Effects of varying hematocrit on intestinal oxygen uptake in neonatal lambs

1985 ◽  
Vol 248 (4) ◽  
pp. G432-G436 ◽  
Author(s):  
I. R. Holzman ◽  
B. Tabata ◽  
D. I. Edelstone

We chronically catheterized 15 newborn lambs (9.5 +/- 2.8 days) and measured intestinal blood flow (Qi) by the radionuclide microsphere technique at hematocrit levels ranging from 10 to 55%. Seven animals were made progressively anemic and eight polycythemic by means of exchange transfusions. Using the Fick principle, we calculated intestinal oxygen delivery (Di o2), oxygen consumption (Vi o2), and oxygen extraction. Initial base-line values were Qi = 195.5 ml . min-1 . 100 g intestine-1, Di o2 = 22.1 ml . min-1 . 100 g-1, Vi o2 = 4.8 ml . min-1 . 100 g-1, and O2 extraction = 22.5%. As the hematocrit was lowered, Di o2 decreased and O2 extraction increased and vice versa when the hematocrit was raised. Vi o2 remained constant, but Qi did not correlate with changes in hematocrit. However, intestinal blood flow, as a percent distribution of total blood flow, decreased with lower hematocrit levels. At no time was there any evidence of anaerobic metabolism as measured by excess lactate production. Our data indicate that the intestines of neonatal lambs are capable of maintaining their metabolic needs over a wide range of oxygen availability induced by a changing hematocrit. The primary mechanism is through alteration of oxygen extraction. Within the range of our experiments, no critically low oxygen availability was attained at which anaerobic metabolism became significant.

1983 ◽  
Vol 244 (3) ◽  
pp. G278-G283
Author(s):  
D. I. Edelstone ◽  
D. R. Lattanzi ◽  
M. E. Paulone ◽  
I. R. Holzman

In 12 chronically catheterized neonatal lambs, we determined intestinal tract blood flow (Qi) and O2 consumption (VO2i) at O2 contents of arterial blood (CaO2) ranging from 15.3 to 3.2 ml O2/dl blood. We measured Qi with the radioactive microsphere technique and computed intestinal O2 delivery (DO2i), VO2i, and O2 extraction (VO2i/DO2i) using the Fick principle. In lambs breathing air, mean Qi = 214 ml X min-1 X 100 g intestine-1, DO2i = 27.0 ml O2 X min-1 X 100 g-1, O2 extraction = 21%, and VO2i = 5.6 ml O2 Xmin-1 X 100 g-1. During reductions in CaO2, Qi and DO2i decreased. Intestinal O2 extraction increased sufficiently, however, so that VO2i was maintained over the range of CaO2 from 15.3 to about 6.5 ml O2/dl blood. VO2i was independent of Qi at Qi greater than 160 ml X min-1 X 100 g-1. When CaO2 was reduced below values of 6.5 ml O2/dl blood, corresponding to Qi less than 160 ml X min-1 X 100 g-1, VO2i fell in association with increases in the H+ concentration difference between mesenteric venous and arterial blood. These data indicate that the intestinal tract of the neonatal lamb can meet its oxygen requirements when O2 supply varies over a wide range. When O2 availability reaches a critically low level, intestinal anaerobic metabolism develops as the O2 supply to the neonatal intestinal tract becomes inadequate for the O2 demand.


1988 ◽  
Vol 254 (1) ◽  
pp. E45-E51 ◽  
Author(s):  
A. A. van Lambalgen ◽  
H. C. Runge ◽  
G. C. van den Bos ◽  
L. G. Thijs

High serum lactate may not reflect the severity of endotoxin shock: the lactate load could even be formed immediately after the endotoxin challenge. During the first 30 min after endotoxin injection (Escherichia coli; 1.5 mg/kg iv) into anesthetized dogs (4 mg.kg-1.h-1 etomidate, n = 19) we studied arterial lactate concentration; contributions of portal and splanchnic (n = 6), renal and pulmonary (n = 7), and femoral (n = 6) vascular beds to the early lactate rise; and regional O2 extraction and blood flow (microspheres). In control dogs (n = 5, no endotoxin), we found no significant hemodynamic and biochemical changes. Endotoxin caused an immediate decrease in blood pressure, cardiac output, and organ perfusion, followed by recovery after approximately 5 min to approximately 75% of preshock values at t = 30 min (except for renal blood flow, which remained low). Arterial lactate concentration started to increase almost immediately after endotoxin and increased rapidly until t = 15 min (to 300%) and then leveled off, but in spite of the hemodynamic recovery it remained elevated. A major part of the early increase in lactate concentration can be explained by splanchnic lactate production. The total splanchnic bed released more lactate than the portal bed, indicating that the liver produces lactate. We conclude that the lactate concentration later in canine endotoxin shock depends on events that occur during early shock in which the liver may play a crucial role.


