scholarly journals Hindlimb glucose and lactate metabolism during umbilical cord compression and acute hypoxemia in the late-gestation ovine fetus

2003 ◽  
Vol 284 (4) ◽  
pp. R954-R964 ◽  
Author(s):  
D. S. Gardner ◽  
D. A. Giussani ◽  
A. L. Fowden
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Oxygen Delivery ◽  
Lactate Concentration ◽  
Cord Compression ◽  
Oxygen Extraction ◽  
Metabolic Adaptation ◽  
Umbilical Blood ◽  
Time Flow ◽  
Lactate Output

The metabolic adaptation of the hindlimb in the fetus to a reversible period of adverse intrauterine conditions and, subsequently, to a further episode of acute hypoxemia has been examined. Sixteen sheep fetuses were chronically instrumented with vascular catheters and transit-time flow probes. In nine of these fetuses, umbilical blood flow was reversibly reduced by 30% from baseline for 3 days (umbilical cord compression), while the remaining fetuses acted as sham-operated, age-matched controls. Acute hypoxemia was subsequently induced in all fetuses by reducing maternal fractional inspired oxygen concentration for 1 h. Paired hindlimb arteriovenous blood samples were taken at appropriate intervals during cord compression and acute hypoxemia, and by using femoral blood flow and the Fick principle, substrate delivery, uptake, and output were calculated. Umbilical cord compression reduced blood oxygen content and delivery to the hindlimb and increased hindlimb oxygen extraction and blood glucose and lactate concentration in the fetus. However, hindlimb glucose and oxygen consumption were unaltered during umbilical cord compression. In contrast, hindlimb oxygen delivery and uptake were significantly reduced in all fetuses during subsequent acute hypoxemia, but glucose extraction, oxygen extraction, and hindlimb lactate output significantly increased in sham-operated control fetuses only. Preexposure of the fetus to a temporary period of adverse intrauterine conditions alters the metabolic response of the fetal hindlimb to subsequent acute stress. Additional data suggest that circulating blood lactate may be derived from sources other than the fetal hindlimb under these circumstances. The lack of hindlimb lactate output during acute hypoxemia in umbilical cord-compressed fetuses, despite a significant fall in oxygen delivery to and uptake by the hindlimb, suggests that the fetal hindlimb may not respire anaerobically after exposure to adverse intrauterine conditions.

Dynamics of cardiovascular responses to repeated partial umbilical cord compression in late-gestation sheep fetus

1997 ◽  
Vol 273 (5) ◽  
pp. H2351-H2360 ◽  
Author(s):  
Dino A. Giussani ◽  
Nobuya Unno ◽  
Susan L. Jenkins ◽  
Richard A. Wentworth ◽  
Jan B. Derks ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Cardiovascular Responses ◽  
Cord Compression ◽  
Secondary Response ◽  
Fetal Sheep ◽  
Compression Phase ◽  
Umbilical Blood ◽  
Group I ◽  
Umbilical Blood Flow

We characterized the detailed hemodynamics of fetal blood pressure, heart rate, common umbilical blood flow, and femoral blood flow responses to partial compression of the umbilical cord and tested the hypothesis that repeated cord compression modulates fetal cardiovascular responses in 10 chronically instrumented fetal sheep at ∼130 days of gestation. In five fetuses ( group I), partial compression of the umbilical cord was induced 12 times, each for 5 min at 15-min intervals. Each cord compression reduced common umbilical blood flow by 50% and produced modest falls in fetal pH (7.33 ± 0 to 7.29 ± 0) and arterial [Formula: see text] (21.1 ± 0.2 to 16.8 ± 0.2 mmHg) and a mild increase in arterial[Formula: see text] (49.9 ± 0.5 to 54.9 ± 0.4 mmHg). Sham experiments were performed in five other fetuses ( group II). Second-by-second analysis of group I fetal cardiovascular data revealed a clear biphasic response to partial cord compression. Phase I (1st min of cord compression) was characterized by a rapid bradycardia and a rapid femoral vasoconstriction (primary response); phase II ( minutes 2–5of cord compression) was characterized by a delayed bradycardia and a return of femoral vascular resistance toward baseline (secondary response). Repeated cord compression abolished the primary, but not the secondary, cardiovascular responses. These results demonstrate that fetal cardiovascular responses to stress may be modified by preexposure to repeated intrauterine challenges.

