Critical O2 transport values at lowered body temperatures in rats

1983 ◽  
Vol 55 (6) ◽  
pp. 1713-1717 ◽  
Author(s):  
S. M. Cain ◽  
W. E. Bradley
Keyword(s):  
Cardiac Output ◽  
Body Temperature ◽  
Critical Value ◽  
Whole Body ◽  
Body Temperatures ◽  
O2 Uptake ◽  
O2 Transport ◽  
Normal Ranges ◽  
O2 Concentration ◽  
Lowered Body

Whole-body O2 uptake (VO2) in rats was reported not to increase when total O2 transport (TOT = cardiac output X arterial O2 concentration) was increased above normal ranges when body temperature was kept at 38 degrees C (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 53: 660-664, 1982). Similar experiments were performed to see if hypothermic rats at 34 degrees C would increase VO2 with an increased TOT in an effort to generate heat. Anesthetized rats were ventilated with 9 or 12% O2 (hypoxia), room air (normoxia), and O2 (hyperoxia) to vary TOT from 52.6 to 6.6 ml X kg-1 X min-1. VO2 was measured in a closed-circuit, double servospirometer system. Although VO2 was significantly lower at 34 degrees C than the values previously found at 38 degrees C with normoxia and hyperoxia, there was no increase with increasing values of TOT. In spite of a lower plateau value of VO2 at 34 degrees C, the critical value of TOT below which VO2 could not be maintained was nearly the same as at 38 degrees C (22 ml X kg-1 X min-1). The reason for this was that O2 was less completely extracted as TOT was lowered below the critical value in the hypothermic animal. Some of the difficulty in extracting O2 at the tissues was probably due to the decrease in P50 (PO2 at 50% saturation) that occurs with decreased body temperature.

O2 transport during two forms of stagnant hypoxia following acid and base infusions

1983 ◽  
Vol 54 (6) ◽  
pp. 1518-1524 ◽  
Author(s):  
S. M. Cain ◽  
R. P. Adams
Keyword(s):  
Skeletal Muscle ◽  
Control Period ◽  
Pericardial Tamponade ◽  
The Other ◽  
Whole Body ◽  
O2 Uptake ◽  
Volume Depletion ◽  
O2 Transport ◽  
Organ Systems ◽  
Acid And Base

Cardiac output and mean arterial pressure were decreased in two groups of 16 anesthetized paralyzed dogs ventilated by pump. Pericardial tamponade was used in one group, and hemorrhagic hypotension was used in the other. After a 30-min control period and 30 min of circulatory shock by either method, 0.3N HCl was infused into half the dogs in each group and 1.0N NaHCO3 into the other half so that pH was separated by 0.3–0.4 units. The slope of the line relating O2 uptake to total O2 transport (blood flow X arterial O2 concentration) was used to evaluate how well the tissues extracted O2 relative to O2 supply. During the initial shock period before infusion, the slope of the line relating O2 uptake of left hindlimb skeletal muscle to total O2 transport in the limb was almost twice as great as that for the whole body. Acid infusion increased the slope of the whole-body line but did not alter that for the hindlimb. Base infusion, on the other hand, decreased the slope of the line for the limb during hemorrhagic shock but had no other effect. We concluded that acid either improved the distribution of a limiting blood supply to nonmuscle organ systems, or increased tissue capillary PO2 and O2 diffusion by decreasing hemoglobin O2 affinity (HOA), or both. The effect of an increased HOA with base infusion was noticeable in hindlimb skeletal muscle only when volume depletion by hemorrhage presumably greatly increased the normally short intercapillary diffusion distance in muscle.

Heat exchanges in wet suits

1985 ◽  
Vol 58 (3) ◽  
pp. 770-777 ◽  
Author(s):  
A. H. Wolff ◽  
S. R. Coleshaw ◽  
C. G. Newstead ◽  
W. R. Keatinge
Keyword(s):  
Body Temperature ◽  
Water Temperature ◽  
Cold Water ◽  
Whole Body ◽  
Metabolic Responses ◽  
Body Temperatures ◽  
Postural Changes ◽  
Wide Range ◽  
Heat Exchanges ◽  
Skin Temperatures