1977 ◽  
Vol 233 (1) ◽  
pp. H106-H113 ◽  
Author(s):  
K. M. Jan ◽  
S. Chien

Twenty-five closed-chest pentobarbitalized dogs were used for studying coronary flow dynamics and myocardial oxygen utilization following variations of hematocrit (Hct) by isovolumetric exchange of blood with plasma or packed red cells. Coronary blood flow (133Xe washout) and cardiac output varied inversely with Hct. Coronary systemic, and pulmonary flow resistances varied in the same direction with Hct. Blood viscosity played a significant role in determining the flow resistances in these three regions. Analysis of vascular hindrance (vascular resistance/blood viscosity) suggested that coronary vasodilation occurred following Hct changes beyond the range of 20-60%. In systemic and pulmonary circulations, however, there was vasoconstriction following hemodilution. The range of optimum Hct for maximum O2 transport (blood flow X arterial O2 content) was much wider in coronary (20-60% Hct) than in systemic circulation (40-60% Hct). The O2 consumptions in total body and in myocardium were essentially constant over a wide range of Hct (20-60%). The maintenance of total body O2 consumption over the Hct range of 20-40% was attributable to an increase in A-V O2 extraction. The O2 extraction ratio in the coronary circulation was constant over the entire range of Hct studied, suggesting that the myocardial O2 consumption was primarily determined by the coronary O2 transport.


2019 ◽  
Vol 31 (4) ◽  
pp. 683 ◽  
Author(s):  
G. Rizzoto ◽  
C. Hall ◽  
J. V. Tyberg ◽  
J. C. Thundathil ◽  
N. A. Caulkett ◽  
...  

There is a paradigm that testicular hyperthermia fails to increase testicular blood flow and that an ensuing hypoxia impairs spermatogenesis. However, in our previous studies, decreases in normal and motile spermatozoa after testicular warming were neither prevented by concurrent hyperoxia nor replicated by hypoxia. The objective of the present study was to determine the effects of increasing testicular temperature on testicular blood flow and O2 delivery and uptake and to detect evidence of anaerobic metabolism. Under general anaesthesia, the testicular temperature of nine crossbred rams was sequentially maintained at ~33°C, 37°C and 40°C (±0.5°C; 45min per temperature). As testicular temperature increased from 33°C to 40°C there were increases in testicular blood flow (13.2±2.7 vs 17.7±3.2mLmin−1 per 100g of testes, mean±s.e.m.; P<0.05), O2 extraction (31.2±5.0 vs 47.3±3.1%; P<0.0001) and O2 consumption (0.35±0.04 vs 0.64±0.06mLmin−1 per 100g of testes; P<0.0001). There was no evidence of anaerobic metabolism, based on a lack of change in lactate, pH, HCO3− and base excess. In conclusion, these data challenge the paradigm regarding scrotal–testicular thermoregulation, as acute testicular hyperthermia increased blood flow and tended to increase O2 delivery and uptake, with no indication of hypoxia or anaerobic metabolism.


1996 ◽  
Vol 85 (4) ◽  
pp. 817-822 ◽  
Author(s):  
Michael E. Ward

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 < 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.


1987 ◽  
Vol 253 (4) ◽  
pp. E349-E353 ◽  
Author(s):  
M. Takeuchi ◽  
P. A. Low

We studied the dynamic effects of exsanguination of approximately one-third of rat blood volume over 3-12 min on energy metabolism and blood flow in rat sciatic nerves. Nerve high-energy phosphate compounds were relatively well maintained. There was a modest stimulation of anaerobic metabolism at slow rates of exsanguination, and glucose stores were slightly increased. These findings indicate that when stressed because of significant blood loss, compensatory mechanisms, presumably adrenosympathetic mediated, are effective in vivo. We recorded nerve blood flow (NBF), endoneurial oxygen tension, and mean arterial pressure simultaneously; NBF was linearly related to blood pressure (BP) over a wide range of BPs, confirming that NBF does not significantly autoregulate. Endoneurium underwent oxygen-exchange, indicating that peripheral nerve microvasculature is physiologically nutritive. NBF fell before and at a faster rate than BP, indicating that it is a capacitive system. Nerves also adapted to declining oxygen supplies, presumably by reducing their oxygen consumption. The physiological implications of such a system are discussed.


