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.

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.

Pathological supply dependence of O2 uptake during bacteremia in dogs

1987 ◽  
Vol 63 (4) ◽  
pp. 1487-1492 ◽  
Author(s):  
D. P. Nelson ◽  
C. Beyer ◽  
R. W. Samsel ◽  
L. D. Wood ◽  
P. T. Schumacker
Keyword(s):  
Bacterial Infection ◽  
Venous Blood ◽  
Extraction Ratio ◽  
Control Group ◽  
Systemic Delivery ◽  
O2 Uptake ◽  
Critical Limit ◽  
Peripheral Tissues ◽  
O2 Extraction ◽  
O2 Delivery

When systemic delivery of O2 [QO2 = cardiac output X arterial O2 content (CaO2)] is reduced, the systemic O2 extraction ratio [(CaO2-concentration of O2 in venous blood/CaO2] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by delivery. Many patients with adult respiratory distress syndrome exhibit supply dependence of VO2 even at high levels of QO2, which suggests that a peripheral O2 extraction defect may be present. Since many of these patients also suffer from serious bacterial infection, we tested the hypothesis that bacteremia might produce a similar defect in the ability of tissues to maintain VO2 independent of QO2, as QO2 reduced. The critical O2 delivery (QO2crit) and critical extraction ratio (ERcrit) were compared in a control group of dogs and a group receiving a continuous infusion of Pseudomonas aeruginosa (5 x 10(7) organisms/min). Dogs were anesthetized, paralyzed, and ventilated with room air. Systemic QO2 was reduced in stages by hemorrhage as hematocrit was maintained. At each stage, systemic VO2 and QO2 were measured, and the critical point was determined from a plot of VO2 vs. QO2. The mean QO2crit and ERcrit of the bacteremic group (11.4 +/- 2.2 ml.min-1.kg-1 and 0.51 +/- 0.09) were significantly different from control (7.4 +/- 1.2 and 0.71 +/- 0.10) (P less than 0.05). These results suggest that bacterial infection can reduce the ability of peripheral tissues to extract O2 from a limited supply, causing VO2 to become limited by O2 delivery at a stage when a smaller fraction of the delivered O2 has been extracted.(ABSTRACT TRUNCATED AT 250 WORDS)

Systemic and intestinal limits of O2 extraction in the dog

1987 ◽  
Vol 63 (1) ◽  
pp. 387-394 ◽  
Author(s):  
D. P. Nelson ◽  
C. E. King ◽  
S. L. Dodd ◽  
P. T. Schumacker ◽  
S. M. Cain
Keyword(s):  
Extraction Ratio ◽  
Whole Body ◽  
Systemic Delivery ◽  
O2 Uptake ◽  
Critical Limit ◽  
O2 Extraction ◽  
Isolated Segment ◽  
O2 Supply ◽  
O2 Delivery ◽  
Arterial Tone

When systemic delivery of O2 (QO2 = QT X CaO2, where QT is cardiac output and CaO2 is arterial O2 content) is reduced by bleeding, the systemic O2 extraction ratio [ER = (CaO2 - CVO2)/CaO2, where CVO2 is venous O2 content] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by O2 delivery. During hypovolemia, reflex increases in mesenteric arterial tone may preferentially reduce gut blood flow so that the onset of O2 supply dependence occurs in the gut before other regions. We compared the critical O2 delivery (QO2c) and critical extraction ratio (ERc) of whole body and an isolated segment (30–50 g) of small bowel in seven anesthetized paralyzed dogs ventilated with room air. Systemic QO2 was reduced in stages by controlled hemorrhage as arterial O2 content was maintained, and systemic and gut VO2 and QO2 were measured at each stage. Body QO2c was 7.9 +/- 1.9 ml X kg-1 X min-1 (ERc = 0.69 +/- 0.12), whereas gut O2 supply dependency occurred when gut QO2 was 34.3 +/- 11.3 ml X min-1 X kg gut wt-1 (ERc = 0.63 +/- 0.09). O2 supply dependency in the gut occurred at a higher systemic QO2 (9.7 +/- 2.7) than whole-body QO2c (P less than 0.05). The extraction ratio at the final stage (maximal ER) was less in the gut (0.80 +/- 0.05) than whole body (0.87 +/- 0.06). Thus during reductions in systemic QO2, gut VO2 was maintained by increases in gut extraction of O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal O2 consumption during progressive hemorrhage

