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Stroke. 1995;26:2347-2352

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(Stroke. 1995;26:2347-2352.)
© 1995 American Heart Association, Inc.


Articles

Characterization of an Anterior Circulation Rat Subarachnoid Hemorrhage Model

A. Piepgras, MD; C. Thomé, MD P. Schmiedek, PhD

From the Department of Neurosurgery, Klinikum Mannheim, Ruprecht-Karls-Universität Heidelberg, Mannheim, Germany.

Correspondence to Dr Axel Piepgras, Neurochirurgische Klinik, Klinikum Mannheim/Ruprecht-Karls-Universität Heidelberg, Theodor-Kutzer-Ufer 1-3, 68135 Mannheim, Germany. E-mail fa8@ix.urz.uni-heidelberg.de.

Background and Purpose Our aim was to demonstrate the feasibility of an angiographically controlled rat model for the study of macrocirculatory and microcirculatory changes of the anterior intracranial circulation after subarachnoid hemorrhage.

Methods Subarachnoid hemorrhage was induced by transorbital injection of 0.3 mL of nonheparinized autologous arterial blood into the chiasmatic cistern. Changes in regional cerebral blood flow were continuously recorded with the use of laser-Doppler flowmetry over the parietal cortex. Angiographic verification of middle cerebral artery diameter was performed by carotid catheterization at baseline and 2 days after injection of blood or artificial cerebrospinal fluid. We monitored intracranial and systemic blood pressure during and after injections.

Results Injection of artificial cerebrospinal fluid in the control group did not change the diameter of the middle cerebral artery. Injection of blood caused a significant arterial narrowing of 17.5%, from 0.37±0.04 mm to 0.31±0.04 mm after 2 days (P=.0001). In the control group regional cerebral blood flow decreased to 75.9±16.8% of preinjection control but quickly recovered to 99.7±19.4%. Intracranial pressure increased for 5 minutes after the injection to a maximum of 27.3±8.9 mm Hg, accompanied by a 10% decrease in mean arterial pressure. A fall in cerebral blood flow to 53.1±26.3% in blood-injected animals that recovered to only 80.7±16.9% of baseline values during the observation period of 30 minutes was noted. A peak intracranial pressure of 45.7±11.5 mm Hg occurred 2 minutes after injection with a decrease in mean arterial pressure of 13%, resulting in a markedly lower cerebral perfusion pressure than in the control group.

Conclusions An angiographically controlled model of subarachnoid hemorrhage primarily involving the anterior circulation is feasible in the rat. The resulting narrowing of the middle cerebral artery reflects moderate vasospasm and will allow further microcirculatory studies with cranial windows.


Key Words: angiography • cerebral blood flow • intracranial pressure • subarachnoid hemorrhage • rats • vasospasm




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