Arteriolar Contribution to Microcirculatory CO2/O2 Exchange

Ye, Guo-Fan; Buerk, Donald G.; Jaron, Dov

doi:10.1006/mvre.1995.1063

Cited by 10 publications

(4 citation statements)

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“…Similar progressive declines in the oxygen levels inside precapillary vessels have also been observed in other tissues: cat pia [11]; hamster retractor muscle [17,18,33]; hamster dorsal skinfold [14], and rat mesentery [35]. In addition, earlier modeling studies of microvascular oxygen transport predicted significant diffusion of oxygen from the arteriolar network [24,37]. In postcapillary vessels, we found no statistical difference in the centerline PO 2 between two orders of venules.…”

Section: Discussionsupporting

confidence: 85%

“…In addition, comparisons of oxygen measurements between microelectrodes and microspectrophotometry [ 20 ], as well as microelectrodes and phosphorescence quenching [ 3 , 21 ], have demonstrated good agreement among the methods. Further, mathematical modeling studies of microvascular oxygen transport [ 23 , 24 , 37 ] predict significant diffusion of oxygen from the arteriolar network. At the present time, the importance of this arteriolar loss of oxygen and the destination of the oxygen are not completely understood.…”

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confidence: 99%

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Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Carvalho

Pittman

2008

Microcirculation

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Section: Discussionsupporting

confidence: 85%

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confidence: 99%

Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Carvalho

Pittman

2008

Microcirculation

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“…For large vessels that averaged 29 ± 1.3 μm in diameter the distance to the border of dendritic damage was 40 ± 21 μm ( n = 10, 704 measurements). It is conceivable that these large vessels in part support nearby dendrites through limited gas exchange [19]. However, since large vessels did not define all borders we do not feel they are an absolute requirement for support of dendrites.…”

Section: Resultsmentioning

confidence: 92%

Imaging the Impact of Cortical Microcirculation on Synaptic Structure and Sensory-Evoked Hemodynamic Responses In Vivo

2007

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In vivo two-photon microscopy was used to image in real time dendrites and their spines in a mouse photothrombotic stroke model that reduced somatosensory cortex blood flow in discrete regions of cortical functional maps. This approach allowed us to define relationships between blood flow, cortical structure, and function on scales not previously achieved with macroscopic imaging techniques. Acute ischemic damage to dendrites was triggered within 30 min when blood flow over >0.2 mm2 of cortical surface was blocked. Rapid damage was not attributed to a subset of clotted or even leaking vessels (extravasation) alone. Assessment of stroke borders revealed a remarkably sharp transition between intact and damaged synaptic circuitry that occurred over tens of μm and was defined by a transition between flowing and blocked vessels. Although dendritic spines were normally ~13 μm from small flowing vessels, we show that intact dendritic structure can be maintained (in areas without flowing vessels) by blood flow from vessels that are on average 80 μm away. Functional imaging of intrinsic optical signals associated with activity-evoked hemodynamic responses in somatosensory cortex indicated that sensory-induced changes in signal were blocked in areas with damaged dendrites, but were present ~400 μm away from the border of dendritic damage. These results define the range of influence that blood flow can have on local cortical fine structure and function, as well as to demonstrate that peri-infarct tissues can be functional within the first few hours after stroke and well positioned to aid in poststroke recovery.

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“…There are other implications for coupled NO and O 2 transport that were not fully explored in our simulations. For example, we did not include the longitudinal decrease in intravascular blood P O 2 along vascular networks that has been predicted from our previous O 2 transport models (50)(51)(52)(53) and is observed experimentally, as reviewed by Tsai et al (41). For example, intravascular blood P O 2 values determined by optical phosphorescence quenching in the smallest skinfold arterioles of conscious hamsters decrease to values in the 30-to 40-torr range, which is below the value of 50 torr used in the simulation for a 20-µm-diameter arteriole shown in Figure 5, and significantly below the value of 70 torr used in our simulations for larger arterioles (Figures 3, 4, 6).…”

Section: Discussionmentioning

confidence: 99%

Impact of the Fåhraeus Effect on NO and O₂ Biotransport: A Computer Model

2004

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Nitric oxide (NO) and oxygen (O2) transport in the microcirculation are coupled in a complex manner, since enzymatic production of NO depends on O2 availability, NO modulates vascular tone and O2 delivery, and tissue O2 consumption is reversibly inhibited by NO. The authors investigated whether NO bioavailability is influenced by the well-known Fåhraeus effect, which has been observed for over 70 years. This phenomenon occurs in small-diameter blood vessels, where the tube hematocrit is reduced below systemic hematocrit as a plasma boundary layer forms near the vascular wall when flowing red blood cells (rbcs) migrate toward the center of the bloodstream. Since hemoglobin in the bloodstream is thought to be the primary scavenger of NO in vivo, this might have a significant impact on NO transport. To investigate this possibility, the authors developed a multilayered mathematical model for mass transport in arterioles using finite element numerical methods to simulate coupled NO and O2 transport in the blood vessel lumen, plasma layer, endothelium, vascular wall, and surrounding tissue. The Fåhraeus effect was modeled by varying plasma layer thickness while increasing core hematocrit based on conservation of mass. Key findings from this study are that (1) despite an increase in the NO scavenging rate in the core with higher hematocrit, the model predicts enhanced vascular wall and tissue NO bioavailability due to the relatively greater resistance for NO diffusion through the plasma layer; (2) increasing the plasma layer thickness also increases the resistance for O2 diffusion, causing a larger P(O2) gradient near the vascular wall and decreasing tissue O2 availability, although this can be partially offset with inhibition of O2 consumption by higher tissue NO levels; (3) the Fåhraeus effect can become very significant in smaller blood vessels (diameters <30 microm); and (4) models that ignore the Fåhraeus effect may underestimate NO concentrations in blood and tissue.

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Arteriolar Contribution to Microcirculatory CO2/O2 Exchange

Cited by 10 publications

References 0 publications

Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Imaging the Impact of Cortical Microcirculation on Synaptic Structure and Sensory-Evoked Hemodynamic Responses In Vivo

Impact of the Fåhraeus Effect on NO and O₂ Biotransport: A Computer Model

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Arteriolar Contribution to Microcirculatory CO2/O2 Exchange

Cited by 10 publications

References 0 publications

Longitudinal and Radial Gradients of PO2 in the Hamster Cheek Pouch Microcirculation

Longitudinal and Radial Gradients of PO2 in the Hamster Cheek Pouch Microcirculation

Imaging the Impact of Cortical Microcirculation on Synaptic Structure and Sensory-Evoked Hemodynamic Responses In Vivo

Impact of the Fåhraeus Effect on NO and O2 Biotransport: A Computer Model

Contact Info

Product

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Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Longitudinal and Radial Gradients of PO₂ in the Hamster Cheek Pouch Microcirculation

Impact of the Fåhraeus Effect on NO and O₂ Biotransport: A Computer Model