Micro, surface, and needle oxygen electrodes: comparison of physiological relevance and clinical acceptance.
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Biomedical subjects
Publications and source records attributed to F Kreuzer.
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An index of the efficiency of O2 transport in blood and delivery to tissues, the capacitance coefficient beta, was theoretically analyzed as a function of the position of the blood O2 dissociation curve (ODC). The P50 at which beta reaches its maximum is high at normoxia and decreases with lowering the ambient PO2. At very deep hypoxia this value becomes lower than the normal P50 of human blood. An increase of blood O2 capacity enlarges beta, particularly at deep hypoxia, and also increases the P50 at which maximal beta is reached. Changes of (a-v)O2 have ambivalent effects, depending on both P50 and PaO2. The capacitance coefficient beta was further calculated as a function of PaO2 at three values of P50, simulating the effect of a shift of the ODC. The capacitance coefficient is several times higher at deep hypoxia than at normoxia at all values of P50 used. A shift of the ODC to the left results in a moderate decrease of beta at mild hypoxia but in a large increase at severe hypoxia; a shift to the right has a reverse effect.
Skeletal muscle PO2 was studied during graded hemorrhagic shock in Labrador dogs by means of a polarographic needle PO2 electrode. Compared to hemodynamic, blood gas, biochemical, and hematologic variables, a shift to the left of the cumulative histogram of skeletal muscle PO2 was the earliest and most sensitive indicator of impaired skeletal muscle oxygenation. The mean arterial blood pressure and the mean of the medians of the skeletal muscle PO2, respectively, were as follows: during the control period 125 and 38.1 mm Hg, during the imminent shock period 143 and 24.5 mm Hg, and during the shock period 89 and 5.1 mm Hg. This electrode is suitable for clinical use.
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Quantitative evaluation of the myocardial left ventricular capillarity was performed in three groups of guinea pigs: a) animals native to high altitude collected in Andean mountains, b) animals born at sea level and subjected to a stimulated high altitude postnatally, c) animals born and kept at sea level. The number of capillaries and muscle fibers/mm(2) as well as the fiber capillary ratio and the diffusion distance were similar in all three experimental groups. The only difference found during the detailed analysis of the myocardial capillarity was a slightly lower percentage of the myocardial tissue in the extreme distance from the capillary found in the hearts of high altitude natives when compared to sea level animals. From these morphometric data the distribution of diffusion distances was derived which can be approximated by lognormal distribution. Capillary inhomogeneity expressed as log standard deviation was found to be similar in all three groups.
We studied the steady-state oxygen transfer across thin layers of respiring chicken gizzard smooth muscle and compared three models for oxygen consumption with respect to their influence on the facilitation of oxygen diffusion by myoglobin. These models assumed zero-order, Michaelis-Menten or exponential kinetics. The transport equation was solved for these models with simultaneous oxygen facilitation assuming chemical equilibrium between oxygen and myoglobin. Experimental flux data were obtained in two situations: a) high oxygen pressure throughout the layer of tissue providing maximum oxygen consumption and oxygen permeability, and b) anoxic conditions in part of the layer and with submaximal oxygen consumption and desaturation of myoglobin. Measurements in the presence of functional myoglobin were compared with data obtained after abolishing the transport function of myoglobin by application of 1 kPa carbon monoxide. It was found that oxygen consumption interferes with the facilitation effect. The oxygen pressure at half maximum oxygen consumption in the Michaelis-Menten model was 0.3 +/- 0.1 (S.E) kPa. The facilitation of the oxygen transport by myoglobin was 50 to 100% of the maximum value to be expected on the basis of the prevailing myoglobin concentration.
Adult bovine hemoglobin solutions were studied with respect to the influence of organic phosphates (adenosine-5'-triphosphate, 2,3-diphosphoglycerate, myo-inositolhexaphosphate) on the oxylabile proton binding (fixed-acid Haldane effect). At alkaline pH (less than 7.5) this Haldane effect is increased by organic phosphates, whereas at acid pH (less than 6.5) the effect is decreased; in the neutral pH range no unequivocal trend was found. The influence on the Haldane effect is caused by binding of organic phosphates to both deoxy- and liganded hemoglobin. The binding of 2,3-diphosphoglycerate and myo-inositolhexaphosphate causes a massive proton uptake. In going from deoxy- to liganded hemoglobin in the presence of organic phosphates the proton release due to phosphate release from deoxyhemoglobin and the proton uptake due to phosphate binding by liganded hemoglobin were shown to account for the phosphate-induced part of the fixed-acid Haldane effect.
We investigated oxylabile H+ binding and pH dependent oxygen binding of adult and newborn bovine hemoglobin as influenced by the organic phosphates 2,3-disphosphoglycerate (DPG), adenosine-5'-triphosphate (ATP), and myoinositol hexaphosphate (IHP). The oxygen affinity of newborn bovine hemoglobin is higher than that of adult hemoglobin over a pH over a pH range of 6.5 to 8. Both DPG and IHP decrease the oxygen affinity of adult bovine hemoglobin. IHP not only decreases the oxygen affinity, but also reduces the apparent cooperativity, whereas DPG does not affect cooperativity. The rise in logP50 upon addition of DPG is about equal for adult and newborn bovine hemoglobin: at pH 7.0 we find delta logP50 values of 0.14 and 0.13 respectively upon addition of a fivefold excess of organic phosphate. This agrees with the identical nature of the presumed organic phosphate binding site in these two hemoglobins, but contrasts with the situation in man: newborn human hemoglobin is much less influenced by organic phosphates than adult human hemoglobin.