Flow of water under foam neoprene wet suits could halve insulation that the suits provided, even at rest in cold water. On the trunk conductance of this flow was approximately 6.6 at rest and 11.4 W . m-2 . C-1 exercising; on the limbs, it was only 3.4 at rest and 5.8 W . m-2 . degrees C-1 exercising; but during vasoconstriction in the cold, skin temperatures on distal parts of limbs were lower than were those of the trunk, allowing adequate metabolic responses. In warm water, minor postural changes and movement made flow under suits much higher, approximately 60 on trunk and 30 W . m-2 . degrees C-1 on limbs, both at rest and at work. These changes in flow allowed for a wide range of water temperatures at which people could stabilize body temperature in any given suit, neither overheating when exercising nor cooling below 35 degrees C when still. Even thin people with 4- or 7- mm suits covering the whole body could stabilize their body temperatures in water near 10 degrees C in spite of cold vasodilatation. Equations to predict limits of water temperature for stability with various suits and fat thicknesses are given.

Effects of training on muscle O2 transport at VO2max

1992 ◽  
Vol 73 (3) ◽  
pp. 1067-1076 ◽  
Author(s):  
J. Roca ◽  
A. G. Agusti ◽  
A. Alonso ◽  
D. C. Poole ◽  
C. Viegas ◽  
...  
Keyword(s):  
Blood Flow ◽  
Diffusing Capacity ◽  
O2 Uptake ◽  
O2 Transport ◽  
Straight Line ◽  
O2 Extraction ◽  
O2 Concentration ◽  
Individual Effects ◽  
O2 Supply ◽  
Sedentary Subjects

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.

O2 uptake in bled dogs after resuscitation with hypertonic saline or hydroxyethylstarch

1989 ◽  
Vol 257 (1) ◽  
pp. H238-H243
Author(s):  
K. Reinhart ◽  
T. Rudolph ◽  
D. L. Bredle ◽  
S. M. Cain
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Whole Body ◽  
Base Line ◽  
O2 Uptake ◽  
Shed Blood ◽  
Anesthetized Dogs ◽  
O2 Delivery ◽  
O2 Deficit

Hemodynamic and metabolic variables were measured for the whole body and isolated hindlimb of anesthetized dogs during resuscitation from hemorrhagic shock, using a small volume of hypertonic saline or a larger volume of hydroxyethylstarch. Twelve dogs were bled and maintained at a mean arterial pressure (MAP) of 40 mmHg for 30 min. Six dogs were then infused with 7.5% NaCl in 5 ml/kg hydroxyethylstarch (HTS group), and six received 6% hydroxyethylstarch alone (HES group) in an amount to approximate the maximum MAP achieved with hypertonic saline. Hypertonic saline replacement was approximately 16% of shed blood volume compared with 66% for hydroxyethylstarch. With hypertonic saline, cardiac output returned to base line, but O2 delivery did not. Hydroxyethylstarch increased cardiac output above base line, and O2 delivery was near base line. O2 uptake with hydroxyethylstarch peaked at 40% above control at 10 min of resuscitation. Excess O2 uptake in recovery was higher than O2 deficit in hemorrhage with the HES group but not with the HTS group. In the isolated hindlimb, vascular resistance decreased rapidly on hypertonic saline infusion but reached similar levels at 10 min of resuscitation with both fluids. With progressive lowering of blood flow to the pump-perfused hindlimb, ability of limb muscle to extract O2 was the same for the HTS and HES groups. With hemodilution by volume replacement with acellular fluid after hemorrhage, a seemingly adequate cardiac output and arterial pressure may be underresuscitation if O2 delivery does not meet the increased O2 demand.

Regional hemodynamic responses to hypoxia and hypermetabolism in polycythemic dogs

1989 ◽  
Vol 67 (1) ◽  
pp. 96-102 ◽  
Author(s):  
R. L. Stork ◽  
S. L. Dodd ◽  
C. K. Chapler ◽  
S. M. Cain
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Adverse Effects ◽  
Whole Body ◽  
Metabolic Demand ◽  
O2 Uptake ◽  
O2 Extraction ◽  
Anesthetized Dogs ◽  
Resting Muscle ◽  
Increased Blood Flow

