Occlusion of Middle Cerebral Artery

• Acetazolamide was given to five of ten cats for 48 to 54 hours after extradural occlusion of a middle cerebral artery (MCA). At seven to eight days later, measurements of regional cerebral blood flow (CBF) and estimates of the sizes of the ischemic and infarcted areas of the brains were made. Neurological deficits were more severe and the ischemic and infarcted regions were larger in the cats given acetazolamide. Cerebral edema (brain swelling) was present and reactive hyperemia was common in the treated cats, even one week after MCA occlusion. The hypercapnia and decreases of pH of nonischemic brain tissue that are caused by acetazolamide are harmful for ischemic brain tissue, presumably because of vasodilatation in nonischemic brain tissue with resultant increases of intracranial pressure and decreases of CBF of ischemic regions. ADDITIONAL KEY WORDS antipyrine-14C autoradiography Pacoo r e s p o n s e reactive hyperemia carbonic anhydrase treatment of cerebral ischemia hyperemia CO2 transport cerebral circulation • In the following article in this issue1 it was found that the intravenous injection of acetazolamide could cause an increase of blood flow in ischemic as well as nonischemic cerebral cortex of cats with craniectomies, an occluded middle cerebral artery (MCA), and controlled respiration. The increases of blood flow were, in part, independent of increases of arterial carbon dioxide tension (PaCOo)- However, in animals with crani-ectomies, vasodilatation and brain swellin