Effect of graded umbilical cord compression in fetal sheep at 0.6-0.7 gestation

1991 ◽  
Vol 261 (4) ◽  
pp. H1268-H1274 ◽  
Author(s):  
H. S. Iwamoto ◽  
E. Stucky ◽  
C. M. Roman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Umbilical Cord ◽  
Cord Compression ◽  
Plasma Norepinephrine ◽  
Fetal Sheep ◽  
Umbilical Blood ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Umbilical Blood Flow

To define responses of immature fetuses to asphyxia, we occluded the umbilical cord of 11 chronically instrumented fetal sheep at 82-94 days gestation and measured hemodynamic and catecholamine responses. The fetuses became acidemic, hypoxemic, and hypercarbic: arterial pH and PO2 decreased from 7.36 +/- 0.04 and 22 +/- 3 Torr to 7.10 +/- 0.04 (mean +/- SD, P less than 0.01) and 15 +/- 4 Torr (P less than 0.01), respectively, and PCO2 increased from 56 +/- 5 to 86 +/- 8 Torr (P less than 0.01) when umbilical blood flow was reduced by 75-88%. This degree of reduction in umbilical blood flow decreased cardiac output from 606 +/- 101 to 247 +/- 67 ml.min-1.kg-1 (P less than 0.01) and blood flow to hepatic, renal, musculoskeletal, and pulmonary vascular beds. Plasma norepinephrine concentrations increased from 1,557 +/- 975 to 16,718 +/- 14,672 pg/ml (P less than 0.05) with a 75-88% reduction, but mean arterial blood pressure did not increase. The absence of a hypertensive response probably relates to the decrease in cardiac output. These data indicate that asphyxia severely compromises cardiac output and organ perfusion in the midgestation fetus.

Lactate delivery (not oxygen) limits hepatic gluconeogenesis when blood flow is reduced

2006 ◽  
Vol 290 (1) ◽  
pp. E192-E198 ◽  
Author(s):  
Ken D. Sumida ◽  
Jerry H. Urdiales ◽  
Casey M. Donovan
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Oxygen Delivery ◽  
Liver Perfusion ◽  
Lactate Concentration ◽  
Oxygen Availability ◽  
Limiting Factor ◽  
Hepatic Gluconeogenesis ◽  
Experimental Protocols ◽  
The Impact

The purpose of this study was to determine, using the isolated liver perfusion technique, whether the limiting factor for hepatic gluconeogenesis (GNG) from lactate was precursor delivery or oxygen availability during reduced flow rates of 0.85 or 0.60 ml·min−1·g liver−1. After a 24-h fast, three different experimental protocols were employed. Protocol 1 examined the impact on GNG when reservoir lactate concentration was maintained but oxygen delivery was elevated via increases in hematocrit (Hct). Elevating the Hct from 22.5 ± 0.8% to 30.9 ± 0.4% at a blood flow of 0.89 ± 0.01 ml·min−1·g liver−1 increased the oxygen consumption (V̇o2) but did not augment GNG. Similarly, when the Hct was elevated from 22.5 ± 0.8% to 41.5 ± 0.7% at 0.59 ± 0.04 ml·min−1·g liver−1, V̇o2 was increased, but GNG was unaffected. Protocol 2 examined the impact on GNG when Hct was maintained but precursor delivery was elevated via increases in reservoir lactate concentration ([LA]). Specifically, elevating the [LA] from 2.31 ± 0.07 to 3.61 ± 0.33 mM at a flow rate of 0.82 ± 0.04 ml·min−1·g liver−1 significantly increased GNG. Similarly, elevating the [LA] from 2.31 ± 0.07 to 4.24 ± 0.37 mM at a flow rate of 0.58 ± 0.02 ml·min−1·g liver−1 increased GNG. Finally, we examined the impact of increasing both the oxygen and lactate delivery ( Protocol 3). Again, V̇o2 was elevated with increased oxygen delivery, but GNG was not augmented beyond that observed with elevations in lactate delivery alone, i.e., Protocol 2. The results indicate that, during decrements in blood flow, GNG is limited primarily by precursor delivery, not oxygen availability.

Relationship between the umbilical cord coiling index and the umbilical blood flow at 11-13 weeks of gestation

2013 ◽  
Vol 33 (8) ◽  
pp. 764-769 ◽  
Author(s):  
Junichi Hasegawa ◽  
Masamitsu Nakamura ◽  
Shoko Hamada ◽  
Ryu Matsuoka ◽  
Kiyotake Ichizuka ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Umbilical Blood ◽  
Umbilical Blood Flow

Differences between the effects of noradrenaline and the β-adrenoceptor agonist BRL 28410 in brown adipose tissue and hind limb of the anaesthetized rat

1986 ◽  
Vol 64 (8) ◽  
pp. 1111-1114 ◽  
Author(s):  
Peter L. Thurlby ◽  
Rodney D. M. Ellis
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Uptake ◽  
Brown Adipose Tissue ◽  
Oxygen Delivery ◽  
Hind Limb ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Adrenoceptor Agonist ◽  
Brown Adipose