1991 ◽  
Vol 70 (5) ◽  
pp. 1957-1962 ◽  
Author(s):  
R. Schlichtig ◽  
D. J. Kramer ◽  
J. R. Boston ◽  
M. R. Pinsky
Keyword(s):  
Extraction Ratio ◽  
Whole Body ◽  
O2 Consumption ◽  
Direct Proportion ◽  
Initial Value ◽  
Wide Range ◽  
Mammalian Tissues ◽  
O2 Extraction ◽  
O2 Delivery ◽  
The Relationship

Most mammalian tissues regulate O2 utilization such that O2 consumption (VO2) is relatively constant at O2 delivery (DO2) higher than a critical value (DO2c). We studied the relationship between VO2 and DO2 of kidney and whole body during graded progressive exsanguination. The relationship between whole body VO2 and DO2 was biphasic, and whole body VO2 decreased by 5.6 +/- 14.4% (P = NS) from the initial value to the value nearest whole body DO2c. Kidney DO2 decreased in direct proportion to whole body DO2 such that the average R2 value describing the linear regression of kidney DO2 vs. whole body DO2 was 0.94 +/- 0.02. The relationship between kidney, like whole body, VO2 and DO2 appeared biphasic; however, kidney VO2 decreased by 63.3 +/- 10.4% (P less than 0.0001) from the initial value to the value nearest kidney DO2c. Renal O2 extraction ratio was relatively constant over a wide range of kidney DO2, whereas whole body O2 extraction ratio increased progressively at all whole body DO2 values as whole body DO2 decreased. However, final values of O2 extraction ratio were indistinguishable for whole body (0.86 +/- 0.1) and kidney (0.86 +/- 0.06) (P = NS). We conclude that the pattern of kidney and whole body VO2 response to decreasing DO2 differs during hemorrhage, particularly in the range of DO2 normally associated with tissue wellness.

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.

Adrenergic vasoconstriction augments tissue O2 extraction during reductions in O2 delivery

1994 ◽  
Vol 76 (4) ◽  
pp. 1454-1461 ◽  
Author(s):  
L. A. Maginniss ◽  
H. Connolly ◽  
R. W. Samsel ◽  
P. T. Schumacker
Keyword(s):  
Blood Volume ◽  
Supply And Demand ◽  
Sympathetic Tone ◽  
Whole Body ◽  
Metabolic Demand ◽  
O2 Extraction ◽  
Limit Blood Flow ◽  
Anesthetized Dogs ◽  
O2 Supply ◽  
O2 Delivery

When systemic O2 delivery is reduced, increases in systemic O2 extraction are facilitated by sympathetically mediated increases in vascular resistance that limit blood flow to regions with low metabolic demand. Local metabolic vasodilation competes with this vasoconstriction, thereby effecting a balance between tissue O2 supply and demand. This study examined the role of sympathetically mediated vasoconstriction on the critical level of O2 extraction in hindlimb and whole body during progressive reductions in O2 delivery. In anesthetized dogs, the left hindlimb was vascularly isolated and its O2 delivery was decreased in stages by reducing the speed of an occlusive pump. In a normovolemic group (n = 6), blood volume was maintained to minimize sympathetic tone while flow to the hindlimb was reduced. In a hypovolemic group (n = 6), blood volume was removed in stages to augment sympathetic tone progressively while flow to the limb was reduced simultaneously. A phenoxybenzamine group (n = 6) was identical to the hypovolemic group, except that alpha-adrenergic effects were inhibited with phenoxybenzamine (3 mg/kg). The systemic critical O2 extraction ratio in the phenoxybenzamine group (0.60 +/- 0.06) was less than for the hypovolemic group (0.71 +/- 0.04; P = 0.004). In the hindlimb, critical O2 extractions were significantly less in the normovolemic (0.46 +/- 0.17) and phenoxybenzamine (0.49 +/- 0.10) groups compared with the hypovolemic group (0.72 +/- 0.10; P < or = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of hematocrit on tissue O2 extraction capabilities during acute hemorrhage

1993 ◽  
Vol 264 (6) ◽  
pp. H1942-H1947 ◽  
Author(s):  
P. Van der Linden ◽  
E. Gilbart ◽  
P. Paques ◽  
C. Simon ◽  
J. L. Vincent
Keyword(s):  
The Body ◽  
Acute Hemorrhage ◽  
O2 Extraction ◽  
Normovolemic Hemodilution ◽  
Group 3 ◽  
Group 2 ◽  
Lactate Levels ◽  
O2 Delivery ◽  
Blood Lactate Levels ◽  
Group 1

