63 research outputs found
CBF in Patients with Ischemic Cerebrovascular Disease Studied with 133Xe Inhalation and Single Photon Emission Tomography
No full textEffect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen.
No full textThe 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 O2 pressure, partial CO2 pressure, pH, and O2 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 133xenon injection technique. In addition, changes in CBF were estimated from the arteriovenous oxygen content difference. CBF increased in all patients after acetazolamide, by approximately 55 and 70% after 3 and 20 min, respectively. The CBF changes were of the same order whether calculated from the 133Xe clearance or from the arteriovenous oxygen differences (A-V)O2. CMRO2, calculated from (A-V)O2 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.</p
Cell density in the border zone around old small human brain infarcts.
No full textNine brain autopsy cases of small old cerebral infarcts were selected for neuropathological studies. Eight of the patients had cortical infarcts, in two cases with extension into the striate body. In one case the infarct involved the striate body only. The density of neurons and glial cells was measured in the coronal and the horizontal planes at various distances from the margin of the infarct. Corresponding counting points in the contralateral hemisphere served as control. On light microscopy, the infarcted cortex was irregularly shaped, but on serial sections the bulging parts appeared to be cut off from the infarcted tissue ("pseudo-infarct islands"). The zone of transition from infarcted to normal brain tissue was less than a few mm wide. In one patient, tomographic measurements of the cerebral blood flow (CBF) and a CT scan could be compared with the neuropathological findings. In this patient, CBF in the surroundings of the infarct was decreased despite a normal neuronal density. The study supports the traditional view held by pathologists that a sharp transition exists between infarcted and normal brain tissue and suggests that the hypoperfusion zone surrounding the region of complete infarction may be due to mechanisms other than selective loss of neurons.</jats:p
Evaluation of the cerebral vasodilatory capacity by the acetazolamide test before EC-IC bypass surgery in patients with occlusion of the internal carotid artery.
No full textCerebral blood flow (CBF) was measured by xenon-133 inhalation tomography in 18 patients with cerebrovascular disease before and 4 months after extracranial-intracranial bypass surgery. Only patients who showed a reduced CBF in areas that were intact on the CT scan and relevant to the clinical and angiographical findings were operated. The majority of the patients had suffered a minor stroke with or without subsequent transient ischemic attacks. They were studied at least 6 weeks following the stroke. All patients had an occlusion of the relevant internal carotid artery. To identify preoperatively the patients with a compromised collateral circulation and hence reduced CBF due to reduced perfusion pressure, a cerebral vasodilatory stress test was performed using acetazolamide (Diamox). In normal subjects, Diamox has been shown to increase tomographic CBF without change of the flow distribution. In the present series 9 patients showed a significant redistribution of flow in favor of the non-occluded side ("positive" Diamox test). Two of these 9 patients showed even a paradoxical decrease in focal CBF preoperatively, i.e., a "steal" effect. These 2 patients were the only patients who improved in focal CBF after shunting. The remaining 9 patients all showed uniform flow responses ("negative" Diamox test), and none of these increased in focal CBF postoperatively. The finding of an unchanged flow map postoperatively confirmed that the low flow areas were not due to restricted flow via collateral pathways. However, an increase in the regional vasodilatory capacity was observed postoperatively in the majority of patients.</jats:p
CBF decreases after calcium antagonist treatment in acute ischemic stroke
No full textThe effect of the possible influence of a new calcium antagonist, PY 108-068, on regional cerebral blood flow (CBF) was studied in patients suffering acute ischemic stroke. The dosage was 1.5 + 2.5 mg intravenously in six patients (series 1) and 2.5 + 5.0 mg intravenously in five other patients (series 2). CBF was measured before and after treatment by xenon-133 inhalation and single photon emission computed tomography (Tomomatic 64). In the first series, no changes in hemispheric CBF, arterial blood pressure, or clinical symptoms were noted after treatment, but one patient showed an increase of CBF in part of the peri-infarct area. In the second series, slight increases in mean hemispheric flow values were seen, but in three of the five patients CBF decreased even further in the ischemic area. Arterial blood pressure decreased by 13%, and the clinical symptoms were unchanged. In conclusion the results shows, that calcium antagonist may be harmful in acute ischemic strokes since it can decrease the cerebral blood flow further in the ischemic areas. A potential beneficial metabolic effect of an calcium antagonist in ischemic tissue may thus be overshadowed by a harmful flow decrease.</p
rCBF After Tia and during Migraine Attacks
No full text TIA is usually caused by embolism from a carotid stenosis. The stenosis has no hemodynamic significance, but recent studies of regional cerebral blood flow have indicated that this occurs in a few cases. Traditionally, TIA are not considered to cause cerebral damage, but CT-studies have revealed a number of silent infarcts and rCBF measurements have shown even more persistent abnormalities of blood flow. In classic migraine, alterations of rCBF are completely different, indicating a mechanism progressing in the cerebral cortex, probably the spreading depression of Leao. Similar blood flow changes are not seen in common migraine, where tomographic rCBF determinations have been normal. </jats:p
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