In mature (450–600 g) 21 °C-acclimated male rats, anaesthetized with urethane, blood flow (measured by the radioactive microsphere technique) to brown adipose tissue (BAT) was determined during the infusion of the β-adrenoceptor agonist BRL 28410 or noradrenaline bitartrate at doses chosen to give similar increases in whole body oxygen uptake. Blood flow to BAT during BRL 28410 infusion was only about one third of that found during noradrenaline infusion although increases in whole body thermogenesis were similar (55 and 77% for BRL 28410 and noradrenaline, respectively). This suggests that BAT may be less involved in the thermogenic response to BRL 28410 than to noradrenaline. In a separate experiment using slightly smaller rats (350–500 g) hind limb oxygen uptake was measured in situ using a venous bypass preparation. BRL 28410, at a dose having a maximum effect on whole body thermogenesis (53% increase), had no effect on oxygen delivery to the hind limb but significantly increased oxygen extraction by 33% (p < 0.001). In contrast, noradrenaline, also at a dose that maximally increased whole body thermogenesis, led to a 35% decrease in oxygen delivery to the hind limb and no change in oxygen extraction. For the thermogenic β-agonist BRL 28410 the hind limb, and presumably muscular tissue in general, may be contributing to thermogenesis.

Effect of Acute Respiratory Acidosis on the Limits of Oxygen Extraction during Hemorrhage

1996 ◽  
Vol 85 (4) ◽  
pp. 817-822 ◽  
Author(s):  
Michael E. Ward
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Oxygen Content ◽  
Oxygen Delivery ◽  
Tissue Oxygenation ◽  
Respiratory Acidosis ◽  
Oxygen Availability ◽  
Oxygen Extraction ◽  
Oxygen Extraction Ratio ◽  
Critical Oxygen

Background Hypercapnia can impair cells' capacity to maintain energy status anerobically and enhances the risk of hypoxic injury when oxygen availability is reduced. The ability to maintain tissue oxygenation is determined by both bulk blood flow and the efficiency of oxygen extraction. Bulk blood flow is maintained during hypercapnia through increased sympathetic activity. The effect of hypercapnia on oxygen extraction, however, is unknown. This study evaluates the effect of hypercapnia on cells' capacity to adapt to reductions in oxygen availability by increasing oxygen extraction. Methods In three groups of paralyzed, mechanically ventilated dogs that were anesthetized with alpha-chloralose, the concentration of carbon dioxide in the inhaled gas mixture was adjusted to achieve normocapnia, moderate hypercapnia (Paco2 = 72 +/- 3 [SE] mmHg) or severe hypercapnia (Paco2 = 118 +/- 4 [SE] mmHg). Stepwise hemorrhage was induced until each dog's blood pressure was destabilized. At each stage in the hemorrhage protocol, the oxygen delivery, oxygen consumption, and oxygen extraction ratios (ratio of arteriovenous oxygen content difference to arterial oxygen content) were determined. Results At the point of onset of delivery dependence of oxygen consumption, the oxygen delivery rate (critical oxygen delivery) was 7.8 +/- 1.5 (SE) ml.kg-1.min-1 and the oxygen extraction ratio (critical oxygen extraction ratio) was 0.72 +/- 0.04 (SE) in the normocapnic dogs. Moderate hypercapnia had no effect on these parameters. In the severely hypercapnic dogs, the critical values for oxygen delivery and extraction ratios were 12.5 +/- 1.8 (SE) ml.kg-1.min-1 and 0.54 +/- 0.035 (SE), respectively (P &lt; 0.05 for differences from the normocapnic dogs). Conclusions The results identify a previously unrecognized threat to tissue oxygenation and emphasize the importance of ensuring adequate oxygen delivery when adopting mechanical ventilatory strategies that permit respiratory acidosis to develop.

The effect of vasopressin on fetal oxygenation in sheep

1984 ◽  
Vol 62 (1) ◽  
pp. 27-30 ◽  
Author(s):  
D. W. Rurak ◽  
N. C. Gruber
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Base Excess ◽  
Percentage Increase ◽  
Umbilical Blood ◽  
Umbilical Blood Flow ◽  
Fetal Oxygenation

