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Subarachnoid hemorrhage fails to produce vasculopathy or chronic blood flow changes in rats.

Dale M. Swift, Robert A. Solomon

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Abstract

Cerebral blood flow was measured by a [14C]butanol indicator fractionation technique in rats subjected to subarachnoid hemorrhage, in control rats, and in rats given injections of buffered saline into the subarachnoid space (sham hemorrhage). Cerebral blood flow was significantly decreased in both the subarachnoid hemorrhage and sham hemorrhage rats 3 hours after injection. However, blood flow returned to control levels by 24 hours, and measurement for 14 days after subarachnoid hemorrhage failed to show any delayed decrease in cerebral blood flow. Electron microscopic studies of basilar arteries from rats subjected to subarachnoid hemorrhage 72 hours before killing failed to show any of the morphologic changes that have been associated with vasospasm in humans or in higher animal models. Our studies indicate that the rat model of subarachnoid hemorrhage has limited applicability to the study of subarachnoid hemorrhage following ruptured cerebral aneurysms in humans. However, although rats are not a perfect model of this clinical condition, some pathophysiologic changes similar to those observed in human subarachnoid hemorrhage have been demonstrated in this model and deserve further investigation.

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Cerebral blood flow was measured by a [14C]butanol indicator fractionation technique in rats subjected to subarachnoid hemorrhage, in control rats, and in rats given injections of buffered saline into the subarachnoid space (sham hemorrhage). Cerebral blood flow was significantly decreased in both the subarachnoid hemorrhage and sham hemorrhage rats 3 hours after injection. However, blood flow returned to control levels by 24 hours, and measurement for 14 days after subarachnoid hemorrhage failed to show any delayed decrease in cerebral blood flow. Electron microscopic studies of basilar arteries from rats subjected to subarachnoid hemorrhage 72 hours before killing failed to show any of the morphologic changes that have been associated with vasospasm in humans or in higher animal models. Our studies indicate that the rat model of subarachnoid hemorrhage has limited applicability to the study of subarachnoid hemorrhage following ruptured cerebral aneurysms in humans. However, although rats are not a perfect model of this clinical condition, some pathophysiologic changes similar to those observed in human subarachnoid hemorrhage have been demonstrated in this model and deserve further investigation.

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Available abstract

Cerebral blood flow was measured by a [14C]butanol indicator fractionation technique in rats subjected to subarachnoid hemorrhage, in control rats, and in rats given injections of buffered saline into the subarachnoid space (sham hemorrhage). Cerebral blood flow was significantly decreased in both the subarachnoid hemorrhage and sham hemorrhage rats 3 hours after injection. However, blood flow returned to control levels by 24 hours, and measurement for 14 days after subarachnoid hemorrhage failed to show any delayed decrease in cerebral blood flow. Electron microscopic studies of basilar arteries from rats subjected to subarachnoid hemorrhage 72 hours before killing failed to show any of the morphologic changes that have been associated with vasospasm in humans or in higher animal models. Our studies indicate that the rat model of subarachnoid hemorrhage has limited applicability to the study of subarachnoid hemorrhage following ruptured cerebral aneurysms in humans. However, although rats are not a perfect model of this clinical condition, some pathophysiologic changes similar to those observed in human subarachnoid hemorrhage have been demonstrated in this model and deserve further investigation.

Key concepts: Subarachnoid hemorrhage, Medicine, Subarachnoid space, Anesthesia, Cerebral vasospasm, Cerebral blood flow, Vasospasm, Pathophysiology

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Subarachnoid hemorrhage fails to produce vasculopathy or chronic blood flow changes in rats. — Research Paper | ScholarLens