of the adventitial cerebrospinal fluid spaces with erythrocytes. Angiographically visible spasm was resistant to vasodilators. These data suggest that infiltration of blood elements into the arterial wall is an important concomitant feature of morphological and angiographic vasospasm.

Comparison of three rat models of cerebral vasospasm

“…Despite the fact that all subarachnoid hemorrhage models in the present study developed sufficient vasospasm, the most severe arterial contraction in both arteries was found after induction in the double-hemorrhage model on day 7. Similar results have been previously reported: that the single injection of blood produced less vasospasm, especially on day 7, and a second one (double hemorrhage) was required to produce a more reliable vasospasm model in rabbits and dogs (26,43,46).…”

“…The unavailability of a vehicle group for research on the role of blood in the pathophysiology in the endovascular puncture model is another area of concern (5, 47). In the production of vasospasm, the most important factor, as shown in both experimental (12,26,43,44,46) and clinical studies (16,29), is the amount of blood in contact with cerebral arteries. Rats are unable to maintain an adequate amount of periarterial clotting because of the rapid clearance time, which usually occurs 48 h after subarachnoid hemorrhage induction (12,19,30).…”

Cerebral vasospasm in a double-injection model in rabbit

“…Perhaps the effects owing to raised ICP in this experimental model might be minimized by removing an equal amount of cerebrospinal fluid prior to blood injection. No particular problems were encountered when performing angi- 13,14,16,19,20,24,26]. Moreover, the reduction in the diameter of "spastic" basilar artery was statistically significant.…”

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

“…Injections of homologous blood into the cisterna magna twice (second injection usually 2 days after the 302 TODA AND OKAMURA first) evokes experimentally induced delayed vasospasm in dogs, rabbits, cats, monkeys, baboons, and rats (Echlin, 1965;Liszczak et al, 1983;Svendgaard et al, 1983;Sasaki et al, 1985;Baker et al, 1987;Otsuji et al, 1994). Mechanisms underlying the vasospasm have been analyzed intensively in these animal models to provide effective prophylactic maneuvers.…”