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)

Pathological supply dependence of systemic and intestinal O2 uptake during endotoxemia

1988 ◽  
Vol 64 (6) ◽  
pp. 2410-2419 ◽  
Author(s):  
D. P. Nelson ◽  
R. W. Samsel ◽  
L. D. Wood ◽  
P. T. Schumacker
Keyword(s):  
Blood Flow ◽  
Small Intestine ◽  
Reactive Hyperemia ◽  
Extraction Ratio ◽  
Whole Body ◽  
Control Group ◽  
Base Line ◽  
O2 Uptake ◽  
Critical Limit ◽  
O2 Extraction

When systemic delivery of oxygen (QO2 = blood flow X arterial O2 content) is reduced, the systemic O2 extraction ratio [(CaO2 - CVO2)/CaO2; where CaO2 is arterial O2 content and CVO2 is venous O2 content] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by delivery. Patients with adult respiratory distress syndrome and sepsis exhibit supply dependence of VO2 even at high levels of QO2, which suggests that a peripheral O2 extraction defect may be present. We tested the hypothesis that endotoxemia might produce a similar defect in the efficacy of tissue O2 extraction by determining the whole-body critical systemic QO2 (QO2 c) and critical extraction ratio in a control group of dogs and a group receiving a 5-mg/kg dose of Escherichia coli endotoxin. QO2 c was determined in each group by measuring VO2 as QO2 was gradually reduced by bleeding. The VO2 and QO2 of an isolated segment of small intestine were also measured to determine whether O2 extraction was impaired within a local region of tissue. The dogs were anesthetized, paralyzed, and ventilated with room air. Systemic QO2 was reduced in stages by hemorrhage as hematocrit was maintained. The systemic and intestinal critical points were determined from a plot of VO2 vs. QO2. The mean systemic QO2 c and critical O2 extraction ratio of the endotoxemic group (12.8 +/- 2.0 and 0.54 +/- 0.11 ml.min-1.kg-1) were significantly different from control (6.8 +/- 1.2 and 0.78 +/- 0.04) (P less than 0.001), indicating that endotoxin administration impaired systemic extraction of O2. Endotoxin also increased base-line systemic VO2 [6.1 +/- 0.7 (before) to 7.4 +/- 0.1 (after)] (P less than 0.001). The critical and maximal intestinal O2 extraction ratios of the endotoxemic group (0.47 +/- 0.10 and 0.71 +/- 0.04) were significantly less than control (0.69 +/- 0.06 and 0.83 +/- 0.05) (P less than 0.001). In addition, intestinal reactive hyperemia disappeared in six of seven endotoxemic dogs, whereas it remained intact in all control dogs. Thus endotoxin reduced the ability of tissues to extract O2 from a limited supply at the whole body level as well as within a 40- to 50-g segment of small intestine. These results could be explained by a defect in microvascular regulation of blood flow that interfered with the optimal distribution of a limited QO2 in accordance with tissue O2 needs.

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.

Adenosine infusion does not improve maximal O2 uptake in isolated working dog muscle

1994 ◽  
Vol 76 (6) ◽  
pp. 2820-2824 ◽  
Author(s):  
S. S. Kurdak ◽  
M. C. Hogan ◽  
P. D. Wagner
Keyword(s):  
Vascular Resistance ◽  
Gastrocnemius Muscle ◽  
Venous Blood ◽  
Blood Gases ◽  
O2 Uptake ◽  
Vascular Perfusion ◽  
Fick Principle ◽  
O2 Extraction ◽  
Before And After ◽  
O2 Delivery

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)

Effects of hyperthermia and hypothermia on oxygen extraction by tissues during hypovolemia

1987 ◽  
Vol 63 (3) ◽  
pp. 1246-1252 ◽  
Author(s):  
P. T. Schumacker ◽  
J. Rowland ◽  
S. Saltz ◽  
D. P. Nelson ◽  
L. D. Wood
Keyword(s):  
Extraction Ratio ◽  
Whole Body ◽  
Lower Body ◽  
Body Temperatures ◽  
Systemic Delivery ◽  
O2 Uptake ◽  
Mechanically Ventilated ◽  
O2 Extraction ◽  
Stepwise Reduction ◽  
O2 Supply

