The rate of oxygen release and its effect on capillary O2 tension: A mathematical analysis

Gutiérrez, Guillermo

doi:10.1016/0034-5687(86)90032-0

Cited by 92 publications

(51 citation statements)

References 16 publications

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“…Although it is dependent on multiple factors, optimal oxygen off-loading in skeletal muscle is achieved within a narrow range of VRBC (41). In the present study, the mean VRBC of the EDL muscle was no different in the CLP rats when compared with the SHAM rats, but this was primarily due to an increase in the number of stopped-flow (0 mLmls) capillaries.…”

Section: Methodscontrasting

confidence: 50%

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Lam¹,

Tyml²,

Martin³

et al. 1994

J. Clin. Invest.

334

208

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We hypothesized that normotensive sepsis affects the ability of the microcirculation to appropriately regulate microregional red blood cell (RBC) flux. An extensor digitorum longus muscle preparation for intravital study was used to compare the distribution of RBC flux and the functional hyperemic response in SHAM rats and rats made septic by cecal ligation and perforation (CLP). Using intravital microscopy, we found that sepsis was associated with a 36% reduction in perfused capillary density (from 35.3±+1.5 to 22.5±1.0 capillaries/mm of test line) and a 265% increase in stopped-flow capillaries (from 0.9±0.2 to 3.3±0.4 capillaries/mm); the spatial distribution of perfused capillaries was also 72% more heterogeneous. Mean intercapillary distance (ICD) increased 30% (from 25.7±0.8 to 33.5±1.6 ,um), and the proportion of capillary pairs with intercapillary distances > 33.8 ,um (the 75th percentile of ICDsHAM) was greater with sepsis. Mean capillary RBC velocity increased 17% in CLP rats (391 vs 333 ,um/s). Laser Doppler flowmetry was used to assess the functional hyperemic response of the extensor digitorum longus muscle before and after a period of maximal twitch contraction designed to increase oxygen demand. RBC flux was 36% lower in the CLP rats at rest. After contraction, RBC flux increased in both SHAM and CLP rats; however, the relative increase was less in the CLP group. We concluded that sepsis affects the ability of the skeletal muscle microcirculation to appropriately distribute RBC flux and to respond to increases in oxygen need. (J. Clin. Invest. 1994. 94

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Section: Methodscontrasting

confidence: 50%

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Lam¹,

Tyml²,

Martin³

et al. 1994

J. Clin. Invest.

334

208

View full text Add to dashboard Cite

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“…Two obvious consequences that affect oxygen transport are 1) a reduced surface area for the exchange of oxygen, and 2) a reduced transit time of RBCs through the exchange vessels of the SHRs. Gutierrez (8) has shown that under conditions of elevated oxygen demand (muscle contraction) and reduced transit time, a significant disequilibrium for oxygen can develop between the plasma and RBC hemoglobin. At normal hematocrit levels, almost all of the oxygen in blood is bound to the hemoglobin inside RBCs.…”

Section: Discussionmentioning

confidence: 99%

Prolonged tissue Po₂ reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

Smith

Barbee

Ward

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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. Prolonged tissue PO2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 287: H401-H407, 2004. First published February 26, 2004 10.1152/ajpheart.00980.2002We tested the hypothesis that a deficit in oxygen extraction or an increase in oxygen demand after skeletal muscle contraction leads to delayed recovery of tissue oxygen tension (PO2) in the skeletal muscle of hypertensive rats compared with normotensive rats. Blood flow and PO2 recovery at various sites in the spinotrapezius muscle of spontaneously hypertensive rats (SHRs) were evaluated after a 3-min period of muscle contraction and were compared with corresponding values in WistarKyoto rats ( in the SHRs compared with the WKYs can be explained by a decrease in oxygen diffusion from the rarefied microvascular network due to the increased RBC velocity and the shorter residence time in the microcirculation and the consequent disequilibrium for oxygen between plasma and RBCs. The delayed recovery of venular PO 2 in the SHRs is consistent with this explanation, as venular PO 2 is slowly restored to baseline by release of oxygen from the RBCs. This leaves the arterioles in the primary role as oxygen suppliers to restore PO 2 in the tissue after muscle contraction. hypertension; oxygen tension; hypoxia; microvascular blood flow; rarefaction; phosphorescence quenching microscopy; disequilibrium

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“…Many models for oxygen transport from blood into tissue have been investigated [1][2][3][4][5][6][7], but they are mainly concerned with steady state and do not allow for transient solutions. Also, the models are over-simplified and neglect certain critical aspects of the oxygen transport system.…”

Section: Introductionmentioning

confidence: 99%

A computational model of oxygen transport from red blood cells to mitochondria

Beyer¹,

Bassingthwaighte

Deußen

2002

Computer Methods and Programs in Biomedicine

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A computational model of oxygen transport from red blood cells to mitochondria with subsequent reaction to water is presented. This computational model consists of a five region convectiondiffusion-reaction mathematical model which is solved using a standard numerical time-split method. The unique feature of this mathematical model is the treatment of the red blood cells and the plasma as two separate flows. The numerical method is second order accurate overall. This computational model is useful for analyzing residue data from positron emission tomography or data from multiple indicator dilution curves.

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The rate of oxygen release and its effect on capillary O2 tension: A mathematical analysis

Cited by 92 publications

References 16 publications

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Prolonged tissue Po₂ reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

A computational model of oxygen transport from red blood cells to mitochondria

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The rate of oxygen release and its effect on capillary O2 tension: A mathematical analysis

Cited by 92 publications

References 16 publications

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Microvascular perfusion is impaired in a rat model of normotensive sepsis.

Prolonged tissue Po2 reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats

A computational model of oxygen transport from red blood cells to mitochondria

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Product

Resources

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Prolonged tissue Po₂ reduction after contraction in spinotrapezius muscle of spontaneously hypertensive rats