O2 extraction by hind limb versus whole dog during anemic hypoxia

1978 ◽  
Vol 45 (6) ◽  
pp. 966-970 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Blood Flow ◽  
Hind Limb ◽  
Femoral Vein ◽  
Control Level ◽  
The Body ◽  
Stage Ii ◽  
Whole Body ◽  
O2 Uptake ◽  
O2 Extraction ◽  
O2 Delivery

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.

Analysis of oxygen delivery and uptake relationships in the Krogh tissue model

1989 ◽  
Vol 67 (3) ◽  
pp. 1234-1244 ◽  
Author(s):  
P. T. Schumacker ◽  
R. W. Samsel
Keyword(s):  
Blood Flow ◽  
Critical Point ◽  
Real Data ◽  
Whole Body ◽  
O2 Uptake ◽  
Highly Sensitive ◽  
O2 Extraction ◽  
O2 Supply ◽  
Experimental Findings ◽  
O2 Delivery

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.

O2 extraction by canine hindlimb during alpha-adrenergic blockade and hypoxic hypoxia

1980 ◽  
Vol 48 (4) ◽  
pp. 630-635 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Blood Flow ◽  
Femoral Vein ◽  
Recovery Period ◽  
Whole Body ◽  
Adrenergic Blockade ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
Total Blood ◽  
O2 Extraction ◽  
Total Blood Flow

Hindlimb and total blood flow and O2 uptake were measured in anesthetized paralyzed dogs in which venous outflow from the left hindlimb (less paw) was directed through the femoral vein. After ventilation on room air, 10 dogs were given 3 mg/kg phenoxybenzamine + 10 ml/kg dextran and 10 other dogs were isovolemically exchanged with 10 ml/kg dextran without alpha-block while continuing to be ventilated on room air. All animals were then ventilated with 9.1% O2 in N2, followed by a recovery period on room air. Total and limb peripheral resistances were lowered by alpha-block, but total and limb blood flow changed little from control levels. Both total and limb O2 uptake were decreased below control values during hypoxia. Cardiac output and limb blood flow increased during hypoxia in both groups. Although alpha-block caused O2 extraction by the whole body to be less during hypoxia than in unblocked dogs, the hindlimb in both groups extracted O2 equally well. We concluded that skeletal muscle was not overperfused relative to O2 demand when alpha-blocked during hypoxia.

Gastrointestinal blood flow and oxygen consumption in awake newborn piglets: effect of feeding

1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
O2 Consumption ◽  
Gi Tract ◽  
Local Blood Flow ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Gastrointestinal Blood Flow ◽  
O2 Delivery ◽  
Effect Of Feeding

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.

Right and left ventricular O2 uptake during hemodilution and beta-adrenergic stimulation

1993 ◽  
Vol 265 (5) ◽  
pp. H1769-H1777 ◽  
Author(s):  
G. J. Crystal ◽  
S. J. Kim ◽  
M. R. Salem
Keyword(s):  
Blood Flow ◽  
Blood Cells ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
O2 Uptake ◽  
Isovolemic Hemodilution ◽  
Content Difference ◽  
O2 Extraction ◽  
In Series ◽  
O2 Delivery

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)

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
Keyword(s):  
Blood Flow ◽  
Gastrocnemius Muscle ◽  
Dissociation Curve ◽  
Muscle Preparation ◽  
O2 Uptake ◽  
Oxyhemoglobin Dissociation Curve ◽  
O2 Extraction ◽  
O2 Supply ◽  
O2 Delivery ◽  
Oxyhemoglobin Dissociation

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.

