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P Haab

Publications and source records attributed to P Haab.

7 recordsLinked to original sources
PubMed1991

Oxygen supply and uptake in tissue models with unequal distribution of blood flow and shunt.

The effects of unequal distribution of blood flow on O2 uptake are studied on a model composed of 3 tissues compartments with blood flow/O2 requirement ratios in the relation 9:3:1 (unequal blood flow model), a model with 33% shunt blood flow (shunt model), and a single compartment model without shunt (reference model). Diffusion limitation is assumed to be absent. Total blood flow (Q), arterial O2 content (CaO2) and O2 requirement of tissue are varied singly, and the resulting (mixed) venous O2 content (CvO2) and O2 uptake are calculated. In the reference model, CvO2 become zero, and O2 uptake starts falling below the O2 requirement, as soon as the O2 delivery (Q.CaO2) becomes smaller than the O2 requirement. In contrast, in the unequal blood flow model, decrease in the ratio O2 uptake/O2 requirement and in CvO2 sets in earlier, and proceeds more gradually, with decreasing Q or CaO2 or increasing O2 requirement; this is, because O2 delivery limitation sets in sequentially in the compartments, starting with the least perfused compartment. The shunt model behaves similarly to the reference model if Q or O2 requirement is varied, and to the unequal blood flow model if CaO2 is varied. Some features such as the parallel fall of O2 uptake and of CVO2 with decreasing CaO2, common to the unequal blood flow and shunt models, are similar to expected effects of diffusion limitation. Therefore, when the influence of diffusion limitation on tissue O2 supply is to be investigated quantitatively, the effects of a possible unequal distribution of blood flow must be taken into account.

Animals↗
PubMed1990

The effect of carbon monoxide on respiration.

In this review the effects of carbon monoxide on tissular oxygenation, at doses which are compatible with life, are considered. In a first section the relative CO-O2 affinity (M*) of various O2 carrying proteins is compared; M* is about 220 for hemoglobin, 20-25 for myoglobin and close to unity for cytochrome oxidases. Thus most of the acute CO toxicity should not be considered as due to malfunction of the intracellular respiratory chain. In addition the differences in M* are caused more by the changes in O2 affinity than by those in CO affinity. The second section deals with the changes in the O2 equilibrium curve (OEC) induced by the presence of HbCO in blood, i.e. the hyperbolization of this curve due to the progressive loss of allostery due to the preferential binding of CO to Hb. The functional importance of this phenomenon lies in the fact that the lower part of the OEC is shifted to the left, whereas the upper part is shifted to the right to an extent which depends upon the amount of HbCO. Thus the effects of the so-called CO anemia are considered to be due both to the reduction of functional Hb and to the reduced partial pressure in the hypoxic range of the OEC. The third section presents recent data concerning the effect of HbCO on the VO2max of the isolated gastrocnemius preparation. The results were obtained in hypoxia under conditions where perfusion and arterial O2 content, i.e. O2 delivery, were the same with and without 30% HbCO. The salient finding is a 26% reduction of VO2max under conditions of CO anemia as compared to hypoxia alone. Interestingly, the PO2 of the venous effluent of the muscle is found to be the same in both cases which leads to the interpretation that it is not the reduction of the mean capillary PO2 but rather a decrease of the blood-to-mitochondria O2 conductance which causes the fall in VO2max.

Animals↗
PubMed1990

Experimental support for the theory of diffusion limitation of maximum oxygen uptake.