2013 ◽  
Vol 101 (1) ◽  
pp. 9-19 ◽  
Author(s):  
Kelly A. van Bragt ◽  
Hussein M. Nasrallah ◽  
Marion Kuiper ◽  
Joost J. Luiken ◽  
Ulrich Schotten ◽  
...  

1992 ◽  
Vol 263 (2) ◽  
pp. G254-G260 ◽  
Author(s):  
K. D. Crissinger ◽  
D. L. Burney

Age-related differences in the intestinal hemodynamic and oxygenation responses to carbohydrate, protein, and lipid were studied in 1-day-, 3-day-, 2-wk-, and 1-mo-old piglets. A branch of the mesenteric vein draining an isolated loop of jejunoileum was used to measure intestinal blood flow, arteriovenous oxygen content difference, and venous and capillary pressure and to calculate oxygen uptake and vascular resistance. Fractionated intestinal flow was measured with radiolabeled microspheres. Measurements were made before and after luminal placement of either 5% glucose, 2.3% casec, or 5% corn oil. In 1-day-old animals, unlike all older age groups, total intestinal blood flow and vascular resistance were unchanged by any nutrient. Fractionated flow to the mucosa/submucosa levels did, however, increase in the intestine of 1-day-old piglets to a similar extent as that in older age groups. Placement of lipid or protein into the lumen led to increased oxygen uptake in all age groups, whereas carbohydrate absorption resulted in no increase in intestinal oxygen consumption in 1- and 3-day-old animals. In 1-day-olds, the increased oxygen consumption was achieved by enhanced oxygen extraction with no change in total blood flow, whereas all other groups demonstrated increases in blood flow and/or oxygen extraction. Compared with a mixed meal, oxygen consumption was not significantly greater for an individual nutrient component.


1982 ◽  
Vol 242 (1) ◽  
pp. H50-H54 ◽  
Author(s):  
D. I. Edelstone ◽  
I. R. Holzman

In seven chronically catheterized fetal lambs, blood flow and oxygen consumption (VO2) in the combined small and large intestines were determined at various oxygen concentrations in fetal arterial blood (CaO2). Intestinal blood flow (Qi) was measured with the radioactive-microsphere technique; intestinal oxygen delivery (DO2 = Qi X CaO2), VO2 [Qi X C(a-v)O2, where oxygen extraction [C(a-v)O2/CaO2] were computed with the Fick equation. Compared with normally oxygenated fetuses (CaO2 greater than 6.6 ml/dl), moderately hypoxemic fetuses (CaO2 = 4.4-6.6 ml/dl) had decreased intestinal DO2, increased oxygen extraction, and no change in intestinal VO2, Qi, or mesenteric-venous pH and base excess. During severe fetal hypoxemia (CaO2 less than 4.4 ml/dl), DO2 decreased further while oxygen extraction increased substantially. Intestinal VO2 dropped, however, because the rise in oxygen extraction could no longer completely compensate for the reduced DO2. With severe hypoxemia, Qi and mesenteric-venous pH and base excess also fell. These data indicate that the fetal intestinal tract is able to meet its oxygen needs during hypoxemia until a critically low level of oxygenation is reached. Below this level intestinal oxygenation becomes inadequate, and anaerobic metabolism ensures.


1988 ◽  
Vol 254 (4) ◽  
pp. G560-G565 ◽  
Author(s):  
K. D. Crissinger ◽  
P. R. Kvietys ◽  
D. N. Granger

Stimulation of sympathetic fibers or infusion of norepinephrine (NE) into the superior mesenteric artery (SMA) leads to an initial decrease in intestinal blood flow, which is followed by a return of flow toward the base-line value (autoregulatory escape) despite continued nerve stimulation or NE infusion. Although the mechanisms responsible for “autoregulatory escape” have not been defined, accumulation of vasodilator metabolites is frequently invoked to explain this phenomenon. Inasmuch as histamine and adenosine exist in high concentrations in the intestinal mucosa and both are potent vasodilators, we examined the effects of chlorpheniramine (an H1 blocker) and adenosine deaminase (degrades adenosine) on autoregulatory escape from NE infusion. In autoperfused piglet intestinal preparations, we measured SMA blood flow and the arteriovenous oxygen difference during intra-arterial NE infusion before and after blockade with chlorpheniramine or adenosine deaminase. Adenosine deaminase pretreatment increased the peak vasoconstrictor and reduced the steady-state escape responses to NE infusion. Chlorpheniramine did not affect either the vasoconstrictor or escape responses. The oxygen uptake changes induced by NE infusion were not dramatically modified by either treatment. These results indicate that adenosine but not histamine is responsible for at least part of the escape of intestinal blood flow from NE infusion.


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