Régli, F

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.

The right middle cerebral artery was occluded in cats, and Pa o o2 was increased by increasing the amount of oxygen inhaled by the animals at atmospheric pressure. Cortical blood flow (CBF) was measured with Krypton-85, and observations and photographs of the superficial cortical microvasculature were made bilaterally. In two of five animals, increasing the Pa o o2 caused constriction of surface arterioles of the nonischemic hemispheres, with an associated decrease of CBF; in the three other animals, there were no circulatory responses to the increased Pa o o2 . In seven animals, increasing the Pa o o2 had no apparent effect on CBF or arteriolar caliber of the ischemic cerebral hemispheres. In four animals, at Pa o o2 greater than 400 torr, reactivity to increases of Pa CO CO2 was preserved in nonischemic cortex but impaired in ischemic cortex. Reddening of venous blood of the microvasculature of ischemic cerebral cortex occurred when Pa o o2 was increased, indicating that more oxygen was made available to the ischemic cerebral tissue. However, no beneficial effects could be demonstrated on the changes in the microvasculature produced by ischemia.

In cats in which one middle cerebral artery was occluded, cortical blood flow (CBF) was measured and the superficial cortical microvasculature was observed bilaterally before and after the intravenous injection of a vasoactive drug. Aminophylline produced decreased CBF in the nonischemic cerebral hemispheres of five of seven animals and arterial constriction in three. Ergotamine tartrate produced arterial constriction in the nonischemic hemispheres of four animals and decreased CBF in three. Neither drug consistently produced increased CBF in ischemic cerebral tissue. Acetazolamide caused vasodilatation in the nonischemic hemispheres of seven animals and increased CBF in five. Increased CBF was not due entirely to changes of Pa CO 2 . CBF also increased in ischemic hemispheres of four of the seven animals given acetazolamide.

To assess the effects of Pa CO CO 2 on cerebral ischemia and reactive hyperemia, the right middle cerebral artery was occluded in 18 cats. Four to six hours later, Pa CO 2 was adjusted by mechanical ventilation, with or without CO 2 , to less than 20 torr in four cats, 31 to 38 torr in six, and 46 to 68 torr in eight. Regional cerebral blood flow (CBF) then was measured at multiple sites in each hemisphere by autoradiography. In regions of brain tissue outside the distribution of the occluded middle cerebral artery, log 10 CBF correlated positively with Pa CO CO 2 . In ischemic regions, CBF was higher in normocapnic cats. Reactive hyperemia occurred in two cats of the hypocapnic group, in four cats of the normocapnic group, but in only one hypercapnic cat (Pa CO CO 2 = 46 torr). Hyperemia also was found outside potentially ischemic regions in five cats. Multiple hyperemic foci developed in six cats. Neither hypocapnia nor hypercapnia was associated with a smaller size or higher CBF of regions of cerebral ischemia produced by occlusion of a middle cerebral artery, although hypercapnia inhibited the development of hyperemia.