Kovách / Dóra / Kessler Oxygen Transport to Tissue

Satellite Symposium of the 28th International Congress of Physiological Sciences, Budapest, Hungary, 1980
1. Auflage 2013
ISBN: 978-1-4831-9016-7
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)

E-Book, Englisch, 354 Seiten

Advances in Physiological Sciences, Volume 25: Oxygen Transport to Tissue covers the proceedings of the satellite symposium of the 28th International Congress of Physiological Science, held in Budapest, Hungary in 1980. This book mainly focuses on the relation of oxygen transport and delivery to heterogeneities, autoregulation of blood flow, organ function, and rheology. This compilation is divided into five sessions. The first two sessions encompass the models and experiments on the relationship between oxygen transport and heterogeneities. The subsequent session presents papers concerned with autoregulation of blood flow and oxygen delivery. The last two sessions are devoted to presenting papers on oxygen transport and organ function and rheology and oxygen transport. This compendium will be invaluable to those studying oxygen transport and its relationship with other biological processes.

Autoren/Hrsg.

Kovách, A. G. B.

Dóra, E.

Kessler, M.

Leseproben

TISSUE OXYGEN SUPPLY AND CRITICAL OXYGEN PRESSURE

D.W. Lübbers,     Max-Planck-Institut für Systemphysiologie, Rheinlanddamm 201, 4600 Dortmund 1, FRG

Publisher Summary

This chapter discusses tissue oxygen supply and critical oxygen pressure. It is well known that for the whole animal as well as for the isolated organ, in a certain range, the O2 consumption, vO2, is independent of the O2 offered by the respired gas mixture or by the arterial blood. It is found that when oxygen is reduced below this range, a reaction threshold is reached and compensatory mechanisms are put into action to maintain the O2 consumption and, thus, the energy consumption at the same level. There is a point at which the compensatory mechanisms are exhausted. This state can be called critical threshold, critical state of oxygen supply, or simply critical oxygen supply. It means, in this state the oxygen supply limits the oxygen consumption.

Recently it has been questioned whether it is still sensible to use the term “critical oxygen pressure” as an essential parameter to describe tissue hypoxia or anoxia. In the following I like to show the usefulness but also the limitation of this expression. Since the expression was coined from physiological experiments I will begin to discuss these physiological results.

It is well known that for the whole animal as well as for the isolated organ in a certain range the O2 consumption, O2, is independent of the O2 offered by the respired gas mixture or by the arterial blood (see for example 19, 15, 4). When oxygen is reduced below this range a reaction threshold is reached and compensatory mechanisms are put into action to maintain the O2 consumption - and thus the energy consumption - at the same level. But there is a point at which the compensatory mechanisms are exhausted: This state can be called “critical threshold or critical state of oxygen supply” or simply “critical oxygen supply”. It means, in this state the oxygen supply limits the oxygen consumption. The situation of a critical O2 supply has been studied so extensively that it is impossible to review or even mention the main experimental work; instead of that, I shall discuss some examples to elucidate our problem. In the earlier experiments the different criteria for a sufficient oxygen supply that were applied, were: 1) oxygen consumption, 2) lactate balance, and 3) functional state. As later on measurements of tissue concentrations became possible, the tissue concentration of lactate, pyruvate and adenine nucleotides or a relationship such as the lactate/pyruvate ratio, the phosphate potential or the energy charge (see Siesjö, 1978) were used.

1) The O2 consumption criterion was used by Stainsby (1966). He measured the dependence of the O2 consumption of dog skeletal muscles (mm. gastrocnemius - plantaris) on the arterial PO2, PaO2. The critical situation of oxygen supply was produced by reducing PaO2. occurred during rest at a PaO2 of 8 kPa (60 mm Hg) and a PvO2 of 3.33 kPa (25 mm Hg) and during work at a PaO2 of 6.66 (50 mm Hg) and a PvO2 of 1.33 kPa (l0 mm Hg)• Although the O2 consumption during work was 8 times higher than during rest (40/ul O2/g. min as compared to 5/ul O2/g. min), the blood Po2 values during work were smaller. This difference can be explained by the increased number of perfused capillaries in the working muscle which reduce the supply area of a single capillary, and by the increased flow. The experiments demonstrated the strong influence of flow and capillary geometry.

