Waltz, Arthur G.

Correlative studies of cortical blood flow measured by the 85 Kr washout technique and observations of the cortical blood vessels of 10 squirrel monkeys subjected to temporary occlusion of the middle cerebral artery are described. During occlusion, cortical blood flow in core areas of ischemia decreased to 0.12 to 0.90 ml/g/min (20 to 50% of preocclusion values) and became pressure dependent with failure of autoregulation. After release of the occluding clip, cortical blood flow was restored. Correlation between degree of vascular reaction judged by observation of the cortex and degree of hyperemia as determined by cortical blood flow was poor. There was incomplete correlation between the degree of hyperemia and the degree of preceding ischemia. Hyperemia, or "luxury perfusion," manifested by red venous blood, appears to be related to failure of cerebral tissue to utilize available oxygen as well as to "reactive" hyperemia, or supernormal blood flow, in regions previously ischemic. There was no demonstrable gradual failure of collateral circulation during occlusion. Cerebral edema was progressive and even progressed after restoration of cortical blood flow; it was incompletely correlated with the degree of ischemia and degree of hyperemia.

Cerebral blood flow (CBF) was measured during 28 carotid endarterectomies in 25 patients, by injection of 133 Xe into the exposed internal carotid artery (ICA). Twenty-three patients had episodic cerebral or retinal ischemia and five had neurologic deficits before operation. Initial CBF values were variable. Increases of Pa Co Co2 caused CBF to increase in four of six patients, to increase slightly in one, and to decrease in one. In each of 19 procedures, CBF decreased during surgical occlusion of the ICA, 11 times to less than 30 ml/100 g/min, but absence of postoperative worsening indicated that decreased ICA blood flow is not a major risk of the procedure; embolization from the site of operation may be a greater threat to the patient. CBF increased after 14 endarterectomies, perhaps due to failure of autoregulation or to reactive hyperemia. Measurements of jugular PV o o2 and lactate concentration were of little value.

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.