Abstract. The aim of this study was to evaluate the effect of acetazolamide on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). CBF, arterial and jugular venous partial 02 pressure, partial CO2 pressure, pH, and 02 saturation percentage were measured in six patients before and 3 and 20 minutes after intravenous administration of 1 g of acetazolamide. CBF was measured by the intracarotid '33xenon injection technique. In addition, changes in CBF were estimated from the arteriovenous oxygen content difference. CBF increased in all patients after acetazolamide, by 55 and 70% after 3 and 20 min, respectively. The CBF changes were of the same order whether calculated from the '33Xe clearance or from the arteriovenous oxygen differences (A -V)02. CMRO2, calculated from (A -V)02 differences and CBF, remained constant. Except for an increase in the venous oxygen saturation, the blood gases remained constant.Acetazolamide, in a dose sufficient to inhibit the erythrocyte carbonic anhydrase (EC 4.2.1.1), thus induced a rapid and marked increase in CBF, leaving CMRO2 unchanged. This effect of acetazolamide on CBF is probably explained by a decrease in brain pH rather than by brain tissue hypoxia due to inhibition of oxygen unloading in the brain capillaries.
We report the results of 50 angioplasty procedures via the popliteal artery. A 3-year follow-up including control of blood pressures at ankle and toe levels show results comparable to reports in the literature. This new approach for angioplasty of the superficial femoral artery and eventually of coexisting iliac lesions enables treatment of previously inaccessible lesions. The technique is especially suited for lesions close to the takeoff of the superficial femoral artery.
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