In Vivo Comparison of Non-Gaseous Metabolite and Oxygen Transport in the Heart

Rose, Colin P.; Goresky, Carl A.; Bach, Glen G.; Bassingthwaighte, James B.; Little, Stephen

doi:10.1007/978-1-4615-9510-6_5

Cited by 7 publications

(5 citation statements)

References 16 publications

(20 reference statements)

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“…Therefore, for the tissue areas with large blood vessels and relatively high blood velocity, the oxygen exchange between arterioles and venules can be omitted. This conclusion is strongly supported by a lot of previous experiments and theoretical studies [100][101][102][103][104][105]148,149]. Further, one can find that the average oxygen concentration is extremely uniform over the whole intermediate layer, which has been experimentally verified [98].…”

Section: W-j Model Based Oxygen Transport Equationsupporting

confidence: 81%

“…Except for the above efforts, other models have also been formulated to reflect the heterogeneity of capillary architecture and hemodynamics in the brain [103,109]. For example, Ivanov et al [109] studied the distribution of oxygen partial pressure (PO 2 ) in a microvascular unit composed of a spindleshaped neuron surrounded by two capillaries.…”

Section: Overviewmentioning

confidence: 99%

“…Several mathematical models for precapillary and postcapillary transport indicated significant amounts of oxygen exchange between arterioles and the surrounding tissue [10,[97][98][99]. There were also discussions of the possibility of countercurrent exchange of oxygen between paired arterioles and venules [100][101][102][103][104][105]. Of the many existing oxygen transport models, only very limited researches took into consideration the anatomical vascular geometry.…”

Section: Overviewmentioning

confidence: 99%

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Cooling strategies and transport theories for brain hypothermia resuscitation

Jing

2007

Front. Energy Power Eng. China

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The brain is one of the most important organs in a biological body whose normal function depends heavily on an uninterrupted delivery of oxygen. Unlike skeletal muscles that can survive for hours without oxygen, neuron cells in the brain are easily subjected to an irreversible damage within minutes from the onset of oxygen deficiency. With the interruption of cardiopulmonary circulation in many cardiac surgical procedures or accidental events leading to cerebral circulation arrest, an imbalance between energy production and consumption will occur which causes a rapid depletion of oxygen due to the interrupted blood-flow to the brain. Meanwhile, the cooling function of the blood flow on the hot tissue will be stopped, while metabolic heat generation in the tissues still keeps running for awhile. Under such adverse situations, the potential for cerebral protection through hypothermia has been intensively investigated in clinics by lowering brain temperature to restrain the cerebral oxygen demands. The reason can be attributed to the decreased metabolic requirements of the cold brain tissues, which allows a longer duration for the brain to endure reduced oxygen delivery. It is now clear that hypothermia would serve as the principal way for neurologic protection in a wide variety of emergency medicines, especially in cerebral damage, anoxia, circulatory arrest, respiratory occlusion, etc. However, although brain cooling has been found uniquely significant in clinical practices, the serious lack of knowledge on the mechanisms involved prevents its further advancement in brain resuscitation. Compared with the expanded trials in clinics, only very limited efforts were made to probe the engineering issues involved, which turns out to be a major obstacle for the successful operation of brain hypothermia resuscitation. From the viewpoint of biothermal medical engineering, the major theories and strategies for administering brain cooling can generally be classified into three categories: heat transfer, oxygen transport and cooling strategy. Aiming to provide a complete overview of the brain hypothermia resuscitation, this article comprehensively summarizes the recent progresses made in theoretical, practical and experimental techniques in the area. Particularly, attention is paid to the mathematical models to quantify the heat and oxygen transport inside the cerebral tissues. Typical cooling strategies to effectively lower brain temperature and thus decrease oxygen consumption rate in the cerebral tissues are analyzed. Approaches to deliver oxygen directly to the target tissues are discussed. Meanwhile, some future efforts worth pursuing within the area of brain cooling are suggested.

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Section: W-j Model Based Oxygen Transport Equationsupporting

confidence: 81%

Section: Overviewmentioning

confidence: 99%

Section: Overviewmentioning

confidence: 99%

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Cooling strategies and transport theories for brain hypothermia resuscitation

Jing

2007

Front. Energy Power Eng. China

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“…Labeled sucrose does not penetrate the RBCs or the liver cells but does instantaneously equilibrate into the Disse space, so that concentrations in plasma and accessible Disse space are equal at each point along the length (that is, u = v). Accordingly, the single-sinusoid outflow profile for labeled sucrose is found to be (61, (4) where F, is the sinusoidal plasma flow. The tracer sucrose travels as a delayed wave with velocity W/[l + y S J .…”

Section: It Can Be Shownmentioning

confidence: 99%

“…Previous steady-state observations in the heart have demonstrated that in uzuo tissue oxygen tension values in muscle fibers are far below those in coronary artery and vein. Analysis of tracer oxygen studies in the heart indicated unexpected barrier-limited transfer (3) of tracer oxygen from cardiac capillaries to heart muscle; consumption of oxygen beyond this resistance accounted for the observed low tissue oxygen tension values (2,4). The resistance at the interface appeared to arise mainly from the microvascular structure, the continuous capillary endothelial lining in the heart.…”

mentioning

confidence: 98%

Flow-limited tracer oxygen distribution in the isolated perfused rat liver: Effects of temperature and hematocrit

et al. 1992

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We used the multiple-indicator dilution technique to examine the kinetics of tracer oxygen distribution and uptake in the rat liver perfused in a nonrecirculating fashion with blood. 51Cr-labeled 18O2-saturated erythrocytes, labeled albumin, sucrose and water (the tracers for oxygen and vascular, interstitial and cellular references) were injected simultaneously into the portal vein. Timed anaerobic samples were collected from the hepatic vein and analyzed by mass spectrometry for relative 18O2 enrichment and radioactivity. In a set of experiments performed at 32 degrees C, oxygen uptake was substantially diminished; tracer oxygen profiles approached those expected for a completely recovered, flow-limited substance. At 37 degrees C, much larger tracer oxygen sequestration occurred. Experiments were carried out at each temperature at higher and lower hematocrit, and oxygen consumption at each temperature was found to be independent of hematocrit. The tissue space of distribution for tracer oxygen relative to the total sinusoidal vascular content was influenced by the hematocrit: it was smaller at higher hematocrit and larger at lower hematocrit, as expected. The derived partition coefficient of oxygen for liver cells relative to plasma (expressed in terms of the liver and plasma water spaces) was, on average, 2.62 ml/ml; it was independent of the hematocrit. Analysis of the indicator dilution experiments indicates that the tracer oxygen is distributed into tissue in a flow-limited rather than a barrier-limited fashion, and that with this, an ongoing concomitant intracellular sequestration of tracer can be seen.

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