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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

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

I: Journal of Cardiovascular Pharmacology, Bind 16, Nr. 6, 12.1990, s. 1007-10.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Schmidt, JF, Waldemar, G & Paulson, OB 1990, 'The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers', Journal of Cardiovascular Pharmacology, bind 16, nr. 6, s. 1007-10. https://doi.org/10.1097/00005344-199012000-00022

APA

Schmidt, J. F., Waldemar, G., & Paulson, O. B. (1990). The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. Journal of Cardiovascular Pharmacology, 16(6), 1007-10. https://doi.org/10.1097/00005344-199012000-00022

Vancouver

Schmidt JF, Waldemar G, Paulson OB. The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. Journal of Cardiovascular Pharmacology. 1990 dec.;16(6):1007-10. https://doi.org/10.1097/00005344-199012000-00022

Author

Schmidt, J F ; Waldemar, G ; Paulson, O B. / The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers. I: Journal of Cardiovascular Pharmacology. 1990 ; Bind 16, Nr. 6. s. 1007-10.

Bibtex

@article{1c567b728d7447b68a0a98c2d8e73fa3,
title = "The acute effect of captopril on cerebral blood flow, its CO2 reactivity, and cerebral oxygen metabolism in human volunteers",
abstract = "The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arteriovenous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50-56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89-93), and was slightly reduced by 5 mm Hg (4-6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5-3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3-1.6) at baseline compared to 1.4 (1.3-1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1-2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1-3.2) after captopril (p less than 0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.",
keywords = "Adult, Blood Pressure/drug effects, Brain/drug effects, Captopril/pharmacology, Carbon Dioxide/pharmacology, Cerebrovascular Circulation/drug effects, Female, Humans, Male, Oxygen Consumption/drug effects",
author = "Schmidt, {J F} and G Waldemar and Paulson, {O B}",
year = "1990",
month = dec,
doi = "10.1097/00005344-199012000-00022",
language = "English",
volume = "16",
pages = "1007--10",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams & Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - The acute effect of captopril 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 - 1990/12

Y1 - 1990/12

N2 - The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arteriovenous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50-56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89-93), and was slightly reduced by 5 mm Hg (4-6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5-3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3-1.6) at baseline compared to 1.4 (1.3-1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1-2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1-3.2) after captopril (p less than 0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.

AB - The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arteriovenous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50-56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89-93), and was slightly reduced by 5 mm Hg (4-6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5-3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3-1.6) at baseline compared to 1.4 (1.3-1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1-2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1-3.2) after captopril (p less than 0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.

KW - Adult

KW - Blood Pressure/drug effects

KW - Brain/drug effects

KW - Captopril/pharmacology

KW - Carbon Dioxide/pharmacology

KW - Cerebrovascular Circulation/drug effects

KW - Female

KW - Humans

KW - Male

KW - Oxygen Consumption/drug effects

U2 - 10.1097/00005344-199012000-00022

DO - 10.1097/00005344-199012000-00022

M3 - Journal article

C2 - 1704975

VL - 16

SP - 1007

EP - 1010

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 6

ER -

ID: 274927051