A NEW GERBIL MODEL OF HINDBRAIN ISCHEMIA BY EXTRACRANIAL OCCLUSION OFTHE BILATERAL VERTEBRAL ARTERIES

A new gerbil model of hindbrain ischemia was induced by extracranial o cclusion of the bilateral vertebral arteries just before their entry i nto the transverse foramen of the cervical vertebra. Carbon black stud ies, performed at 5 min after occlusion, revealed that the pons-medull a oblongata, and the cerebellum were quite ischemic in all animals. Ca rdiovascular changes in mean arterial blood pressure (MABP) and heart rate were recorded until 30 min after occlusion, and revealed that the typical cerebral ischemic response (i.e., abrupt increase in MABP, br adycardia, and apnea) was elicited in all animals (n = 10). Thirty min utes after occlusion, animals (n = 4) were decapitated and immersion-f ixed. Brain sections were stained with hematoxylin-eosin (HE) and also immunostained for microtubule-associated protein 2 in order to evalua te ischemic neuronal damage from 30 min of ischemia. By HE staining, i schemic lesions were detected bilaterally in the oculomotor, the trige minal motor, the lateral vestibular, and the cerebellar interpositus n ucleus. In addition, immunostaining revealed ischemic lesions in sever al other hindbrain areas. In conclusion, we could successfully establi sh a new gerbil model of hindbrain ischemia. Carbon black perfusion an d hemodynamic studies revealed that severe and reproducible hindbrain ischemia was produced. By histopathological examination, we could also clearly demonstrate symmetrical ischemic lesions in several hindbrain areas.