Testicular hyperthermia increases blood flow that maintains aerobic metabolism in rams

2019 ◽  
Vol 31 (4) ◽  
pp. 683 ◽  
Author(s):  
G. Rizzoto ◽  
C. Hall ◽  
J. V. Tyberg ◽  
J. C. Thundathil ◽  
N. A. Caulkett ◽  
...  
Keyword(s):  
Blood Flow ◽  
General Anaesthesia ◽  
Anaerobic Metabolism ◽  
Base Excess ◽  
O2 Consumption ◽  
O2 Extraction ◽  
Testicular Blood Flow ◽  
Testicular Thermoregulation ◽  
O2 Delivery ◽  
Increased Blood Flow

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.

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.

Intestinal O2 consumption and 86Rb extraction during arterial hypoxia.

1978 ◽  
Vol 234 (3) ◽  
pp. E248
Author(s):  
A P Shepherd
Keyword(s):  
Blood Flow ◽  
Tissue Oxygenation ◽  
Capillary Density ◽  
Mean Value ◽  
O2 Consumption ◽  
Resistance Vessels ◽  
Capillary Bed ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
Increased Blood Flow

Earlier reports indicated that arterial hypoxia not only dilated intestinal resistance vessels but also increased capillary filtration coefficients. The latter finding was interpreted as reflecting an increased number of perfused capillaries. Because both increased blood flow and increased capillary density would tend to maintain tissue oxygenation in spite of arterial hypoxia, the main purpose of this paper was to determine how effectively intestinal O2 utilization is maintained during arterial hypoxia. Therefore, I perfused isolated loops of canine small bowel at constant arterial pressure. Under this condition, reducing arterial PO2 to a mean value of 46 +/- 2.4 mmHg caused blood flow to increase to 146% of control, and O2 consumption was kept within 26% of control. In gut loops perfused at constant blood flow, arterial hypoxia depressed O2 uptake still further, but measurements of 86Rb extraction confirmed that the density of the perfused capillary bed increased. Thus, the responses of both resistance and exchange vessels tend to maintain O2 delivery to intestinal tissue during arterial hypoxia.

Cerebral circulatory response to carbon monoxide and hypoxic hypoxia in the lamb

1982 ◽  
Vol 243 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Hypoxic Hypoxia ◽  
O2 Consumption ◽  
Dissociation Curve ◽  
Oxyhemoglobin Dissociation Curve ◽  
O2 Extraction ◽  
O2 Delivery ◽  
Oxyhemoglobin Dissociation

In 14 unanesthetized newborn lambs the relationship between cerebral blood flow (measured by radiolabeled microspheres) and arterial O2 saturation (SaO2) was compared during two types of hypoxia: hypoxic hypoxia and carbon monoxide (CO) hypoxia. Cerebral venous samples were obtained from the sagittal sinus. The Increase in blood flow was 47% greater during CO than during hypoxic hypoxia. Cerebral O2 consumption and O2 delivery were constant during hypoxic hypoxia. Thus fractional O2 extraction, which equals O2 consumption/O2 delivery, remained constant with hypoxic hypoxia. During CO hypoxia, although O2 consumption remained constant, O2 delivery increased and fractional O2 extraction decreased. This decline in fractional O2 extraction was correlated with the leftward shift of the oxyhemoglobin dissociation curve that accompanied CO hypoxia. We suggest that cerebral blood flow depends on both SaO2 and the position of the oxyhemoglobin dissociation curve in the newborn lamb. However, this correlation does not exclude other potential histotoxic effects contributing to the relative overperfusion with CO hypoxia.

Effects of hemodilution on gastric and intestinal oxygenation

1989 ◽  
Vol 256 (1) ◽  
pp. H171-H178 ◽  
Author(s):  
J. W. Kiel ◽  
G. L. Riedel ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Carrying Capacity ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
O2 Consumption ◽  
O2 Uptake ◽  
O2 Extraction ◽  
The Right ◽  
O2 Delivery

To determine the effects of hemodilution on gastric and intestinal oxygenation, isolated segments of canine stomach and small bowel were perfused by a pressurized reservoir with blood at hematocrits of 40 and 20%. Arteriovenous O2 difference, blood flow, and arterial and venous pressures were monitored continuously as perfusion pressure was reduced in 30-mmHg steps from 180 to 30 mmHg. O2 consumption was calculated as the product of the steady-state arteriovenous O2 difference and blood flow at each perfusion pressure. Gastric and intestinal O2 uptake were relatively well maintained over most of the pressure range when the hematocrit was set at 40%. After hemodilution, gastric O2 uptake decreased significantly only at 90 and 60 mmHg, but intestinal O2 uptake was significantly reduced except at 30 mmHg. When gastric and intestinal O2 uptake were plotted as a function of blood flow, the O2 uptake vs. blood flow relationship were shifted down and to the right by hemodilution. Hemodilution also linearized the O2 uptake vs. blood flow relationship in the intestine. However, when O2 uptake was plotted as function of O2 delivery, the gastric O2 uptake vs. delivery curves at the two hematocrits were superimposed on each other, but the O2 uptake vs. delivery curves for the intestine diverged except at low rates of O2 delivery. We conclude that by reducing the O2-carrying capacity of the blood, hemodilution adversely affects gastric and intestinal oxygenation. Our results also indicate that hemodilution lowers gastric O2 uptake by reducing O2 delivery; however, hemodilution lowers intestinal O2 uptake not only by reducing O2 delivery but also by impairing O2 extraction.

