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  • 1
    ISSN: 1432-1041
    Keywords: propranolol ; cerebral blood flow ; cerebral oxygen metabolism ; CO2 reactivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The effect of acute and long-term treatment with propranolol on cerebral blood flow (CBF) and the cerebral metabolic rate of oxygen (CMRO2) has been studied in 8 young healthy volunteers. CBF was measured by 133Xe-inhalation and single photon emission computer tomography, and CMRO2 was calculated from the arterio-venous oxygen difference and CBF. Studies were done before and 1 h after i. v. injection of 5 mg propranolol and after three weeks on oral propranolol 80 mg/d for 1 week and 160 mg/d for 2 weeks. Cerebrovascular CO2 reactivity in terms of the A – V oxygen difference was tested on all three occasions during hypercapnia and hyperventilation. CBF, CMRO2 and cerebrovascular CO2 reactivity remained stable both after acute and after 3 weeks of treatment with propranolol.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Carbon dioxide ; cerebral blood flow ; cerebral oxygen metabolism ; cerebral vascular reactivity ; ketanserin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the anti-hypertensive agent ketanserin on the cerebral blood flow (CBF) and the cerebrovascular CO2 reactivity was examined in 10 healthy volunteers. Ketanserin was administered as an intravenous bolus of 10 mg followed by an infusion of 6mg/h. Before administration CBF was measured by single photon emission computerized tomography (SPECT) of inhaled133 Xenon. Then arterial CO2 tension was subsequently decreased by voluntary hyperventilation and increased by breathing an air/CO2 mixture. The relative changes in CBF induced by the changes in arterial CO2 tension were estimated by the cerebral arterio-venous oxygen content difference method. One hour following the start of ketanserin infusion the SPECT measurement and CO2 manipulations were repeated. The CO2 reactivity (expressed as the slope of the regression line of the linear relation between CBF and PaCO2), was unchanged, i.e. 3.2%/0.1 kPa before ketanserin and 4. 1%/0.1 kPa during ketanserin, respectively. Using regression lines from a semi-logarithmic plot the CO2 reactivity was also unchanged 3.4%/0.1 kPa and 3.5%/0.1 kPa, respectively. Ketanserin did not change CBF. The cerebral oxygen metabolism (CMRO2) was decreased 19% one hour after the start of infusion of ketanserin. In conclusion administration of ketanserin in a clinically relevant dose to healthy volunteers does not change the regional CBF not the cerebrovascular CO2 reactivity, but a decrease in CMRO2 was observed. However further studies are needed to clarify whether ketanserin in fact has a depressing effect on CMRO2 or whether the different results are caused by methodological errors or stocastic variation.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Intracranial pressure ; cerebral blood flow ; autoregulation ; angiotensin converting enzyme inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fourteen patients with normal pressure hydrocephalus had the autoregulation of cerebral blood flow (CBF) and intracranial pressure (ICP) investigated. In 8 of the patients the effect of Captopril on ICP and CBF was also investigated. The mean arterial blood pressure (MABP) was 109 mmHg (intra-arterially), and ICP was 11 mmHg (intraventricularly). Changes in global CBF were estimated by the arterio-venous oxygen difference method. The autoregulation of CBF was present in 13 of the patients (p 〈 0.01). The lower limit of CBF autoregulation was 86% of the baseline perfusion pressure. One hour after 50 mg of captopril perorally, MABP was reduced 16 mmHg, and ICP and CBF were unchanged. The autoregulation was maintained and the lower limit was decreased 19 mmHg. Thus patients would be expected to benefit from captopril treatment in hypotensive anaesthesia.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 102 (1990), S. 11-13 
    ISSN: 0942-0940
    Keywords: Intracranial pressure ; cerebral blood flow ; perfusion pressure ; nimodipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eight patients with normal-pressure hydrocephalus (NPH) were studied. The resting mean arterial blood pressure (MABP) was 100 (90–125)mmHg and the mean intracranial pressure (ICP) was 11 (5–17)mmHg. ICP and MABP were continuously measured intraventricularly and intra-arterially, respectively. Changes in global cerebral blood flow (CBF) were estimated by the arteriovenous oxygen difference method. Intravenous nimodipine (15 microgram/kg/hour) was given in the first 2 hours and 30 microgram/kg/hour in the next 2 hours. MABP was reduced 23 (4–47)mmHg (p〈0.05). ICP was increased 3 (0–10)mmHg (p 〈 0.05). CBF was unchanged in the group on the whole, but in 4 of patients a major drop in perfusion pressure was seen, and CBF decreased 6, 11, 23 and 34%, respectively. Thus these findings underline the importance of maintaining the perfusion pressure under treatment with nimodipine.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0942-0940
    Keywords: Arterial blood pressure ; calcium antagonist ; cerebral blood flow ; cerebral metabolic rate of oxygen ; carbon dioxide reactivity ; nimodipine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was undertaken in 8 healthy volunteers to examine the effect of a clinically relevant dose of nimodipine (NIM) (15 and 30 microgram/kg/h) on CBF, its CO2 reactivity, and CMRO2. Mean arterial blood pressure (MABP) was measured intra-arterially. Regional CBF was measured by SPECT of inhaled Xenon-133. During the CO2 reactivity tests changes in CBF were estimated by the arterio-venous-oxygen-difference method. Median CBF was 52 ml/ 100 g/min (48–53) with a normal regional distribution, and median baseline MABP was 96 mmHg (92–99). MABP was slightly reduced, by 8 mmHg (7–9), and 9 mmHg (4–11) after infusion of NIM for 2 and 4 hours, respectively. CBF, however, remained constant, although correction for changes in PaCO2, revealed a slight increase after 4 hours (p=0.08). CMRO2 was 3.5 ml/100 g/min (3.2–3.5) and was not changed by the infusion of NIM. At arterial CO2 tensions ranging from 4.0 to 6.5 Kpa the CO2 reactivity was 3.0% CBF/ 0.1 kPa (2.6–3.7) and decreased significantly to 2.6% CBF/0.1 kPa (1.8–3.2) after the infusion of NIM for 3 hours (p=0.02). The median slope of the LnCBFsat/PaCO2 relationship was 1.5 at baseline compared to 1.3 after NIM (p〈0.01). No side effects were observed. The present study shows a decreased CO2 of the cerebral vessels and a maintained coupling of CBF and CMRO2 during the infusion of nimodipine.
    Type of Medium: Electronic Resource
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