O2 Transport in Cerebral Microregions (Mathematical Simulation)

1986 ◽  
Vol 108 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Yu. Ya. Kislyakov ◽  
K. P. Ivanov

The effects of the circulation rate in capillaries, the intensity of O2 consumption by nerve cells and the capillary network density on the O2 tension distribution in the cerebral cortex have been studied, utilizing a mathematical model simulating actual neuron-capillary relationships. The model has been written as a system of equations in partial derivatives, its solution obtained by the net-point method. Regulatory variations of the capillary circulation rate in certain cerebral microregions have been shown to ensure similar changes in oxygen supply throughout the region. A drop of the pO2 level in a cerebral microregion with a rising O2 consumption by nerve cells is shown to be due, by 75 percent, to the increase of O2 consumption and by 25 percent, to the lower pO2 in the capillaries. Conversely, an increase in pO2 in microregions resulting from a lower O2 consumption by neurons is due by 75 percent, to a pO2 rise in capillaries and by 25 percent, at the expense of an O2 consumption decrease. In cerebral regions differing in capillary network density by 20 percent, changes in the conditions for oxygen supply to tissue are due by 1/3 to pO2 variations in the capillaries and by 2/3 to alterations in the diffusion distances.

1989 ◽  
Vol 66 (1) ◽  
pp. 120-127 ◽  
Author(s):  
D. G. Nichols ◽  
S. Howell ◽  
J. Massik ◽  
R. C. Koehler ◽  
C. A. Gleason ◽  
...  

We determined the relationship of diaphragmatic contraction rate to diaphragmatic blood flow (Qdi), metabolism, and contractility in nine open-chested mechanically ventilated newborn lambs. The diaphragm was paced for 15 min at slow (20/min) and fast (100/min) contraction rates each followed by a 30-min rest period. There was a mild reduction in transdiaphragmatic pressure (Pdi) during the slow contraction period accompanied by a shift to the right of the curve relating stimulation frequency (10–100 Hz) to Pdi. Pdi returned to control at the start of the fast contraction period, but then fell by 30% within 2 min with continued fast contraction rates. The frequency-Pdi curve was significantly shifted to the right. Qdi, O2 transport, and O2 consumption increased during slow contraction and to an even greater extent during fast contraction. Fractional O2 extraction reached an apparent maximum during slow contraction. Lactate efflux from the right phrenic vein during slow contraction remained unchanged from control. During fast contraction lactate efflux rose proportionately more than did O2 consumption. We conclude that the energy demands at fast rates of diaphragmatic contraction in newborn lambs cannot be met by aerobic metabolism alone despite increasing O2 transport to the diaphragm.


1982 ◽  
Vol 53 (4) ◽  
pp. 865-872 ◽  
Author(s):  
M. H. LeBlanc ◽  
U. R. Kotagal ◽  
L. I. Kleinman

The effect of hypervolemic polycythemia (Hct 62–77) on O2 transport and O2 consumption (Vo2) was studied in 16 unanesthetized newborn dogs (age 3–10 days). A control group of 10 newborn dogs (3–10 days old) was made hypervolemic but not polycythemic in an otherwise identical experiment. Hypervolemia was attained by infusing 33 ml/kg of either packed red blood cells (polycythemia) or whole blood (controls). In the polycythemic group as a result of the transfusion, cardiac output (CO) decreased by 50% (P less than 0.001), peripheral vascular resistance (PVR) increased by 170% (P less than 0.001), but O2 transport did not change significantly, and Vo2 decreased only slightly by 13% (P less than 0.01). In the 10 control animals there were no significant changes in CO, PVR, O2 transport, or Vo2 as a result of the transfusion. Blood lactate increased only slightly in experimental (35%, P less than 0.04) and control animals (23%, NS). The ability of the animals to increase their O2 transport and Vo2 was tested by measuring the changes induced by cold stress. Cold stress produced a 20% increase in Vo2 (P less than 0.05) in both the polycythemic and the control animals. Thus in spite of a decreased CO in the nonstressed state the polycythemic animals were still able to increase O2 transport and Vo2 in response to cold stress. These results suggest that the newborn animal is capable of regulating CO to maintain O2 transport appropriate to uptake under conditions of hypervolemic, polycythemic hyperviscosity, and environmental cold stress.


