RADIONUCLIDE CBF AND CAROTID ANGIOGRAM/Foo et al. 39territory. Despite perfusion pressures calculated at 110 cm H 2 O and less, we were unable to demonstrate profound capillary collapse, even in areas at high risk to the "noreflow phenomenon" such as thalamus and basal ganglia. In addition, Chiang et al. 5 probably infused their fixative against a much higher cerebrovascular resistance because, in their experiments, the cerebral vasculature had been filled with blood during ischemia, the viscosity of which was undoubtedly increased as a result of the stasis. 4 Thus, it is highly likely that the fixative perfusions of Chiang et al. occurred at pressures and flow rates considerably less than those of the present experiments.The possibility remains that the absence of the formed elements of the blood (red cells, white cells and platelets) from the lumina of the ischemic capillaries might have prevented the endothelial and glial changes from occurring in our experiments. If substances released by these structures are instrumental in causing the pathology in question, they would operate equally in all areas of the brain rather than preferentially in selected areas which is the pattern of the "no-reflow phenomenon."Although the current experiments cannot relate the changes in ischemic cerebral capillaries to postischemic neurological function, we believe that they provide a more accurate picture of the structural state of the ischemic capillaries than was previously offered. 5 Although glial swelling previously seemed to obstruct red cell passage through capillaries within 15 minutes of ischemia, we agree with others that this seems doubtful," as it is quite unlikely that the glial swelling and capillary luminal narrowing found in the present experiments would present an absolute barrier to the flow of red cells. We feel that the impaired flow noted in acute experimental ischemic models 1 " 3 -•• 10 therefore must be better explained by mechanisms other than pericapillary glial swelling, such as precapillary shunting, increased blood viscosity due to red cell settling' or vascular constriction. The following results were obtained. Flow was visually unilaterally diminished in 29 (60%) of 48 patients, including 14 (78%) with occlusion and IS (50%) with stenosis. Sixty-two percent of the subjects with severe stenoses and 46% of the patients with mild stenoses had a positive flow study. Diminished flow was evident in the neck in 80% of the patients, intracranially in 20%. Positive radionuclide angiograms always pointed to the side with occlusion or the greater degree of stenosis even though bilateral internal carotid disease was frequently found (54%). The data leading to the differentiation between major and minor ICA stenosis are not sufficient to justify any conclusion.
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