Cerebral vasospasm is delayed narrowing of the large cerebral arteries in response to blood clots left in the subarachnoid space after subarachnoid hemorrhage (SAH) from any cause, although it is most common after aneurysmal SAH because this process deposits the most dense and voluminous blood in the subarachnoid space, and it is this blood clot that causes vasospasm. Vasospasm is one of the main causes of morbidity and mortality in patients with aneurysmal SAH. Animal models of vasospasm have been developed because of the difficulties modeling delayed vasospasm in vitro. These models use one of three techniques to simulate SAH: (1) an intracranial artery is punctured allowing blood to surround the artery; (2) an artery is surgically exposed and clotted autologous blood obtained from another site is placed around the artery; or (3) autologous blood from another site is injected into the subarachnoid space and allowed to surround the intracranial arteries. Each technique has advantages and disadvantages. In this chapter, we discuss the advantages and disadvantages of and methods for creation of SAH and vasospasm in nonhuman primates. Arterial diameters are easily quantified by angiography, and SAH is created by frontal craniectomy, exposure of the intracranial arteries of the anterior circle of Willis, and placement of autologous clotted blood around these arteries.
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Kawashima, A., Macdonald, R.L. (2009). Nonhuman Primate Blood-Clot Placement Cerebral Vasospasm Model. In: Chen, J., Xu, Z.C., Xu, XM., Zhang, J.H. (eds) Animal Models of Acute Neurological Injuries. Springer Protocols Handbooks. Humana Press. https://doi.org/10.1007/978-1-60327-185-1_27
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