Hepatic oxygen delivery-consumption relationship during anesthesia and hypoxemia in dogs

1995 ◽  
Vol 9 (2) ◽  
pp. 205-206 ◽  
Author(s):  
Nobuyuki Matsumoto ◽  
Yutaka Mizumoto ◽  
Kôichirô Hori ◽  
Yasuo Murakami ◽  
Sinichi Nakamura ◽  
...  
Keyword(s):  
Oxygen Delivery ◽  
Hepatic Oxygen Delivery

Hepatic oxygen delivery-consumption relationship during anesthesia and hypoxemia in dogs

1995 ◽  
Vol 9 (2) ◽  
Author(s):  
Nobuyuki Matsumoto ◽  
Yutaka Mizumoto ◽  
K�ichir� Hori ◽  
Yasuo Murakami ◽  
Sinichi Nakamura ◽  
...  
Keyword(s):  
Oxygen Delivery ◽  
Hepatic Oxygen Delivery

Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs

1990 ◽  
Vol 258 (6) ◽  
pp. G910-G918 ◽  
Author(s):  
K. Nagano ◽  
S. Gelman ◽  
E. L. Bradley ◽  
D. Parks
Keyword(s):  
Reperfusion Injury ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Venous Blood ◽  
Oxygen Demand ◽  
Base Line ◽  
Hepatic Oxygen Delivery ◽  
Normothermic Group

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.

Hepatic oxygen metabolism in porcine endotoxemia: the effect of nitric oxide synthase inhibition

1998 ◽  
Vol 275 (6) ◽  
pp. G1377-G1385 ◽  
Author(s):  
Torunn Saetre ◽  
Yngvar Gundersen ◽  
Otto A. Smiseth ◽  
Tim Scholz ◽  
Hege Carlsen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Delivery ◽  
Statistical Significance ◽  
Liver Blood Flow ◽  
Oxygen Metabolism ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Oxygen Extraction Ratio ◽  
Circulatory Effects ◽  
Hepatic Oxygen Delivery

The role of endotoxin (lipopolysaccharide, LPS) and nitric oxide in hepatic oxygen metabolism was investigated in 36 pigs receiving 1) LPS (1.7 μg ⋅ kg−1 ⋅ h−1) for 7 h and N G-nitro-l-arginine methyl ester (l-NAME; 25 mg/kg) after 3 h, 2) LPS, 3) NaCl andl-NAME, and 4) NaCl. Infusion of LPS reduced hepatic oxygen delivery (Do 2H) from 60 ± 4 to 30 ± 5 ml/min ( P < 0.05) and increased the oxygen extraction ratio from 0.29 ± 0.07 to 0.68 ± 0.04 after 3 h ( P < 0.05). Hepatic oxygen consumption (V˙o 2H) was maintained (18 ± 4 and 21 ± 4 ml/min, change not significant), but acidosis developed. Administration ofl-NAME during endotoxemia caused further reduction of Do 2H from 30 ± 3 to 13 ± 2 ml/min ( P < 0.05) and increased hepatic oxygen extraction ratio from 0.46 ± 0.04 to 0.80 ± 0.03 ( P< 0.05). There was a decrease inV˙o 2H from 13 ± 2 to 9 ± 2 ml/min that did not reach statistical significance, probably representing a type II error. Acidosis was aggravated. Administration of l-NAME in the absence of endotoxin also increased the hepatic oxygen extraction ratio, but no acidosis developed. In a different experiment, liver blood flow was mechanically reduced in the presence and absence of endotoxin, comparable to the flow reductions caused byl-NAME. The increase in hepatic oxygen extraction ratio (0.34) and maximum hepatic oxygen extraction ratio (∼0.90) was similar whether Do 2H was reduced by occlusion or byl-NAME. We concluded thatl-NAME has detrimental circulatory effects in this model. However, neither endotoxin norl-NAME seemed to prevent the ability of the still circulated parts of the liver to increase hepatic oxygen extraction ratio to almost maximum when oxygen delivery was reduced. The effect of l-NAME on oxygen transport thus seems to be caused by a reduction in Do 2H rather than by alterations in oxygen extraction capabilities.