Systemic and diaphragmatic oxygen delivery-consumption relationships during hemorrhage

1994 ◽  
Vol 77 (2) ◽  
pp. 653-659 ◽  
Author(s):  
M. E. Ward ◽  
H. Chang ◽  
F. Erice ◽  
S. N. Hussain
Keyword(s):  
Work Of Breathing ◽  
Venous Blood ◽  
The Body ◽  
Extraction Ratio ◽  
Whole Body ◽  
Critical Threshold ◽  
Inferior Phrenic Artery ◽  
Left Hemidiaphragm ◽  
O2 Extraction ◽  
O2 Delivery

When tissue O2 delivery falls below a critical threshold, tissue O2 uptake (VO2) becomes limited. We compared critical O2 delivery and critical and maximum O2 extraction ratios of the resting and contracting left hemidiaphragm with those of nondiaphragmatic tissues in seven dogs. The left hemidiaphragm was perfused through the left inferior phrenic artery with blood from the left femoral artery. Phrenic venous blood was sampled through a catheter in the inferior phrenic vein. Systemic O2 delivery was reduced in stages by controlled hemorrhage. Left diaphragmatic VO2 during rest and during 3 min of continuous stimulation (3 Hz) of the left phrenic nerve and VO2 of the remaining nonleft hemidiaphragmatic tissues were measured at each stage. Critical diaphragmatic O2 delivery for the resting diaphragm averaged 0.8 +/- 0.16 ml.min-1.100 g-1 with a critical O2 extraction ratio of 65.5 +/- 6%. In the contracting diaphragm, they averaged 5.1 +/- 0.9 ml.min-1.100 g-1 and 81 +/- 5%, respectively. Whole body O2 delivery at which resting diaphragmatic VO2 became supply limited was similar to that for nondiaphragmatic tissues. By comparison, supply limitation of VO2 occurred at a higher systemic O2 delivery in the contracting diaphragm than in the rest of the body despite the increase in critical diaphragmatic extraction ratio. Thus, oxygenation of the isolated diaphragm does not appear to be preferentially preserved during generalized reductions in O2 delivery. These results suggest that, in diseases associated with increased work of breathing and decreased O2 delivery, the diaphragm may become metabolically impaired before limitation of VO2 is observed systemically.

Is peak quadriceps blood flow in humans even higher during exercise with hypoxemia?

1986 ◽  
Vol 251 (5) ◽  
pp. H1038-H1044 ◽  
Author(s):  
L. B. Rowell ◽  
B. Saltin ◽  
B. Kiens ◽  
N. J. Christensen
Keyword(s):  
Blood Flow ◽  
Peak Load ◽  
Mechanical Efficiency ◽  
Dynamic Exercise ◽  
Whole Body ◽  
Peak Exercise ◽  
Active Muscle ◽  
O2 Extraction ◽  
Mean Pressure ◽  
O2 Delivery

Blood flow (Q) to quadriceps muscles was measured by thermal dilution in six men during rest and dynamic exercise [20, 38, and 42.5-60 W (peak load)] restricted to quadriceps of one leg in normoxia (N) and hypoxemia (H; 10-11% O2). Without exception Q and quadriceps vascular conductance were higher in H. Arterial mean pressure, lactate, norepinephrine, and epinephrine all rose when work exceeded 20 W. Q in N was 0.25, 3.28, 4.27, and 5.81 l/min (rest to peak exercise) and in H was 0.25, 4.08, 5.24, and 6.58 l/min. Peak Q per 100 grams of muscle (quadriceps mass = 2.2 kg) was 273.3 (N) and 308.8 ml/min (H). Quadriceps VO2 (Q X femoral A-VO2 difference) was 25, 388, 556, and 771 ml/min (N) and 25, 390, 556, and 743 (lower peak load in H)-net mechanical efficiency was 23%. Muscle O2 delivery (Q X arterial O2 content) was unaffected by H; O2 extraction fell in H but femoral venous O2 content remained near 6 (N) and 5 ml/100 ml (H) at all workloads, in contrast to much lower values in whole body exercise. In H muscle Q can rise to even higher peak values, without apparent limit, when the mass of active muscle is too small to overwhelm the pumping capacity of the heart.

