Angiographic spasm of cerebral arteries was produced in dogs by successive injections of cisternal blood 48 hours apart. Angiograms were taken before and after each cisternal injection. There was progressively greater angiographic vasospasm of the basilar artery. Intravenous aminophylline, 10 mg/kg/hr, reversed vessel constriction on the 1st and 3rd day after one injection of cisternal blood. On the 5th day after two blood injections (on Day 1 and Day 3), intravenous aminophylline, nifedipine (1 mg/kg), and intra-arterial bolus injection of 2 mg/kg papaverine failed to reverse the constriction. The intractable constriction produced in this model resembles that found in patients. The calcium antagonist, nifedipine, is as ineffective as the more traditional vasodilators in reversing vasospasm in this model.
Cerebral blood vessels are devoid of vasa vasorum. Therefore, the authors have studied the microarchitecture of the adventitia of large feline cerebral vessels of the same size, in an effort of determine how the vessels are nourished. The cerebral vessels contain a rete vasorum in the adventitia that is permeable to large proteins and is in continuity with the subarachnoid space. This substructure may be analogous to the systemic vasa vasorum and may contribute to the nutrition of the cerebral arteries.
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.
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