2) The lactate balance criterion was used by Bretschneider (1958). He measured the arteriovenous lactate difference of the dog heart muscle. As long as the O2 supply of the heart muscle was sufficient, lactate was consumed. Insufficient oxygen supply was accompanied by lactate production. Bretschneider showed that the transition point from lactate consumption to lactate production could be related to the magnitude of the venous Po2, independent of the way by which the critical oxygen supply was produced. He found in normal dogs (o2 = 150/ul O2/g. min) the transition point was at about PvO2 = 0.8 kPa (6 mm Hg). At an O2 consumption reduced to a third (o2 = 50 - 80/ul O2/g. min) it was reduced to a PvO2 = 0.26 kPa (2 mm Hg) and at doubled O2 consumption (o2 = 300/ul O2/g. min) it was increased to 1.87 kPa (14 mm Hg). These different transition points are in accordance with the changes of flow and tissue respiration.

3) The functional state criterion for O2 supply was used by Opitz and Schneider (1950) in their review and analysis of the oxygen supply of the brain. They found that the functional state can be at best correlated with the venous Po2 in the sinus sagittalis. The normal Pvo2 of 4.53 kPa (35mm Hg) can decrease to ca 3.73 kPa (28 mm Hg) without any detectable reaction but with a further decrease in Pvo2 blood flow increases to maintain the Pvo2 close to this level. Further reduction of Pvo2 shows first signs of changes in the ECG and in man higher mental functions are impaired. The critical oxygen supply is reached when the Pvo2 becomes smaller than 2.53 - 2.27 kPa (19 - 17 mm Hg). Under this condition man looses consciousness. The changes, however, are still reversible. They become irreversible when Pvo2 is lowered to 1.6 kPa (12 mm Hg) over a certain period of time.

The direct tissue measurements of lactate and adenine nucleotides corroborate these results (17). These examples show the complexity of our system but they also demonstrate that there is a definite state at which a critical O2 supply is reached. The occurrence of a critical O2 supply is influenced by many parameters but the venous Po2 - and not the venous O2 content - seems to be an important indicator of tissue oxygen supply. How can this be explained: It can be easily deduced from the physiological laws of oxygen supply, which concern 1) the O2 transport by blood 2) the O2 transport by diffusion and 3) the behavior of tissue oxygen consumption.

1) O2 transport by blood

    The amount of oxygen which can be supplied to the tissue depends on a) the oxygen content of blood, Co2, and b) blood flow, B.

a) Oxygen content of blood. Under physiological conditions the main amount of oxygen is chemically bound to hemoglobin

Co2(chem) = 1.34. cHb. So2

    CHb, concentration of hemoglobin in g/dl; So2, fractional oxygen saturation; 1.34, ml O2 per g hemoglobin.

    and only a small amount of oxygen is physically dissolved

Co2(phys) = ap. Po2

ap, O2 solubility coefficient of plasma.

    Thus the total amount of oxygen

Co2(blood) = Co2(chem) + Co2(phys)

depends essentially on the hemoglobin concentration and the fractional O2 saturation. The fractional O2 saturation depends on the blood Po2. This dependence is described by the O2 dissociation curve.

b) Effect of flow. The O2 content of the arterial blood is offered and delivered to the tissue. In steady state the difference between the O2 content of arterial and venous blood, the AVDo2 times blood flow corresponds to the tissue respiration

    It is important to note that with constant tissue respiration the AVDo2 is a hyperbolic function: that means that small flow changes are very effective in offering more O2 or in reducing the O2 supply, whereas at high flow the same absolute change has practically no effect.

2) O2 transport by diffusion

    The oxygen transport within the tissue is mainly performed by diffusion. The parameters, which govern the diffusion process can be easily seen from the diffusion equation for a simple layer

    D, diffusion coefficient; x, thickness of diffusion layer.

    The O2 flux, Io2, depends a) on the oxygen conductivity (D.a) and b) on the Po2 gradient, ? Po2/?x.

a) In the product (D.a) D determines the “speed” with which the molecules travel - according to equation s-2 = 6 D.t, s-2 is the square of the mean distance which the molecule travels during time t - and a gives the number of molecules which actually travel. The oxygen conductivity (D.a) characterizes the individual property of the tissue; it increases with temperature as well as with content of water and lipids, but under normal physiological conditions its variation is only small.

b) The Po2 gradient is the important factor for the O2 transport. We should mention that fo£ diffusion of gases the oxygen pressure is the driving force and not the oxygen content. This is especially important for systems with varying values of a. The importance of the oxygen pressure for the O2 transport in the tissue explains why the critical oxygen supply could be correlated to the venous oxygen pressure and not to the venous oxygen content of the blood.

    Two other important factors which influence...