Critical O2 delivery to skeletal muscle at high and low PO2 in endotoxemic dogs

1989 ◽  
Vol 66 (6) ◽  
pp. 2553-2558 ◽  
Author(s):  
D. L. Bredle ◽  
R. W. Samsel ◽  
P. T. Schumacker ◽  
S. M. Cain
Keyword(s):  
Skeletal Muscle ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Adult Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
The Body ◽  
O2 Uptake ◽  
O2 Extraction ◽  
O2 Delivery ◽  
Arterial Po2

An ischemic canine limb model was used to determine whether endotoxin reduces the ability of resting skeletal muscle to extract O2 and whether increasing the arterial PO2 would increase its O2 extraction. Isolated limbs were pump perfused via an extracorporeal circuit with membrane oxygenator at three progressively lower flows and PO2 of both 60 and 200 Torr, whereas the rest of the body remained normoxic and normotensive. Six anesthetized, paralyzed dogs were injected with endotoxin (4 mg/kg, ENDO), and another six were controls (CONT). Limb critical O2 delivery was higher (P less than 0.05) in ENDO than CONT (8.3 vs. 6.1 ml.kg-1.min-1). Critical venous PO2 was also higher (P less than 0.05) in ENDO than CONT (38 vs. 30 Torr). Critical O2 extraction ratio was lower (P less than 0.05) in ENDO than CONT (0.60 vs. 0.73). There were no differences in these variables between low and high arterial PO2. We concluded that 1) endotoxin can cause a small but significant O2 extraction defect in skeletal muscle, 2) increasing arterial PO2 did not correct such a defect, nor did it improve O2 uptake in ischemic, but otherwise healthy, muscle, and 3) skeletal muscle may contribute to the peripheral O2 extraction defect in adult respiratory distress syndrome insofar as endotoxin effects model those found in adult respiratory distress syndrome.

Relationship between body and leg VO2 during maximal cycle ergometry

1992 ◽  
Vol 73 (3) ◽  
pp. 1114-1121 ◽  
Author(s):  
D. R. Knight ◽  
D. C. Poole ◽  
W. Schaffartzik ◽  
H. J. Guy ◽  
R. Prediletto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Asymptotic Behavior ◽  
Cycle Ergometry ◽  
The Body ◽  
Whole Body ◽  
Constant Infusion ◽  
Concentration Difference ◽  
Leg Blood Flow ◽  
O2 Extraction ◽  
Total Leg

It is not known whether the asymptotic behavior of whole body O2 consumption (VO2) at maximal work rates (WR) is explained by similar behavior of VO2 in the exercising legs. To resolve this question, simultaneous measurements of body and leg VO2 were made at submaximal and maximal levels of effort breathing normoxic and hypoxic gases in seven trained male cyclists (maximal VO2, 64.7 +/- 2.7 ml O2.min-1.kg-1), each of whom demonstrated a reproducible VO2-WR asymptote during fatiguing incremental cycle ergometry. Left leg blood flow was measured by constant-infusion thermodilution, and total leg VO2 was calculated as the product of twice leg flow and radial arterial-femoral venous O2 concentration difference. The VO2-WR relationships determined at submaximal WR′s were extrapolated to maximal WR as a basis for assessing the body and leg VO2 responses. The differences between measured and extrapolated maximal VO2 were 235 +/- 45 (body) and 203 +/- 70 (leg) ml O2/min (not significantly different). Plateauing of leg VO2 was associated with, and explained by, plateauing of both leg blood flow and O2 extraction and hence of leg VO2. We conclude that the asymptotic behavior of whole body VO2 at maximal WRs is a direct reflection of the VO2 profile at the exercising legs.

Contribution of excising legs to the slow component of oxygen uptake kinetics in humans

1991 ◽  
Vol 71 (4) ◽  
pp. 1245-1260 ◽  
Author(s):  
D. C. Poole ◽  
W. Schaffartzik ◽  
D. R. Knight ◽  
T. Derion ◽  
B. Kennedy ◽  
...  
Keyword(s):  
Blood Flow ◽  
Radial Artery ◽  
Slow Component ◽  
Femoral Vein ◽  
Lactate Concentration ◽  
Oxygen Uptake Kinetics ◽  
The Body ◽  
O2 Uptake ◽  
Mechanistic Basis ◽  
Highly Correlated

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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