To examine the effects of vasopressin on fetal oxygenation the hormone was infused intravenously for 1 h (1.4–3.5 mU∙min−1∙kg fetal weight−1) to chronically catheterized fetal lambs in utero (113–137 days gestation). Arterial pressure rose (48.3 to 59.6 mmHg) (1 mmHg = 133.322 Pa) and heart rate fell (185.3 to 141.0 beats/min) during the infusion. There was a significant increase in fetal arterial [Formula: see text] (20.0 to 23. 1 mmHg) and significant declines in pH (7.414 to 7.381) and base excess. Umbilical blood flow rose, and the percentage increase in flow (23%) was identical to the proportional rise in arterial pressure. Accompanying the rise in umbilical blood flow was a rise in umbilical oxygen delivery. But as there was no change in fetal oxygen consumption, fractional oxygen extraction by the fetus fell significantly (0.31 to 0.25). These data indicate that the vasopressin-induced rise in fetal vascular [Formula: see text] results from an increase in umbilical oxygen delivery and concomitant fall in fractional extraction. Fetal vasopressin levels are greatly elevated during hypoxia, and under conditions of reduced oxygen supply, the effects of the hormone on umbilical oxygen delivery and vascular [Formula: see text] could have definite survival value.

Effects of afferent neural stimulation on critical oxygen delivery: a hemodynamic explanation

1995 ◽  
Vol 269 (6) ◽  
pp. R1448-R1454 ◽  
Author(s):  
E. Kirkman ◽  
H. Zhang ◽  
H. Spapen ◽  
R. A. Little ◽  
J. L. Vincent
Keyword(s):  
Blood Flow ◽  
Oxygen Delivery ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Oxygen Extraction ◽  
Whole Body ◽  
Afferent Nerve Fibers ◽  
Femoral Blood Flow ◽  
Critical Oxygen ◽  
Renal Flow

Injury and activation of somatic afferent nerve fibers may alter critical oxygen delivery (DO2C), the point at which oxygen consumption becomes dependent upon delivery, and hence reduce tolerance to hypovolemia. The present study investigated the mechanism of this. Anesthetized mongrel dogs were divided into two groups: control (n = 6) and those subject to brachial nerve stimulation (BNS; n = 5). Whole body oxygen delivery (DO2I) and consumption were initially similar in both groups. DO2I was reduced by cardiac tamponade to determine DO2C. DO2C was significantly higher in BNS compared with control (11.5: 11.0-16.7 vs. 7.5: 6.9-9.5 ml.min-1.kg-1; median: Q1 - Q3), whereas critical oxygen extraction ratios were lower (54.8: 39.7-61.2 vs. 78.3: 53.5-92.4%). At approximately DO2C, normalized femoral blood flow was lower than renal flow in control (renal-femoral difference 17.4: 8.7-40.0%) but not in BNS (-7.8: -14.8 to +11.8%). These results indicate that activation of somatic afferent nerve fibers elevates DO2C. This could be due to an impairment in peripheral oxygen extraction as a consequence of a redistribution of blood flow away from metabolically active vital organs toward relatively inactive skeletal muscle.

Group B Streptococcus-induced acidosis in newborn swine: regional oxygen transport and lactate flux

1992 ◽  
Vol 72 (1) ◽  
pp. 272-277 ◽  
Author(s):  
E. S. Barefield ◽  
W. Oh ◽  
B. S. Stonestreet
Keyword(s):  
Metabolic Acidosis ◽  
Oxygen Uptake ◽  
Oxygen Delivery ◽  
Group B Streptococcus ◽  
Lactate Concentration ◽  
Oxygen Metabolism ◽  
Oxygen Extraction ◽  
Vascular Bed ◽  
Vascular Beds ◽  
Group B

To investigate the mechanism of metabolic acidosis resulting from group B streptococcal sepsis, oxygen metabolism and lactate flux of the cerebrum, hindlimb, liver, splanchnic organs, and systemic vascular bed as a whole were examined. Nine 3- to 5-day-old awake and spontaneously breathing piglets were studied before and after 3, 4, and 5 h of continuous live group B Streptococcus infusion. After 5 h, oxygen delivery was decreased to all organs and to the whole systemic vascular bed. Increased oxygen extraction compensated for reduced oxygen delivery in the liver and splanchnic organs; however, it only partially offset reduced oxygen delivery to the hindlimb and systemic vascular bed. Cerebral oxygen extraction did not increase. As a result, oxygen uptake was reduced in the cerebrum, hindlimb, and systemic vascular bed. At 5 h of bacterial infusion, arterial lactate concentration was increased with regional lactate efflux from the cerebrum and hindlimb and influx to the liver (P less than 0.05 vs. zero or no net flux). We conclude that group B Streptococcus-induced metabolic acidosis is associated with regional lactate efflux from vascular beds in which oxygen uptake is reduced. We speculate that the quantity of net lactate efflux from vascular beds with insufficient oxygen uptake exceeds the net influx into organs such as the liver, resulting in metabolic acidosis.

Sign in / Sign up

Export Citation Format

Share Document