Leif Henriksen

Effect of acetazolamide on cerebral blood flow and cerebral metabolic rate for oxygen.

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 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.

Spreading Cerebral Oligemia in Classical‐ and Normal Cerebral Blood Flow in Common Migraine

SYNOPSIS

Regional Cerebral Blood Flow Assessed by 133Xe Inhalation and Emission Tomography: Normal Values

Regional cerebral blood flow (rCBF) in the cerebral hemispheres and the cerebellum was measured by single photon emission computed tomography with inhalation of l33Xe in 39 normal volunteers at test. The goal of this study was to assess the normal flow pattern and its variations. Five parallel tomographic slices through the brain were recorded with a resolution element of 1.7 × 1.7 × 2.0 cm (full width at half maximum). The blood flow distribution showed that the predominantly gray matter areas displayed flow approximately double that of the predominantly white matter regions. The CBF distribution was practically symmetrical with a side-to-side difference averaging 1.4 ± 1.4 ml/100 g/min. This means that a difference exceeding 4.2 ml/100 g/min (approximately 9% of mean CBF) is abnormal with a confidence level of below 5%. The measured average CBF and cerebellar blood flow were 56 ± 7 and 54 ± 6 ml/100 g/min (mean ± 1 SD), respectively. A significant correlation was found between CBF and Pco2, and between CBF and age. Repeat measurements in an additional 30 subjects showed a day-to-day variability of −0.2 ± 6.4 ml/100 g/min of the difference between the first and the second measurement. This corresponds to random methodological and biological errors of 6.4√2 = 4.6 ml/100 g/min and is a measure of the overall intraindividual variability. Xenon-133 tomography is atraumatic and affords rCBF images free of the superposition artifacts that practically invalidate the nontomographic approaches in the studies of cerebrovascular disease. The rCBF tomograms are blurred, particularly due to Compton scatter. Relative to this factor, the errors caused by local variations in the tissue: blood partition coefficient are less important.

Brain Luxury Perfusion during Cardiopulmonary Bypass in Humans. A Study of the Cerebral Blood Flow Response to Changes in CO2, O2, and Blood Pressure

CBF and related parameters were studied in 68 patients before, during, and following cardiopulmonary bypass. CBF was measured using the intraarterial 133Xe injection method. The extracorporeal circuit was nonpulsatile with a bubble oxygenator administering 3–5% CO2 in the main group of hypercapnic patients (n = 59) and no CO2 in a second group of hypocapnic patients. In the hypercapnic patients, marked changes in CBF occurred during bypass. Evidence was found of a brain luxury perfusion that could not be related to the effect of CO2 per se. Mean CBF was 29 ml/100 g/min just before bypass, 49 ml/100 g/min at steady-state hypothermia (27°C), reached a maximum of 73 ml/100 g/min during the rewarming phase (32°C), fell to 56 ml/100 g/min at steady-state nor-mothermic bypass (37°C), and was 48 ml/100 g/min shortly after bypass was stopped. Addition of CO2 evoked systemic vasodilation with low blood pressure and a rebound hyperemia. The hypocapnic group responded more physiologically to the induced changes in hematocrit (Htc) and temperature, CBF being 25, 23, 25, 34, and 35 ml/100 g/min, respectively, during the five corresponding periods. Carbon dioxide was an important regulator of CBF during all phases of cardiac surgery, the responsiveness of CBF being ∼4% for each 1-mm Hg change of Paco2. The level of MABP was important for the CO2 response. At low blood pressure states, the CBF responsiveness to changes in Paco2 was almost abolished. An optimal level of Paco2 during hypothermic bypass of ∼25 mm Hg (at actual temperature) is recommended. A normal autoregulatory response of CBF to changes in blood pressure was found during and following bypass. The lower limit of autoregulation was at pressure levels of ∼50–60 mm Hg. CBF autoregulation was almost abolished at Paco2 levels of >50 mm Hg. The degree of hemodilution neither affected the CO2 response nor impaired CBF autoregulation, although, as would be expected, it influenced CBF: In 33 women CBF was 55 ml/100 g/min at an Htc of 24%, as compared with 42 ml/100 g/min in 35 men (Htc = 28%). High Pao2 was a vasoconstrictor, the autoregulatory plateau being narrowed. The lower limit of autoregulation was shifted to a higher pressure when Pao2 was low.

Regional cerebral blood flow in chronic alcoholics measured by single photon emission computerized tomography.