Regulation of Local Hepatic Oxygen Delivery Following Stress

2006 ◽  
pp. 147-154
Author(s):  
Mark G. Clemens ◽  
Markus Paxian ◽  
Walid Kamoun ◽  
Jean Ashburn ◽  
M. Nicole Kresge ◽  
...  
Keyword(s):  
Oxygen Delivery ◽  
Hepatic Oxygen Delivery

Modulators of Nitric Oxide in Porcine Endotoxemia: Effects on Hepatic Oxygen Delivery and Consumption

1997 ◽  
Vol 29 (4) ◽  
pp. 237-245 ◽  
Author(s):  
Y. Gundersen ◽  
T. S&aelig;tre ◽  
H. Carlsen ◽  
T. Scholz ◽  
P. Lilleaasen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Delivery ◽  
Hepatic Oxygen Delivery

Dopamine and hepatic oxygen supply – demand relationship

1990 ◽  
Vol 68 (8) ◽  
pp. 1165-1169 ◽  
Author(s):  
Leonid Roytblat ◽  
Simon Gelman ◽  
Edwin L. Bradley ◽  
Todd Henderson ◽  
Dale Parks
Keyword(s):  
Oxygen Uptake ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Sodium Pentobarbital ◽  
Uptake Ratio ◽  
Maximal Increase ◽  
Dopamine Infusion ◽  
Blood Flows ◽  
Hepatic Oxygen Delivery

The present study examined the effect of small, vasodilating doses of dopamine on the hepatic oxygen supply – uptake ratio. Thirteen miniature pigs weighing 18–27 kg were studied under sodium pentobarbital anesthesia. Hepatic arterial and portal blood flows were measured. Oxygen content in arterial, portal, and hepatic venous blood was determined. Dopamine was infused in doses of 5, 10, and 15 μg∙kg−1∙min−1. Dopamine infusion was associated with a dose-related increase in hepatic oxygen uptake and a dose-independent increase in hepatic oxygen delivery with a maximal increase (30%) in the hepatic oxygen delivery at 10 μg∙kg−1∙min−1. The hepatic oxygen delivery–uptake ratio remained unchanged during dopamine infusion in doses of 5 and 10 μg∙kg−1∙min−1 and significantly decreased during the dose of 15 μg∙kg−1∙min−1. The study demonstrated that an increase in cardiac output and hepatic oxygen delivery during dopamine administration was not associated with an improvement in hepatic oxygen supply – demand relationship since hepatic oxygen uptake also increased.Key words: dopamine, hepatic blood flow, hepatic oxygenation.

The biochemistry of drugs and doping methods used to enhance aerobic sport performance

2008 ◽  
Vol 44 ◽  
pp. 63-84 ◽  
Author(s):  
Chris E. Cooper
Keyword(s):  
Oxygen Uptake ◽  
Oxygen Content ◽  
Oxygen Delivery ◽  
Sport Performance ◽  
Blood Substitutes ◽  
Altitude Training ◽  
Blood Oxygen ◽  
Oxygen Carriers ◽  
Sports Performance ◽  
Blood Doping

Optimum performance in aerobic sports performance requires an efficient delivery to, and consumption of, oxygen by the exercising muscle. It is probable that maximal oxygen uptake in the athlete is multifactorial, being shared between cardiac output, blood oxygen content, muscle blood flow, oxygen diffusion from the blood to the cell and mitochondrial content. Of these, raising the blood oxygen content by raising the haematocrit is the simplest acute method to increase oxygen delivery and improve sport performance. Legal means of raising haematocrit include altitude training and hypoxic tents. Illegal means include blood doping and the administration of EPO (erythropoietin). The ability to make EPO by genetic means has resulted in an increase in its availability and use, although it is probable that recent testing methods may have had some impact. Less widely used illegal methods include the use of artificial blood oxygen carriers (the so-called ‘blood substitutes’). In principle these molecules could enhance aerobic sports performance; however, they would be readily detectable in urine and blood tests. An alternative to increasing the blood oxygen content is to increase the amount of oxygen that haemoglobin can deliver. It is possible to do this by using compounds that right-shift the haemoglobin dissociation curve (e.g. RSR13). There is a compromise between improving oxygen delivery at the muscle and losing oxygen uptake at the lung and it is unclear whether these reagents would enhance the performance of elite athletes. However, given the proven success of blood doping and EPO, attempts to manipulate these pathways are likely to lead to an ongoing battle between the athlete and the drug testers.

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