Effect of endotoxin on systemic and skeletal muscle O2 extraction

1988 ◽  
Vol 65 (3) ◽  
pp. 1377-1382 ◽  
Author(s):  
R. W. Samsel ◽  
D. P. Nelson ◽  
W. M. Sanders ◽  
L. D. Wood ◽  
P. T. Schumacker
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
O2 Consumption ◽  
Human Pathology ◽  
O2 Extraction ◽  
O2 Delivery ◽  
And Control

Patients with the adult respiratory distress syndrome (ARDS) show a pathological dependence of O2 consumption (VO2) on O2 delivery (QO2, blood flow X arterial O2 content). In these patients, a defect in tissues' ability to extract O2 from blood can leave tissue O2 needs unmet, even at a normal QO2. Endotoxin administration produces a similar state in dogs, and we used this model to study mechanisms that may contribute to human pathology. We measured systemic and hindlimb VO2 and QO2 while reducing cardiac output by blood withdrawal. At the onset of supply dependence, the systemic QO2 was 11.4 +/- 2.7 ml.kg-1.min-1 in the endotoxin group vs. 8.0 +/- 0.7 in controls (P less than 0.05). At this point, the endotoxin-treated animals extracted only 61 +/- 11% of the arterial O2, whereas control animals extracted 70 +/- 7% (P less than 0.05). Systemic VO2 rose by 15% after endotoxin (P less than 0.05) but did not change in controls. Despite this poorer systemic ability to extract O2 by the endotoxin-treated dogs, isolated hindlimb O2 extraction at the onset of supply dependence was the same in endotoxin-treated and control dogs. At normal levels of QO2, hindlimb VO2 in endotoxin-treated dogs was 23% higher than in controls (P less than 0.05). Fractional blood flow to skeletal muscle did not differ between control and endotoxin-treated dogs. Thus skeletal muscle was not overperfused in endotoxemia and did not contribute to a systemic extraction defect by stealing blood flow from other tissues. Skeletal muscle in endotoxin-treated dogs demonstrated an increase in VO2 but no defect in O2 extraction, differing in both respects from the intestine.

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.

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)

Adequacy of tissue oxygenation in intact dog intestine

1984 ◽  
Vol 56 (4) ◽  
pp. 1065-1069 ◽  
Author(s):  
C. M. Grum ◽  
R. G. Fiddian-Green ◽  
G. L. Pittenger ◽  
B. J. Grant ◽  
E. D. Rothman ◽  
...  
Keyword(s):  
Critical Point ◽  
Tissue Oxygenation ◽  
Base Line ◽  
O2 Consumption ◽  
Diffusion Limitation ◽  
Ischemic Group ◽  
O2 Extraction ◽  
The Face ◽  
O2 Delivery ◽  
Hypoxic Group

Changes in O2 consumption, O2 extraction, and intramural pH, resulting from a decreasing O2 delivery, were studied in the intact dog intestine. The O2 delivery was decreased by ischemia, hypoxia, and combined hypoxia-ischemia. A noninvasive approach for determining intramural pH based on the principle of tonometry was used. There was a strong correlation between the changes in intramural pH and intestinal O2 consumption as O2 delivery was decreased. Intramural pH and O2 consumption were initially maintained in the face of decreasing O2 delivery, but after a critical point they decreased. This critical point was 60.3 +/- 1.6% of base-line O2 delivery in the ischemic group and 51.3 +/- 2.7% of base line in the hypoxic-ischemic group. Despite a decrease to 36.0 +/- 5.6% of base-line O2 delivery, the intramural pH and O2 consumption did not decrease in the hypoxic group. O2 extraction increased with decreasing O2 delivery but did not plateau, indicating no diffusion limitation. The data suggest that blood flow is the major factor limiting intestinal O2 consumption. It is concluded that the noninvasive measure of intramural pH is a good marker of the adequacy of tissue oxygenation in canine intestine.

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.

Fetal oxygen uptake, oxygenation, and acid-base balance as a function of uterine blood flow

1983 ◽  
Vol 244 (6) ◽  
pp. H749-H755 ◽  
Author(s):  
R. B. Wilkening ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Base Excess ◽  
Umbilical Vein ◽  
Delivery Rate ◽  
Uterine Blood Flow ◽  
O2 Uptake ◽  
Acid Base Balance ◽  
Venous Pco2 ◽  
Base Balance ◽  
O2 Delivery

The rate of O2 delivery to the pregnant uterus (FaO2) was decreased in chronic sheep preparations by mechanical occlusion of uterine blood flow. The relationship of uterine venous O2 saturation (SVO2) to FaO2 was curvilinear with convexity toward the SVO2 axis. As SVO2 decreased, there was a decrease in uterine and umbilical venous O2 tension (PO2), with no appreciable reduction of the PO2 difference between the two veins and a decrease in the umbilical vein O2 delivery rate. Fetal O2 uptake and base excess remained normal as the umbilical vein O2 delivery rate was reduced from 1.1 to 0.6 mmol . min-1 . kg-1 but decreased markedly at an O2 delivery rate less than 0.5. Umbilical venous CO2 tension (PCO2) was higher than, and strongly correlated with, uterine venous PCO2 (R = 0.954). These observations support a venous equilibration model of ovine placental exchange and demonstrate that under normal physiological conditions the O2 supply to the fetal lamb is approximately twice the value necessary to maintain an adequate fetal O2 uptake and a normal fetal base excess.

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