1996 ◽  
Vol 271 (2) ◽  
pp. H721-H737 ◽  
Author(s):  
T. K. Roy ◽  
A. S. Popel

Characterizing the resistances to O2 transport from the erythrocyte to the mitochondrion is important in understanding potential transport limitations. A steady-state model of this process was developed to predict the minimum (critical) end-capillary PO2 required to prevent hypoxia at maximal O2 consumption (VO2max) in a circular region of tissue surrounding the venular end of a capillary. Capillary density was used as a measure of O2 delivery, and mitochondrial density was used as a measure of O2 consumption. The effects of oxyhemoglobin dissociation kinetics and diffusion facilitation by hemoglobin in the erythrocytes and facilitation by myoglobin in the tissue were taken into account. Calculations made for selected skeletal muscles, diaphragm, and myocardium in three adaptive animal pairs (dog and goat, horse and cow, and pony and calf) yielded values of end-capillary PO2 that were consistent with measured values of mixed venous PO2 in maximally working animals. Values of end-capillary PO2 were found to be uncorrelated with values of VO2max in different muscles. No significant difference in end-capillary PO2 was found between similar muscles of athletic versus nonathletic animals. Predicted intracapillary O2 transport resistance ranged from 18 to 54% of the total transport resistance in the O2 pathway. Further investigation is required to explore the extent to which spatial and temporal heterogeneities in O2 delivery and consumption play a role in O2 transport.


1987 ◽  
Vol 252 (2) ◽  
pp. R341-R347 ◽  
Author(s):  
D. G. Covell ◽  
J. A. Jacquez

We have examined the role of myoglobin to facilitate O2 diffusion to active mitochondria in skeletal muscle by constructing computer-simulation experiments. Steady-state mitochondrial O2 consumption under different conditions of supply partial pressure of O2 (PO2) in a system with and without myoglobin were examined for a one-dimensional slab of tissue. O2 consumption by mitochondria was saturable with the mitochondria located in bands at uniform intervals throughout the tissue. Under these conditions, myoglobin provides a measurable increase in O2 transport for supply PO2 below 10 Torr and diffusion lengths expected for skeletal muscle fibers. We conclude that under circumstances where hypoxia lowers PO2 below 10 Torr that myoglobin begins to provide a measurable increase in O2 delivery to mitochondria.


1992 ◽  
Vol 263 (1) ◽  
pp. H208-H217
Author(s):  
A. Saltiel ◽  
D. J. Sanfilippo ◽  
R. Hendler ◽  
G. Lister

We tested whether digoxin would limit tissue hypoxia during severe anemia by improving peripheral O2 distribution or decreasing O2 demands. Hematocrit (Hct) was reduced in eight control and eight digoxin-treated pigs from 27-28% to 17-18, 11-12, and 7-8%. Whole body and hindlimb blood flow, O2 transport, O2 extraction, and O2 consumption and serum catecholamines (epinephrine and norepinephrine) were determined at each Hct. Arterial and femoral venous lactate and O2 deficit were obtained to reflect tissue hypoxia. Cardiac output was significantly greater (P less than 0.05) with digoxin, as expected, but there were no differences in hindlimb blood flow. Also, whole body and hindlimb O2 extractions were equal in both groups for similar levels of O2 transport, suggesting that digoxin did not alter the relationship of O2 flow to metabolism in regional circulations. As whole body O2 consumption fell, controls accumulated more (P less than 0.05) O2 deficit and arterial lactate than the digoxin group. Furthermore, the slope demonstrating the linear increase of lactate with respect to O2 deficit was much steeper in controls (y = 1.11 + 0.06x) than in digoxin (y = 1.36 + 0.02x), suggesting that there were differences in the degree of tissue hypoxia for comparable O2 deficit. This may be attributed to the marked differences in catecholamine response: epinephrine was higher in controls at Hct of 7-8% and norepinephrine was higher at Hcts of 11-12 and 7-8%. Digoxin may have inhibited the release of catecholamine or reduced the stimulus for catecholamine secretion during anemia. We speculate that digoxin markedly improved the balance between peripheral O2 supply and demand during anemia by inhibiting catecholamine thermogenesis, thereby decreasing O2 demands. This may explain some of the salutary effects of glycosides in high-output cardiac failure with normal ventricular function.


