The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers

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The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. / Schmidt, J F; Waldemar, G; Paulson, O B.

I: Acta Neurochirurgica, Bind 111, Nr. 1-2, 1991, s. 49-53.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Schmidt, JF, Waldemar, G & Paulson, OB 1991, 'The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers', Acta Neurochirurgica, bind 111, nr. 1-2, s. 49-53. https://doi.org/10.1007/BF01402513

APA

Schmidt, J. F., Waldemar, G., & Paulson, O. B. (1991). The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. Acta Neurochirurgica, 111(1-2), 49-53. https://doi.org/10.1007/BF01402513

Vancouver

Schmidt JF, Waldemar G, Paulson OB. The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. Acta Neurochirurgica. 1991;111(1-2):49-53. https://doi.org/10.1007/BF01402513

Author

Schmidt, J F ; Waldemar, G ; Paulson, O B. / The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. I: Acta Neurochirurgica. 1991 ; Bind 111, Nr. 1-2. s. 49-53.

Bibtex

@article{524228c502f9497ca9335c21311d8613,
title = "The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers",
abstract = "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/100g/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 less than 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.",
keywords = "Adult, Blood Pressure/drug effects, Carbon Dioxide/blood, Cerebrovascular Circulation/drug effects, Female, Humans, Male, Nimodipine/pharmacology, Oxygen/blood, Reference Values, Tomography, Emission-Computed, Single-Photon, Xenon Radioisotopes",
author = "Schmidt, {J F} and G Waldemar and Paulson, {O B}",
year = "1991",
doi = "10.1007/BF01402513",
language = "English",
volume = "111",
pages = "49--53",
journal = "Acta Neurochirurgica",
issn = "0001-6268",
publisher = "Springer Wien",
number = "1-2",

}

RIS

TY - JOUR

T1 - The acute effect of nimodipine on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers

AU - Schmidt, J F

AU - Waldemar, G

AU - Paulson, O B

PY - 1991

Y1 - 1991

N2 - 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/100g/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 less than 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.

AB - 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/100g/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 less than 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.

KW - Adult

KW - Blood Pressure/drug effects

KW - Carbon Dioxide/blood

KW - Cerebrovascular Circulation/drug effects

KW - Female

KW - Humans

KW - Male

KW - Nimodipine/pharmacology

KW - Oxygen/blood

KW - Reference Values

KW - Tomography, Emission-Computed, Single-Photon

KW - Xenon Radioisotopes

U2 - 10.1007/BF01402513

DO - 10.1007/BF01402513

M3 - Journal article

C2 - 1927624

VL - 111

SP - 49

EP - 53

JO - Acta Neurochirurgica

JF - Acta Neurochirurgica

SN - 0001-6268

IS - 1-2

ER -

ID: 275016924