This study was performed to test the hypothesis that tissue O2 extraction capabilities during hemorrhage may be greater when hematocrit (Hct) is initially reduced. Twenty-four anesthetized and splenectomized dogs were randomly assigned in three groups of eight dogs each: group 1 (Hct 40), 40–45% Hct; group 2 (Hct 30), 30–35% Hct; and group 3 (Hct 20), 20–25% Hct. In each animal, the desired Hct was obtained by normovolemic hemodilution using hydroxyethyl starch 450/0.7 and maintained throughout the experiment. O2 delivery (DO2) was progressively reduced by hemorrhage. At each step, DO2 and O2 consumption (VO2) were measured separately. Critical DO2 obtained from a plot of VO2 vs. DO2 was lower in the Hct 30 and Hct 20 groups than in the Hct 40 group [(in ml.min-1.kg-1) Hct 30, 7.9 +/- 2.2; Hct 20, 7.8 +/- 1.0; Hct 40, 10.4 +/- 1.1; P < 0.05]. Critical DO2 obtained from blood lactate levels was also significantly lower in the Hct 30 and Hct20 groups than in the Hct 40 group. Critical O2 extraction ratio was also greater in the Hct 30 and Hct 20 groups than in the Hct 40 group (Hct 30, 73.0 +/- 13.9%; Hct 20, 70.1 +/- 9.6%; Hct 40, 57.1 +/- 11.5%; P < 0.05). In the conditions of our study, moderate hemodilution was associated with an improvement of the O2 extraction capabilities of the body, probably related to the reduction in blood viscosity.

The physiologic reserve in oxygen carrying capacity: studies in experimental hemodilution

1986 ◽  
Vol 64 (1) ◽  
pp. 7-12 ◽  
Author(s):  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Supply ◽  
The Body ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Oxygen Extraction Ratio ◽  
Acute Anemia ◽  
Total Body Oxygen

The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. Several factors are discussed which contribute to the increase in cardiac output during acute anemia including the reduction in blood viscosity, sympathetic innervation of the heart, and increased venomotor tone. The latter has been shown to be dependent on intact aortic chemoreceptors. With respect to peripheral vascular responses, the rise in coronary and cerebral blood flows which occur following hemodilution is proportionally greater than the increase in cardiac output while the opposite is true for kidney, liver, spleen, and intestine. Skeletal muscle does not contribute to a redistribution of blood flow to more vital areas during acute anemia despite its relatively large anaerobic capacity. Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.

Glutamine and glutamate kinetics in humans

1986 ◽  
Vol 251 (1) ◽  
pp. E117-E126 ◽  
Author(s):  
D. Darmaun ◽  
D. E. Matthews ◽  
D. M. Bier
Keyword(s):  
Venous Blood ◽  
The Body ◽  
Glutamine Metabolism ◽  
Whole Body ◽  
Turnover Rates ◽  
Healthy Young Adult ◽  
Appearance Rate ◽  
N Rates ◽  
Male Subjects ◽  
Fractional Turnover

To study glutamate and glutamine kinetics, 4-h unprimed intravenous infusions of L-[15N]glutamate, L-[2-15N]glutamine, and L-[5-15N]-glutamine were administered to healthy young adult male subjects in the postabsorptive state. Arterialized-venous blood samples were drawn and analyzed for glutamate and glutamine 15N enrichments. The fractional turnover rates of the tracer-miscible glutamate and glutamine pools were fast, 8.0 and 2.8% min-1, respectively. The glutamate tracer-miscible pool accounted for less than one-tenth the estimated free glutamate pool in the body. The plasma glutamate amino N, glutamine amino N and glutamine amide N rates of appearance were 83 +/- 22 (means +/- SD), 348 +/- 33, and 283 +/- 31 mumol X kg-1 X h-1, respectively. The glutamine amide N appearance rate was 20% slower than the amino N appearance rate, indicating that glutamine transaminase is an active pathway in human glutamine metabolism. From measurement of transfer of tracer 15N, we found that only 5% of the glutamine synthesized in cells and released into plasma was derived from intracellular glutamate that had mixed with plasma. These data demonstrate that intravenously administered tracers of glutamate or glutamine do not mix thoroughly with the intracellular pools, and their measured kinetics reflect transport rates through plasma rather than whole-body fluxes.

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.

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