The effect of a shift of the blood O2 dissociation curve (ODC) on the alveolar-arterial O2 gradient was studied in computer models of the lung with several degrees of VA/Q inequality during air breathing. A shift to the left decreases and a shift to the right increases not only the mixed-venous but also the arterial PO2. Consequently the alveolar-arterial O2 gradient is larger with a left and smaller with a right shift of the ODC. This effect of a shift of the ODC on the alveolar-arterial O2 gradient is negligible in a healthy lung but becomes quite considerable in a diseased lung with a severe mismatching of VA/Q.
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The oxygenation of layers of hemoglobin solutions thick enough to ensure chemical equilibrium between oxygen and hemoglobin has been analyzed theoretically assuming simultaneous diffusion of oxygen and oxyhemoglobin. The dimensionless transfer equation was solved for the finite and semi-infinite situation, the parameters being 1) the ratio of bound to physically dissolved oxygen after equilibration (H), 2) the ratio of carrier-mediated to free oxygen flux at steady state (D), and 3) the dimensionless saturation curve (characterized by phi 50). A parametric analysis provided plots of the dimensionless oxygenation time against these three dimensionless parameters. In this way, from the oxygenation times plotted as a function of the reciprocal oxygen driving pressure in any particular hemoglobin solution, the values of the oxygen permeability (or, knowing oxygen solubility, of the oxygen diffusion coefficient) and of the hemoglobin diffusion coefficient can be derived simultaneously.
The oxygenation of layers of deoxygenated hemoglobin solutions after a sudden exposure to a gas containing oxygen at a partial pressure P1 has been studied by a photometric method. Layer thicknesses varied between 50 and 250 micron, hemoglobin concentrations between 0.1 and 0.34kg/l, and oxygen partial pressures between 4.65 and 93.1 kPa (35 and 700 mmHg). The diffusion chamber containing the layer of hemoglobin solution permitted a step change in gas atmosphere without changing the optical apparatus constant. The following results were obtained: 1. The oxygen saturation increase is independent of the layer thickness when expressed as a function of time divided by layer thickness squared (normalized oxygenation time). This justifies the assumption of chemical equilibrium between oxygen and hemoglobin in the range considered. 2. The oxygen saturation increases proportionally to the square root of time over a wide range of oxygenation as expected. This range reaches to almost 100% oxygenation at P1=93.1kPa (700mmHg) but less far as P1 is lower. Thus at high P1 values there is a sharp boundary between the oxygenated and deoxygenated part of the layer allowing the application of the advancing front concept. 3. Fitting the theoretical equations derived in a preceding paper to the experimental results provides simultaneous values of the oxygen permeability (or, knowing oxygen solubility, of the oxygen diffusion coefficient) and of the hemoglobin diffusion coefficient. These values agree fairly well with values obtained by other authors from experiments yielding the diffusion coefficients of oxygen or hemoglobin separately.
In stress incontinence, urinary leakage can be controlled by support of the anterior vaginal wall by applying pressure directly at the bladder neck (the Marshall test) or applying pressure remotely. In the latter maneuver, a cotton ball, gripped in the jaws of a sponge stick, engages the vaginal vault near the apex and rotates it posteriorly and horizontally. This tenses the anterior vaginal wall thereby controlling stress-induced leakage. The mechanism of action and some surgical implications are discussed.
A new mathematical treatment is presented which simplifies the solution of carrier-diffusion problems. The method is generally applicable and is illustrated and tested for a specific, commonly occurring situation: facilitated diffusion of a single substrate through flat layers. Results predicted for total substrate flux are in excellent agreement with control computer calculations. The method also can be used to obtain concentration profiles for each species; here the results are good only if conditions at the boundaries are predicted correctly.
The effect of variation of blood hydrogen ion concentration on arterial and mixed venous PO2, ideal alveolar-arterial O2 pressure difference (PAiO2--PaO2), venous admixture (Qs/Qt), arterio-alveolar CO2 pressure difference (a--A)DCO2, physiological dead space to tidal volume ratio (VD/VT), cardiac output (Qt) and mean pulmonary arterial pressure (PAP) has been studied. Arterial and mixed venous PO2 increased and (PAiO2--PaO2) decreased with increasing blood hydrogen ion concentration. No change in Qs/Qt, (a--A)DCO2, VD/VT, Qt and PAP was observed. The effect of hydrogen ion concentration on arterial and mixed venous PO2 and on (PAiO2--PaO2) is mainly due to a shift of the blood oxyhemoglobin dissociation curve (ODC), i.e. due to the Bohr effect. The upper part of the ODC is more flat in alkalosis (shift to the left) than in acidosis (shift to the right). Therefore the same end-capillary to arterial O2 content difference results in a greater (PAiO2--PaO2) in alkalosis than in acidosis. Any factor influencing the slope of the upper part of the ODC is expected to affect the arterial PO2 and the (PAiO2--PaO2) by this mechanism. Similarly any factor shifting the steep part of the ODC is expected to affect the PO2 of the mixed venous blood.
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