Normovolemic polycythemia did not improve the ability of either resting muscle or gut to maintain O2 uptake (VO2) during severe hypoxia because of the adverse effects of increased viscosity on blood flow to those regions. The present study tested whether increased metabolic demand would promote vasodilation sufficiently to overcome those effects. We measured whole body, muscle, and gut blood flow, O2 extraction, and VO2 in anesthetized dogs after increasing hematocrit to 65% and raising O2 demand with 2,4-dinitrophenol (n = 8). We also tested whether regional denervation (n = 8) and hypervolemia (n = 6) affected these responses. After raising hematocrit and metabolism, the dogs were ventilated with air, with 9% O2–91% N2, and again with air for 30-min periods. Reduced blood flow and increased O2 demand, caused by increased blood viscosity and 2,4-dinitrophenol, respectively, increased O2 extraction so that muscle VO2 was nearly supply limited in normoxia. Denervation showed that vasoconstriction had increased in gut and muscle with hypoxia onset but this was overcome after 15 min. By then, muscle was receiving a major portion of cardiac output, whereas gut showed little change. With hypervolemia cardiac output increased in hypoxia but neither gut nor muscle increased blood flow in those experiments. Because regional and whole body VO2 fell in all groups during hypoxia to the same extent found earlier in normocythemic dogs, any real benefit of polycythemia under the conditions of these experiments was dubious at best.

A critical value for O2 transport in the rat

1982 ◽  
Vol 53 (3) ◽  
pp. 660-664 ◽  
Author(s):  
R. P. Adams ◽  
L. A. Dieleman ◽  
S. M. Cain
Keyword(s):  
Cardiac Output ◽  
O2 Uptake ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Normal Limits ◽  
O2 Transport ◽  
Anesthetized Rats ◽  
O2 Extraction ◽  
Normal Blood Flow ◽  
Heart Blood

Rat skeletal muscle O2 uptake (VO2) has been reported to be supply dependent even at normal blood flow rates. To find the point at which whole-animal VO2 became dependent on total O2 transport (TOT), intact anesthetized rats were ventilated under hypoxic, normoxic, and hyperoxic conditions while either normovolemic or hypovolemic. In this manner, TOT (cardiac output X arterial O2 content) was varied over a range of 513;80 ml . kg-1 . min-1 . VO2 was measured in a closed-circuit, double servospirometer system. O2 contents were measured in carotid artery and right heart blood. Arterial PCO2, pH, and rectal temperature were kept within normal limits. Above a TOT of 23 ml . kg-1 . min-1, reciprocal changes in O2 extraction and cardiac output maintained VO2 independently of TOT (VO2 = 17.9 +/- 1.3 ml . kg-1 . min-1). Below a TOT of 23 ml . kg-1 . min-1, Vo2 became linearly dependent upon TOT. For TOT between 5 and 16 ml . kg-1 . min-1, VO2 = 0.89 + 0.78 TOT (r = 0.98). These data indicate that above a critical TOT of approximately 23 ml . kg-1 . min-1, VO2 in anesthetized rats does not depend on TOT.

Gastrointestinal tract O2 uptake and regional blood flows during digestion in conscious newborn lambs

1981 ◽  
Vol 241 (4) ◽  
pp. G289-G293 ◽  
Author(s):  
D. I. Eldelstone ◽  
I. R. Holzman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Whole Body ◽  
O2 Uptake ◽  
Blood Flows ◽  
O2 Extraction ◽  
Regional Blood Flows ◽  
Gastrointestinal Blood Flow

We determined gastrointestinal tract O2 uptake, cardiac output, regional blood flows, and whole-body O2 uptake before and for 1-6 h after feeding in 10 chronically catheterized unanesthetized lambs (9-15 days of age). Total gastrointestinal blood flow (sum of blood flows to the stomach, small intestine, and colon, as calculated with the radioactive microsphere technique) increased 23% at 1 h postprandially. This increased flow at 1 h was due to a large increase in blood flow to the stomach, whereas blood flows to the small intestine and colon did not change significantly. By 2 h, stomach blood flow and thus total gastrointestinal blood flow had returned to fasting values. In contrast, total O2 uptake by the gastrointestinal tract organs (stomach, small intestine, and colon) increased 65% at 1 h, 51% at 2 h, and 28% at 3 h postprandially in association with increases in O2 extraction (O2 uptake/O2 delivery) of 41% at 1 h, 45% at 2 h, and 27% at 3 h. There were no digestion-related changes in whole-body O2 uptake or in cardiac output and its distribution to the brain, heart, kidney, liver (hepatic artery), and carcass. Our data indicate that postprandial increases in O2 demand by gastrointestinal tract organs of the newborn animal are met primarily by enhanced tissue O2 extraction, rather than by metabolic hyperemia, because the postprandial hyperemia observed in the neonate is of short duration and is confined to the stomach.

