O2 delivery to contracting muscle during hypoxic or CO hypoxia

1987 ◽  
Vol 63 (2) ◽  
pp. 726-732 ◽  
Author(s):  
C. E. King ◽  
S. L. Dodd ◽  
S. M. Cain

The consequences of a decreased O2 supply to a contracting canine gastrocnemius muscle preparation were investigated during two forms of hypoxia: hypoxic hypoxia (HH) (n = 6) and CO hypoxia (COH) (n = 6). Muscle O2 uptake, blood flow, O2 extraction, and developed tension were measured at rest and at 1 twitch/s isometric contractions in normoxia and in hypoxia. No differences were observed between the two groups at rest. During contractions and hypoxia, however, O2 uptake decreased from the normoxic level in the COH group but not in the HH group. Blood flow increased in both groups during hypoxia, but more so in the COH group. O2 extraction increased further with hypoxia (P less than 0.05) during concentrations in the HH group but actually fell (P less than 0.05) in the COH group. The O2 uptake limitation during COH and contractions was associated with a lesser O2 extraction. The leftward shift in the oxyhemoglobin dissociation curve during COH may have impeded tissue O2 extraction. Other factors, however, such as decreased myoglobin function or perfusion heterogeneity must have contributed to the inability to utilize the O2 reserve more fully.

1982 ◽  
Vol 243 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman

In 14 unanesthetized newborn lambs the relationship between cerebral blood flow (measured by radiolabeled microspheres) and arterial O2 saturation (SaO2) was compared during two types of hypoxia: hypoxic hypoxia and carbon monoxide (CO) hypoxia. Cerebral venous samples were obtained from the sagittal sinus. The Increase in blood flow was 47% greater during CO than during hypoxic hypoxia. Cerebral O2 consumption and O2 delivery were constant during hypoxic hypoxia. Thus fractional O2 extraction, which equals O2 consumption/O2 delivery, remained constant with hypoxic hypoxia. During CO hypoxia, although O2 consumption remained constant, O2 delivery increased and fractional O2 extraction decreased. This decline in fractional O2 extraction was correlated with the leftward shift of the oxyhemoglobin dissociation curve that accompanied CO hypoxia. We suggest that cerebral blood flow depends on both SaO2 and the position of the oxyhemoglobin dissociation curve in the newborn lamb. However, this correlation does not exclude other potential histotoxic effects contributing to the relative overperfusion with CO hypoxia.


1989 ◽  
Vol 67 (3) ◽  
pp. 1234-1244 ◽  
Author(s):  
P. T. Schumacker ◽  
R. W. Samsel

Normally, tissue O2 uptake (VO2) is set by metabolic activity rather than O2 delivery (QO2 = blood flow X arterial O2 content). However, when QO2 is reduced below a critical level, VO2 becomes limited by O2 supply. Experiments have shown that a similar critical QO2 exists, regardless of whether O2 supply is reduced by progressive anemia, hypoxemia, or reduction in blood flow. This appears inconsistent with the hypothesis that O2 supply limitation must occur by diffusion limitation, since very different mixed venous PO2 values have been seen at the critical point with hypoxic vs. anemic hypoxia. The present study sought to begin clarifying this paradox by studying the theoretical relationship between tissue O2 supply and uptake in the Krogh tissue cylinder model. Steady-state O2 uptake was computed as O2 delivery to tissue representative of whole body was gradually lowered by anemic, hypoxic, or stagnant hypoxia. As diffusion began to limit uptake, the fall in VO2 was computed numerically, yielding a relationship between QO2 and VO2 in both supply-independent and O2 supply-dependent regions. This analysis predicted a similar biphasic relationship between QO2 and VO2 and a linear fall in VO2 at O2 deliveries below a critical point for all three forms of hypoxia, as long as intercapillary distances were less than or equal to 80 microns. However, the analysis also predicted that O2 extraction at the critical point should exceed 90%, whereas real tissues typically extract only 65–75% at that point. When intercapillary distances were larger than approximately 80 microns, critical O2 extraction ratios in the range of 65–75% could be predicted, but the critical point became highly sensitive to the type of hypoxia imposed, contrary to experimental findings. Predicted gas exchange in accord with real data could only be simulated when a postulated 30% functional peripheral O2 shunt (arterial admixture) was combined with a tissue composed of Krogh cylinders with intercapillary distances of less than or equal to 80 microns. The unrealistic efficacy of tissue O2 extraction predicted by the Krogh model (in the absence of postulated shunt) may be a consequence of the assumed homogeneity of tissues, because real tissues exhibit many forms of heterogeneity among capillary units. Alternatively, the failure of the original Krogh model to fully predict tissue O2 supply dependency may arise from basic limitations in the assumptions of that model.