1977 ◽  
Vol 233 (1) ◽  
pp. H106-H113 ◽  
Author(s):  
K. M. Jan ◽  
S. Chien

Twenty-five closed-chest pentobarbitalized dogs were used for studying coronary flow dynamics and myocardial oxygen utilization following variations of hematocrit (Hct) by isovolumetric exchange of blood with plasma or packed red cells. Coronary blood flow (133Xe washout) and cardiac output varied inversely with Hct. Coronary systemic, and pulmonary flow resistances varied in the same direction with Hct. Blood viscosity played a significant role in determining the flow resistances in these three regions. Analysis of vascular hindrance (vascular resistance/blood viscosity) suggested that coronary vasodilation occurred following Hct changes beyond the range of 20-60%. In systemic and pulmonary circulations, however, there was vasoconstriction following hemodilution. The range of optimum Hct for maximum O2 transport (blood flow X arterial O2 content) was much wider in coronary (20-60% Hct) than in systemic circulation (40-60% Hct). The O2 consumptions in total body and in myocardium were essentially constant over a wide range of Hct (20-60%). The maintenance of total body O2 consumption over the Hct range of 20-40% was attributable to an increase in A-V O2 extraction. The O2 extraction ratio in the coronary circulation was constant over the entire range of Hct studied, suggesting that the myocardial O2 consumption was primarily determined by the coronary O2 transport.


1980 ◽  
Vol 14 (1-2) ◽  
pp. 233-243 ◽  
Author(s):  
W. Meier-Ruge ◽  
O. Hunziker ◽  
U. Schulz ◽  
H.-J. Tobler ◽  
A. Schweizer

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 454A ◽  
Author(s):  
Mattias Casutt ◽  
Burkhardt Seifert ◽  
Thomas Pasch ◽  
Edith R. Schmid ◽  
Marko I. Turina ◽  
...  

1991 ◽  
Vol 70 (4) ◽  
pp. 1845-1853 ◽  
Author(s):  
Z. Turek ◽  
K. Rakusan ◽  
J. Olders ◽  
L. Hoofd ◽  
F. Kreuzer

A model of myocardial oxygenation was developed that allows calculation of Po2 histograms under varying conditions. The model consists of parallel tissue cylinders with varying radii, simulating the heterogeneity of capillary spacing, in agreement with our previous experimental results. The facilitated diffusion of O2 by myoglobin, an additional resistance to diffusion at the capillary level, and the Michaelis-Menten type of O2 consumption were also incorporated. The shape of the histograms depends on input data. When no additional barrier to O2 transport is included, the histograms resemble those obtained with Po2 surface electrodes, and they are strongly dependent on heterogeneity in capillary spacing and capillary blood flow. On the other hand, an inclusion of an additional capillary barrier combined with the Michaelis-Menten type of O2 consumption can generate Po2 histograms similar to those derived from myoglobin cryospectroscopy. In this case, the Po2 histograms are relatively independent of heterogeneity of capillary spacing and blood flow. The facilitation of O2 diffusion by myoglobin has only a modest effect on the form of the histograms in all situations considered.


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