Surface oxygen pressure distributions in rabbit skeletal muscle: dependence on arterial pO2.

Per Thorborg, L. A. Malmqvist, N. Lund

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.

Original languageEnglish (US)
Pages (from-to)169-192
Number of pages24
JournalMicrocirculation, endothelium, and lymphatics
Volume4
Issue number2
StatePublished - Apr 1988
Externally publishedYes

Fingerprint

Skeletal Muscle
Oxygen
Rabbits
Pressure
Muscles
Striated Muscle
Critical Illness
Ventilation
Healthy Volunteers
Electrodes
Animal Models

ASJC Scopus subject areas

  • Pharmacology

Cite this

Surface oxygen pressure distributions in rabbit skeletal muscle : dependence on arterial pO2. / Thorborg, Per; Malmqvist, L. A.; Lund, N.

In: Microcirculation, endothelium, and lymphatics, Vol. 4, No. 2, 04.1988, p. 169-192.

Research output: Contribution to journalArticle

@article{d5af911522a640c094f665a6db208b60,
title = "Surface oxygen pressure distributions in rabbit skeletal muscle: dependence on arterial pO2.",
abstract = "Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.",
author = "Per Thorborg and Malmqvist, {L. A.} and N. Lund",
year = "1988",
month = "4",
language = "English (US)",
volume = "4",
pages = "169--192",
journal = "Microcirculation, Endothelium and Lymphatics",
issn = "0740-9451",
number = "2",

}

TY - JOUR

T1 - Surface oxygen pressure distributions in rabbit skeletal muscle

T2 - dependence on arterial pO2.

AU - Thorborg, Per

AU - Malmqvist, L. A.

AU - Lund, N.

PY - 1988/4

Y1 - 1988/4

N2 - Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.

AB - Previous reports indicate that hyperoxemia disturbs the striated muscle tissue oxygenation in both critically ill patients and in healthy human volunteers. We believe that further studies of this problem can most conveniently be carried out in an animal model. A systematic study on the influence of higher than normal arterial pO2 levels on striated muscle surface tissue oxygen pressure distributions (OPD) was performed using an MDO oxygen electrode. Experiments were carried out during controlled ventilation in a rabbit model conceived to maintain exceptional cardiovascular stability. The PaO2 level was varied by altering FiO2 (the fraction of inspired oxygen) randomly between 0.21 (mean PaO2 10.7 kPa), 0.30 (mean PaO2 19.2 kPa), 0.5 (mean PaO2 29.1 kPa) and 0.70 (mean PaO2 44.0 kPa) with only small variations in PaCO2 (4-5 kPa). There was a clear relationship between the degree of hyperoxemia and the degree of abnormality of the muscle tissue OPD: the higher the PaO2 level, the more abnormal was the muscle tissue OPD. Slightly disturbed (scattered) muscle tissue OPD:s appeared at PaO2 levels around 19 kPa, while increasingly scattered OPD:s appeared at PaO2 29 kPa and 44 kPa, respectively. At normal baseline PaO2 levels (mean PaO2 10.7 kPa) muscle OPD:s were normal. The time needed to achieve stable muscle tissue oxygen pressure levels after PaO2 had been increased was longer than expected, i.e., on average 45 min. The OPD shapes as well as the mode of reaction to hyperoxemia were found to be the same in the rabbit as in man. Our model displayed good macro- and microvascular stability and should be useful for studies on regulatory mechanisms of skeletal muscle oxygenation.

UR - http://www.scopus.com/inward/record.url?scp=0023987665&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023987665&partnerID=8YFLogxK

M3 - Article

C2 - 3374446

AN - SCOPUS:0023987665

VL - 4

SP - 169

EP - 192

JO - Microcirculation, Endothelium and Lymphatics

JF - Microcirculation, Endothelium and Lymphatics

SN - 0740-9451

IS - 2

ER -