1984 ◽  
Vol 4 (1) ◽  
pp. 115-122 ◽  
Author(s):  
Raymond C. Koehler ◽  
Richard J. Traystman ◽  
Scott Zeger ◽  
Mark C. Rogers ◽  
M. Douglas Jones

Cerebral blood flow (CBF) responses to two types of isocapnic hypoxia, hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH), were examined in seven unanesthetized adult sheep by the radiolabeled microsphere technique. Comparisons were made with newborn lambs (5–12 days old) previously studied under similar conditions. The arterial O2 content (Cao2) was reduced in a graded manner to 50–60% of the control value. During HH, CBF increased to maintain cerebral O2 delivery (Cao2 x CBF) in both adults and newborns; however, cerebral O2 uptake (CMRO2) did not change. Although CMRO2 was higher in newborns, the responses of CBF/CMRO2 to HH did not differ significantly in newborns and adults. In newborns, regional CBF showed that brainstem areas were particularly responsive to HH. In both age groups, CBF increased to a greater extent with COH than with HH for similar reductions in Cao2. This resulted in an increase in cerebral O2 delivery with COH. The degree to which COH differed from HH correlated with the magnitude of the leftward shift of the oxyhemoglobin dissociation curve that accompanies COH. In adults, CMRO2 fell by 16% with COH but was maintained in newborns. We conclude that maintenance of cerebral O2 delivery during acute, isocapnic HH is a property of CBF regulation common to both newborn and adult sheep. During COH, the position of the oxyhemoglobin dissociation curve is an additional factor that sets the level of O2 delivery. The fetal conditions of low Cao2 and a left-shifted oxyhemoglobin dissociation curve may have provided the newborn with a microcirculation better suited for maintaining CMRO2 during COH.


1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.


1993 ◽  
Vol 265 (5) ◽  
pp. H1769-H1777 ◽  
Author(s):  
G. J. Crystal ◽  
S. J. Kim ◽  
M. R. Salem

Myocardial O2 uptake (MVO2) and related variables were compared in right and left ventricles (RV and LV, respectively) during isovolemic hemodilution (HD) alone and combined with isoproterenol (Iso) infusion in 13 isoflurane-anesthetized open-chest dogs. Measurements of myocardial blood flow (MBF) obtained with radioactive microspheres were used to calculate MVO2. Lactate extraction (Lacext) was determined. The study consisted of two experimental series: 1) graded HD (dextran) to hematocrit (Hct) of 10% and 2) Iso (0.1 microgram.kg-1.min-1 iv) during moderate HD (Hct = 18 +/- 1%). In series 1, arteriovenous O2 content difference in both ventricles decreased in parallel with reduced arterial O2 content caused by HD, i.e., percent O2 extraction was constant; MVO2 was maintained by proportional increases in MBF. In series 2, Iso during moderate HD raised MVO2 (RV, +156%; LV, +80%). Higher MVO2 was satisfied by combination of increased MBF and O2 extraction in RV and by increased MBF alone in LV. Lacext remained consistent with adequate myocardial O2 delivery throughout study. Conclusions were that 1) both RV and LV tolerated extreme HD (Hct = 10%) because blood flow reserves were sufficient to fully compensate for reduced arterial O2 content; 2) significant cardiac reserve was evident during HD, which could be recruited Iso; and 3) because increase in MVO2 in RV caused by Iso in presence of HD was partially satisfied by increased O2 extraction, the absence of augmented O2 extraction during HD alone was not due to impaired release of O2 from diluted red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 45 (6) ◽  
pp. 966-970 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler

