Summary: In situ hybridization was used to estimate re gional levels of heat shock protein-70 (HSP-70) mRNA and c-fos mRNA in two related models of focal cerebral ischemia. In the first model, permanent occlusion of the distal middle cerebral artery (MCA) alone caused a patchy increase in HSP-70 mRNA by 1 h in the central zone of the MCA territory of the ipsilateral neocortex. Tissue levels of HSP-70 mRNA continued to increase for several hours and remained elevated at 24 h. In contrast to the focal expression of HSP-70, c-fos mRNA was in creased throughout the ipsilateral cerebral cortex by 15 min and remained elevated for least 3 h. The wide distri bution of c-fos expression suggests it may have been caused by spreading depression. In the second model, severe focal ischemia was produced with a combination of transient (l-h) bilateral carotid artery occlusion and permanent MCA occlusion. Combined occlusion for 1 h Cerebral ischemia induces increased synthesis of a number of specific proteins, despite an overall reduction in the rate of protein synthesis (Kleihues and Hossmann, 1971; Dienel et aI., 1980 Dienel et aI., , 1986Nowak, 1985). Several of the induced proteins are members of a group of "heat shock" or "stress" proteins that are expressed in the central nervous system following a number of stresses, including heat shock (Brown and Rush, 1990), trauma (Gower et aI., 1989), as well as ischemia. Although the func tion of the stress proteins is not well understood, their induction has been correlated with increased resistance to injury in many cell types (for review, see Lindquist and Craig, 1988). In brain, induction of stress proteins prior to an episode of cerebral 204without reperfusion caused expression of HSP-70 mRNA only in regions adjacent to the central zone of the MCA territory of the neocortex. However, reperfusion of the carotids for 2 h generated intense expression of HSP-70 mRNA throughout most of the ipsilateral cerebral cortex, white matter, striatum, and hippocampus. The wide spread increase in HSP-70 mRNA suggests that reperfu sion triggered expression in all previously ischemic re gions. However, at 24 h of reperfusion, increased levels of HSP-70 mRNA were restricted primarily to the isch emic core of the neocortex. These results suggest that expression of HSP-70 mRNA is prolonged in regions un dergoing injury, but is transient in surrounding regions that recover. Key Words: Heat shock protein-70--c-fos Focal ischemia-In situ hybridization-Messenger ribo nucleic acid-Middle cerebral artery.

Background and Purpose: Brain temperature during ischemia is known to strongly influence the extent of cellular injury. The objectives of the present study were to determine the effect of severe focal ischemia on brain temperature and to assess the influence of those changes on focal infarction.Methods: Severe focal ischemia was produced in rats using permanent occlusion of the distal middle cerebral artery combined with transient (60-minute) bilateral carotid artery occlusion. The temperature of the ischemic focus was measured with a small subdural probe. Three groups of rats were studied. In the first group, brain temperature was permitted to decline spontaneously to 32°C after occlusion. In the second, brain temperature was maintained at 37.5°C during occlusion. In the third group, the brain temperature was maintained at 37.5°C for 40 minutes postocclusion before cooling. After recovery for 24 hours, the volume of infarction was measured in histological sections.Results: In the absence of cranial heating, the brain temperature fell to 33°C by 10 minutes postocclusion, and infarct volume was 19±9 mm 3 (mean±SEM; n=6). Maintaining brain temperature at 37.5°C increased the volume of infarction to 82 ±16 mm 3 (n=7;p<0.001). Delayed cooling did not prevent the increase in infarct volume (75±16 mm

A case of anomalous origin of the anterior choroidal and posterior communicating arteries in a 36-year-old woman with aneurysmal subarachnoid hemorrhage is presented. Preoperative four-vessel angiography revealed a reverse relationship of these vessels, wherein the anterior choroidal artery origin was proximal to the origin of the posterior communicating artery. This arrangement is extremely rare; the only other reported case was in a patient undergoing angiography prior to acoustic neurinoma resection. It is believed that this is the first case reported in a patient with subarachnoid hemorrhage from rupture of an aneurysm arising from a vessel of such anomalous origin.