As systemic delivery of O2 (QO2 = QT X CaO2) is reduced during progressive hemorrhage, the O2 extraction ratio [(CaO2 - CVO2)/CaO2] increases until a critical delivery is reached below which O2 uptake (VO2) becomes limited by delivery (O2 supply dependence). When tissue metabolic activity and O2 demand are increased or reduced, the critical QO2 required to maintain VO2 should rise or fall accordingly, unless other changes in the distribution of a limited QO2 precipitate the onset of O2 supply dependence at a different critical extraction ratio. We compared the critical QO2 and critical extraction ratio in 23 normothermic (38 degrees C), hyperthermic (41 degrees C), or hypothermic (34 decrees C) dogs during stepwise reduction in delivery produced by bleeding, as arterial O2 content was maintained. Dogs were anesthetized, paralyzed, and mechanically ventilated. Hypothermia reduced whole-body VO2 by 31%, whereas hyperthermia increased VO2 by 20%. The critical QO2 was significantly reduced during hypothermia (5.6 +/- 0.95 ml.min-1.kg-1) (P less than 0.05) and increased during hyperthermia (8.9 +/- 1.1) (P approximately equal to 0.06) compared with normothermic controls (7.4 +/- 1.2). The extraction ratio at the onset of supply dependency was significantly increased in hyperthermia (0.76 +/- 0.05) compared with hypothermia (0.65 +/- 0.10) (P less than 0.05), and the normothermic critical extraction was 0.71 +/- 0.1. These results suggest that higher body temperatures are associated with an improved ability to maintain a VO2 independent of QO2, since a higher fraction of the delivered O2 can be extracted before the onset of O2 supply dependence, relative to lower body temperatures.

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.

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.

Blood respiratory properties in pigeons at high altitudes: effects of acclimation

1985 ◽  
Vol 249 (6) ◽  
pp. R765-R775 ◽  
Author(s):  
Y. Weinstein ◽  
M. H. Bernstein ◽  
P. E. Bickler ◽  
D. V. Gonzales ◽  
F. C. Samaniego ◽  
...  
Keyword(s):  
High Altitude ◽  
Venous Blood ◽  
Hypoxia Tolerance ◽  
Control Group ◽  
Mixed Venous Blood ◽  
High Altitudes ◽  
Simulated High Altitude ◽  
O2 Extraction ◽  
Columbia Livia ◽  
Venous Blood Gas

Many birds thrive at high altitudes where environmental temperatures are low. Previous studies have shown that tolerance of and acclimation to hypoxia involve cardiopulmonary and hematological adaptations. We investigated blood respiratory properties during exposure to simulated high altitude (hypobaric hypoxia) and low temperature in unanesthetized resting pigeons (Columbia livia, mean mass 0.38 kg). A control group (C) and a group acclimated to 7 km above sea level (ASL) in a hypobaric chamber at 25 degrees C (HA group) were used. All were acutely exposed to altitudes through 9 km ASL at 5 or 25 degrees C. Arterial and mixed venous blood gas tensions and O2 and CO2 content during steady state decreased with increased altitude, whereas blood lactate increased in both groups at both temperatures. Acute high-altitude exposure did not affect hematocrit, hemoglobin concentrations, or O2 carrying capacity, but at any altitude these were all greater in HA than in C birds. At 5 degrees C blood pH increased with altitude in controls but remained unchanged in HA birds. At 25 degrees C in both groups mean intracellular pH did not change, averaging 6.97, whereas extracellular (venous) pH increased with altitude. At the highest altitudes tissue O2 extraction was virtually complete in both groups. Acclimation changed blood O2 and CO2 combining properties in ways likely to improve gas transport at high altitudes. The previously unreported shifts in blood respiratory and acid-base properties with acclimation indicate that innate extrapulmonary adaptations contribute to avian hypoxia tolerance.

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