The ability of the hind limb to obtain oxygen and maintain its O2 uptake in relation to the whole body during isovolemic hemodilution with dextran was measured in eight anesthetized, paralyzed dogs kept at constant ventilation. Hind limb venous outflow (ankle to upper thigh) was restricted by tourniquets to femoral vein. Hind limb blood flow, O2 uptake (VO2), cardiac output, and total VO2 were measured at normal hematocrit, at hematocrits just above (16%, stage 2) and just below (10%, stage II) that at which total VO2 could be maintained at the control level, and following isovolemic reinfusion of recovered red blood cells (Hct = 23%). VO2 was maintained at the control level in whole body and hind limb during stage I. Total VO2 decreased significantly in stage II (P less than 0.05), whereas limb VO2 did not. Hind limb had a consistently greater extraction ratio for O2 (P less than 0.01) and lower venous oxygen partial pressure than the body as a whole (P less than 0.01). In spite of limitations of O2 delivery by anemia to the point that total O2 demand was not met, there was no redistribution of blood flow away from or decreased demand for O2 by the hind limb, which was mostly skeletal muscle.


1994 ◽  
Vol 77 (3) ◽  
pp. 1093-1100 ◽  
Author(s):  
W. S. Kim ◽  
M. E. Ward ◽  
S. N. Hussain

Our aim was to assess whether endotoxemia impairs the ability of the diaphragm to extract O2 and whether this defect leads to a greater dependence of O2 uptake on O2 delivery. In two groups of anesthetized mechanically ventilated dogs, the left hemidiaphragm was vascularly isolated. Diaphragmatic blood flow and cardiac output (CO) were measured simultaneously in all animals. Saline (S group) or Escherichia coli endotoxin (100 mg; E group) was infused intravenously over 60 min. In both groups, CO was reduced in stages by controlled hemorrhage, and systemic and diaphragmatic O2 deliveries and consumptions were measured at each stage to construct the O2 delivery-O2 consumption relationships. In the S group, the average systemic O2 delivery below which O2 uptake became supply dependent was 7.2 ml.kg-1.min-1. At this O2 delivery, systemic O2 extraction ratio (ER) averaged 67.9%, whereas the maximum O2 ER was 91.3%. Critical diaphragmatic O2 delivery and critical and maximum diaphragmatic O2 ER, by comparison, averaged 9.0 ml.kg-1.min-1, 65%, and 81.9%, respectively. Endotoxin infusion raised critical systemic O2 delivery to 16.7 ml.kg-1.min-1 (P < 0.05) and reduced critical and maximum systemic O2 ER to 55.5 and 77% (P < 0.05), respectively. Similarly, critical diaphragmatic O2 delivery in the E group increased to 14.8 ml.kg-1.min-1 (P < 0.05), whereas critical and maximum O2 ER declined to 51.8 and 72.8%, respectively (P < 0.05). Thus, endotoxemia impairs diaphragmatic O2 extraction. This, in turn, leads to a greater dependence of diaphragmatic O2 uptake on O2 delivery.


1992 ◽  
Vol 73 (3) ◽  
pp. 1067-1076 ◽  
Author(s):  
J. Roca ◽  
A. G. Agusti ◽  
A. Alonso ◽  
D. C. Poole ◽  
C. Viegas ◽  
...  

To quantify the relative contributions of convective and peripheral diffusive components of O2 transport to the increase in leg O2 uptake (VO2leg) at maximum O2 uptake (VO2max) after 9 wk of endurance training, 12 sedentary subjects (age 21.8 +/- 3.4 yr, VO2max 36.9 +/- 5.9 ml.min-1.kg-1) were studied. VO2max, leg blood flow (Qleg), and arterial and femoral venous PO2, and thus VO2leg, were measured while the subjects breathed room air, 15% O2, and 12% O2. The sequence of the three inspirates was balanced. After training, VO2max and VO2leg increased at each inspired O2 concentration [FIO2; mean over the 3 FIO2 values 25.2 +/- 17.8 and 36.5 +/- 33% (SD), respectively]. Before training, VO2leg and mean capillary PO2 were linearly related through the origin during hypoxia but not during room air breathing, suggesting that, at 21% O2, VO2max was not limited by O2 supply. After training, VO2leg and mean capillary PO2 at each FIO2 fell along a straight line with zero intercept, just as in athletes (Roca et al. J. Appl. Physiol. 67: 291–299, 1989). Calculated muscle O2 diffusing capacity (DO2) rose 34% while Qleg increased 19%. The relatively greater rise in DO2 increased the DO2/Qleg, which led to 9.9% greater O2 extraction. By numerical analysis, the increase in Qleg alone (constant DO2) would have raised VO2leg by 35 ml/min (mean), but that of DO2 (constant Qleg) would have increased VO2leg by 85 ml/min, more than twice as much. The sum of these individual effects (120 ml/min) was less (P = 0.013) than the observed rise of 164 ml/min (mean). This synergism (explained by the increase in DO2/Qleg) seems to be an important contribution to increases in VO2max with training.