The four experiments summarized above demonstrate that there is a strong relationship between both measured muscle venous PO2 and calculated mean muscle capillary PO2 and VO2max. This is true for whole body or exercising muscle VO2max, and is seen both in isolated canine gastrocnemius and intact man. This behavior is exactly what would be expected if the diffusing properties for oxygen in skeletal muscle play a constraining role in setting maximum VO2. These data therefore support the hypothesis we advanced (Wagner, 1988a; Wagner, 1988b), that it is a quantitative integrative relationship between convective and diffusive phenomena that combine to set maximum VO2. A specific prediction of this integrative hypothesis (i.e., the non-uniqueness of VO2max as a function of convective oxygen delivery) was confirmed (Experiment 3). While at this point in time phenomena such as perfusion heterogeneity and muscle shunts cannot be quantitatively taken into account in such analyses, the remarkable concurrence between expectations of the hypothesis and experimental data continue to lend support to the basic idea that maximum VO2 is not limited by any single step of the oxygen transport pathway from atmosphere to mitochondria, but rather by the way in which each and every step combines with every other step to determine oxygen supply.

Animals↗
PubMed1989

Evidence for tissue diffusion limitation of VO2max in normal humans.

We recently found [at approximately 90% maximal O2 consumption (VO2max)] that as inspiratory PO2 (PIO2) was reduced, VO2 and mixed venous PO2 (PVO2) fell together along a straight line through the origin, suggesting tissue diffusion limitation of VO2max. To extend these observations to VO2max and directly examine effluent venous blood from muscle, six normal men cycled at VO2max while breathing air, 15% O2 and 12% O2 in random order on a single day. From femoral venous, mixed venous, and radial arterial samples, we measured PO2, PCO2, pH, and lactate and computed mean muscle capillary PO2 by Bohr integration between arterial (PaO2) and femoral venous PO2 (PfvO2). VO2 and CO2 production (VCO2) were measured by expired gas analysis, VO2max averaged 61.5 +/- 6.2 (air), 48.6 +/- 4.8 (15% O2), and 38.1 +/- 4.1 (12% O2) ml.kg-1.min-1. Corresponding values were 16.8 +/- 5.6, 14.4 +/- 5.0, and 12.0 +/- 5.0 Torr for PfVO2; 23.6 +/- 3.2, 19.1 +/- 4.2, and 16.2 +/- 3.5 Torr for PVO2; and 38.5 +/- 5.4, 30.3 +/- 4.1, and 24.5 +/- 3.6 Torr for muscle capillary PO2 (PmCO2). Each of the PO2 variables was linearly related to VO2max (r = 0.99 each), with an intercept not different from the origin. Similar results were obtained when the subjects were pushed to a work load 30 W higher to ensure that VO2max had been achieved. By extending our prior observations 1) to maximum VO2 and 2) by direct sampling of femoral venous blood, we conclude that tissue diffusion limitation of VO2max may be present in normal humans. In addition, since PVO2, PfVO2, and PmCO2 all linearly relate to VO2max, we suggest that whichever of these is most readily obtained is acceptable for further evaluation of the hypothesis.

Adult↗
PubMed1989

Effects of altitude acclimatization on pulmonary gas exchange during exercise.

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

Acclimatization↗
PubMed1979

Pulmonary O2 diffusing capacity estimates from assumed log-normal VA/Q distributions.

Steady-state pulmonary gas exchange has been measured in hypoxia in 33 mongrel dogs with the aim of comparing DLO2 estimates obtained with three procedures differing by the models assumed for functional inhomogeneity. In the first procedure the lung was assumed to be homogeneous and the corresponding DLO2 estimate was 15 mumol . min-1. Torr-1 . kg-1. In the second procedure, which is the one commonly used in respiratory physiology, alveolar dead space was considered as the unique form of functional inhomogeneity and the corresponding DLO2 estimate was 31 mumol . min-1. Torr-1 . kg-1. In the third procedure, which has been specially worked out for this study, functional inhomogeneity was represented by a log-normal distribution of the VA/Q ratios and the corresponding DLO2 estimate was 50 mumol . min-1 . Torr-1 . kg-1. The relation between the DLO2 estimates by the second and by the third procedures was found to depend upon the blood pH. This could be explained on the basis of the effects of acidosis on the blood capacitances for O2 and for CO2. Analysis suggests that in hypoxia where normally the O2 capacitance is about half the CO2 one, the third procedure yields DLO2 estimates about twice as large as those obtained by the second one.

Animals↗