Cat Models

SAH in cats was initially induced by electrical or mechanical stimulation, as well as by laceration of the basilar artery, and vasospasm was determined through diameter measurements under direct microscopic visualization (92-94) after a transclival approach. Vasospasm was also induced by lysed platelets, whole blood, hemolysate, serotonin, angiotensin, and norepinephrin ( 93,95,96 ) and was successfully prevented by treatment with chlorpromazine and papaverine (93,95). Whereas laceration of the basilar artery caused vasospasm that lasted for at least 100 min, mechanical spasm reverted within 15 min (93 ).

Blood injection into the cisterna magna causes angiographic vasospasm of the basilar artery at 4 hr and 1 to 7 days but fails to cause histopathologic changes in the smooth muscle cells (97). Nonetheless, this technique has been used to study CSF absorption after treatment with recombinant tissue plasminogen activator (98) to measure changes in intracranial pulse waves after SAH (99) and to study CBF post-SAH (100), despite reports of rapid clearing of blood from the subarachnoid space (101). Other techniques used include blood injection over the cerebral cortex (102), rupture of the MCA through puncture or incision (97,100), blood injection through a shunt from the abdominal aorta through the chiasmatic cistern (103), and avulsion of the MCA (104) or ICA (105). Cat models of vasospasm, however, have decreased in popularity in recent years due to the limited availability of biologic tools for protein analysis, scarce genetic information, and poor characterization of the onset and progression of vasospasm.

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