1994 ◽  
Vol 76 (6) ◽  
pp. 2820-2824 ◽  
Author(s):  
S. S. Kurdak ◽  
M. C. Hogan ◽  
P. D. Wagner

We asked whether maximally working muscle could increase O2 extraction at fixed O2 delivery [i.e., improve maximal O2 uptake (VO2max)] when vascular resistance was decreased with adenosine (A) infusion. We postulated that a reduction in vascular resistance at the same blood flow (Q) might result in more uniform vascular perfusion and also possibly increase red blood cell transit time, thereby potentially improving the ability of the tissue to extract O2. Pump-perfused isolated dog gastrocnemius muscle (n = 6) was stimulated maximally at each of two levels of Q: 110 +/- 3 and 54 +/- 4 (SE) ml.100 g-1.min-1 [normal control (C) and ischemia (I), respectively], both before and after giving 10(-2) M of A solution in each case. Arterial and venous blood samples were taken to measure blood gases, and the Fick principle was used to calculate O2 uptake. Resistance decreased significantly after A treatment in both groups (1.2 +/- 0.1 vs. 0.9 +/- 0.1 and 1.3 +/- 0.1 vs. 1.1 +/- 0.1 mmHg.ml-1.100 g.min for C vs. C + A and I vs. I + A, respectively; P < 0.01). O2 delivery was lower with I but did not change at either perfusion rate when A was infused. VO2max also decreased significantly with I but was no different when A was added (13.8 +/- 0.7 vs. 13.8 +/- 0.9 and 8.4 +/- 0.5 vs. 8.2 +/- 0.6 ml.100 g-1.min-1 for C vs. C + A and I vs. I + A, respectively). These results show that the decrease in resistance with A did not lead to changes in VO2max.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 74 (4) ◽  
pp. 1742-1747 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
P. D. Wagner

The purpose of this study was to decrease O2 delivery to maximally working muscle by reductions in muscle blood flow (Q), while maintaining hemoglobin concentration and the arterial PO2 (PaO2) constant, to investigate how the decreases in maximal O2 uptake (VO2max) that occur with ischemia are related to changes in the estimated effective muscle O2 diffusing capacity (DO2). Additionally, the relationships among Q, DO2, O2 uptake (VO2), and effluent venous PO2 (PVO2) were used to infer whether the reductions in Q occur uniformly throughout the muscle or whether a nonuniform (greater heterogeneity of Q to VO2) pattern develops. Isolated dog gastrocnemius muscle (n = 6) was stimulated maximally at three levels of muscle blood flow (controlled by pump perfusion): control [C; 119 +/- 3 ml.100 g-1.min-1 (SE)], moderate ischemia (MI; 80 +/- 6), and severe ischemia (SI; 45 +/- 6) in random order. Arterial and venous samples were taken to measure blood gases, O2 concentration, and lactate concentration, whereas a Bohr integration technique using a model based on Fick's law of diffusion was used to estimate mean capillary PO2 and DO2 for each Q condition. VO2max fell progressively (P < 0.05) with Q, even though the O2 extraction ratio (VO2/O2 delivery) increased significantly (C = 67%, MI = 84%, SI = 90%). PVO2 and VO2max fell in proportion to each other from C to MI, but there was not a significant fall in PVO2 from MI to SI. Thus the calculated DO2 did not change between C and MI but fell in proportion to Q between MI and SI. These results suggest that with moderate Q reduction, perfusion falls relatively uniformly throughout the muscle, whereas more severe ischemia leads to nonuniform changes in Q distribution with some areas being poorly perfused to allow more adequate perfusion to other areas.


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