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.

Effects of norepinephrine and alpha-block on O2 uptake and blood flow in dog hindlimb

1981 ◽  
Vol 51 (5) ◽  
pp. 1245-1250 ◽  
Author(s):  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Control Period ◽  
The Other ◽  
Whole Body ◽  
Block Group ◽  
Limb Blood Flow ◽  
O2 Uptake ◽  
O2 Transport ◽  
Constant Rate

Norepinephrine (NE) may increase skeletal muscle O2 demand at the same time that it restricts O2 transport by vasoconstriction. We prevented vasoconstriction with 3.0 mg/kg phenoxybenzamine (alpha-Bl) in 10 anesthetized, paralyzed dogs ventilated at constant rate. Hindlimb and whole-body O2 uptake (VO2) and blood flow were measured for a 20-min control period, 20 min of NE infusion at 1 micrograms . kg-1 . min-1 either intravenously (iv) or intra-arterially (ia), and 20 min of recovery. The sequence was repeated for the other route of infusion. A second group of 10 without alpha-Bl was treated the same. Cardiac output increased with both ia and iv infusions in the no-block group and was unchanged in the alpha-Bl group. Limb blood flow increased 25% during the first 5 min of iv but decreased 40% with ia infusion in the no-block group. Whole-body VO2 was significantly increased 9% in both groups by both routes of NE. Limb VO2 was significantly decreased in the no-block group at 5 min of NE infusion iv when limb blood flow was increased. Limb VO2 did not change significantly in the alpha-Bl group with NE by either route. Hindlimb skeletal muscle did not participate in or contribute to the calorigenic effect of NE on the whole body, and that lack of effect was not due to any effect of NE on rate or distribution of blood flow in the limb.

Canine hindlimb blood flow and O2 uptake after inhibition of EDRF/NO synthesis

1994 ◽  
Vol 76 (3) ◽  
pp. 1166-1171 ◽  
Author(s):  
C. E. King ◽  
M. J. Melinyshyn ◽  
J. D. Mewburn ◽  
S. E. Curtis ◽  
M. J. Winn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Methyl Ester ◽  
Whole Body ◽  
O2 Uptake ◽  
Arterial Inflow ◽  
Anesthetized Dogs ◽  
Nos Inhibitor ◽  
The Right ◽  
Oxide Synthase

The nitric oxide synthase (NOS) inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) was used to determine whether the decrease in canine hindlimb blood flow (QL) with NOS inhibition would limit skeletal muscle O2 uptake (VO2). Arterial inflow and venous outflow from the hindlimb were isolated, and the paw was excluded from the circulation. Pump perfusion from the right femoral artery kept the hindlimb perfusion pressure near the auto-perfused level. Six anesthetized dogs received L-NAME (20 mg/kg i.v.), whereas another group of five dogs received the stereospecific enantiomer N omega-nitro-D-arginine methyl ester (D-NAME 20 mg/kg i.v.). Efficacy of NOS inhibition was tested with intra-arterial boluses of acetylcholine. QL was measured continuously, and whole body and hindlimb VO2 were measured 60 and 120 min after L-NAME or D-NAME. Whole body VO2 remained at control levels, but cardiac output decreased from 117 +/- 17 to 57 +/- 7 ml.kg-1.min-1 60 min after L-NAME (P < 0.05) and remained at that level for the duration of the experiment. Cardiac output was significantly higher in the D-NAME group than in the L-NAME group at 60 min. After L-NAME, QL fell 24% but VO2 increased from 5.2 +/- 0.4 to 7.4 +/- 0.6 ml.kg-1.min-1 (P < 0.05). No change in QL or VO2 occurred after D-NAME. NOS inhibition did not limit hindlimb VO2, despite decreases in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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