Regional cerebral blood flow (CBF) was measured by single photon emission computerized tomography of inhaled 133‐Xe in 20 chronic alcoholic men. Mean CBF was 51 ml/(100 g x min) compared with 53 ml/(100 g x min) in 20 normals. Reduced cerebellar blood flow correlated both to structural abnormalities seen on CT scan and to cognitive dysfunction. Slight abnormalities of the regional CBF was observed in the alcoholics. They had a higher incidence of regional low flow areas than a control group. Low flow areas were found in frontal and posterior parts of the brain not only in patients with atrophia, but also in patients without CT abnormalities, suggesting neuronal dysfunction. The occurrence of regional low flow areas was associated with the severity of alcoholism, cerebral atrophy and intellectual impairment.

Observations on regional cerebral blood flow in cortical and subcortical structures during language production in normal man

Regional cerebral blood flow (rCBF) was studied by single photon emission computerized tomography (SPECT) of inhaled xenon-133 in six normal volunteers during various language, articulatory, and control conditions. Language production increased rCBF in predominantly left-sided cortical and subcortical areas. The involved regions were anatomically related to a left frontal area (Brocas), to both caudate nuclei, to a left thalamic/pallidal area, and bilaterally in retrorolandic areas. The failure to demonstrate lateralized retrorolandic activity is thought to reflect the complexity of the tasks.

Tomographic determination of cerebral blood flow during attacks of cluster headache

A rapidly rotating single-photon emission tomograph was used to study regional cerebral blood flow (rCBF) by 133-Xenon inhalation in 18 patients with cluster headache. Measurements were performed in all patients in the resting state. The patients were given alcohol and/or nitroglycerin to provoke an attack of cluster headache. In eight patients it was possible to obtain satisfactory measurements during their cluster headache attack. All patients had a normal resting CBF with a normal age regression. During the headache phase, no significant changes of mean CBF from baseline occurred. There were no focal changes in the individual patient, but the mean rCBF in all eight patients showed significantly increased rCBF in the central, basal region and a small part of the right parietotemporal region. These changes we interpret as pain activation. It may be concluded that changes in rCBF are not likely to play a pathophysiological role in the development of cluster headache attacks.

Regional cerebral blood flow during rest and skilled hand movements by xenon-133 inhalation and emission computerized tomography

Regional cerebral blood flow (CBF) was studied in 16 normal adult volunteers during rest and in 10 the study was repeated during skilled hand movements. A fast-rotating (“dynamic”), single-photon emission computerized tomograph (ECT) with four detector heads was used. Xenon-133 was inhaled over a 1-min period at a concentration of 10 mCi/L. The arrival and washout of the radioisotope was recorded during four 1-min periods. Two slices, 2 cm thick, 7 and 12 cm above the orbitomeatal line were obtained in every study. CBF averaged 60 ml/100 g/min (SD ± 11) in the lower slice and 51 ml/100 g/min (SD ± 13) in the upper slice. A symmetric pattern comparing right to left sides was found in both slices. Finger tapping and writing with the right hand increased CBF in specific areas of the upper slice: in the contralateral hand area by 35 ± 15% (p < 0.025), and in the supplementary motor area on both sides by 34 ± 15% (p < 0.025).

Cerebral blood flow in chronic toxic encephalopathy in house painters exposed to organic solvents

Cerebral blood flow (CBF) was studied in 11 controls and 9 house painters occupationally exposed to organic solvents for a mean of 22 years. They had mild to moderate intellectual impairment, and no or only minor cerebral atrophy was seen in a CT‐scan of the brain. The 133Xe inhalation technique was used and the flow was calculated from the inital slope of the 133Xe wash out curve (ISI). ISI averaged 36.8 ml/100 g/min in the painters and 45.4 ml/100 g/min in the controls, representing a significant difference (P < 0.05). The reduced CBF in these painters with slight to moderate intellectual impairment might be due to limited neuronal loss or to permanently decreased metabolism of the neurones.

The effects of sodium nitroprusside on cerebral blood flow and cerebral venous blood gases. II. Observations in awake man during successive blood pressure reduction.

Abstract. Cerebral blood flow (CBF) and cerebral venous blood gases were investigated in seven awake patients during hypotension induced with sodium nitroprusside. Infusion of the drug into the internal carotid artery produced no changes in cerebral haemodynamics. Intravenous nitroprusside infusion resulted in a decrease in both CBF and jugular venous PO2 (P<0·01, respectively). Reducing mean arterial blood pressure by 18% and 43% produced a mean CBF fall of 6% and 27% respectively. Arteriovenous oxygen difference increased in consonance with the CBF decrease (P<0·01). Arterial PCO2 fell during the infusion (P<0·01). At 18% blood pressure reduction, the observed PCO2 decrease of 0·25 kPa could account for the 6% CBF decrease. At 43% blood pressure reduction, PCO2 fell by 0·53 kPa, a decrease which could not explain the observed CBF fall of 27%. Dizziness and incipient fainting occurred in the patients at this point. It is concluded that sodium nitroprusside has a minor but significant effect on cerebral haemodynamics in normal awake man.