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.

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.

Thigh oxygen uptake at the onset of intense exercise is not affected by a reduction in oxygen delivery caused by hypoxia

2012 ◽  
Vol 303 (8) ◽  
pp. R843-R849 ◽  
Author(s):  
Peter M. Christensen ◽  
Nikolai Baastrup Nordsborg ◽  
Lars Nybo ◽  
Stefan P. Mortensen ◽  
Mikael Sander ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Delivery ◽  
Venous Blood ◽  
Knee Extensor ◽  
Intense Exercise ◽  
Muscle Lactate ◽  
Flow Measurements ◽  
Arterial Blood ◽  
Blood Flow Measurements

In response to hypoxic breathing most studies report slower pulmonary oxygen uptake (V̇o2) kinetics at the onset of exercise, but it is not known if this relates to an actual slowing of the V̇o2 in the active muscles. The aim of the present study was to evaluate whether thigh V̇o2 is slowed at the onset of intense exercise during acute exposure to hypoxia. Six healthy male subjects (25.8 ± 1.4 yr, 79.8 ± 4.0 kg, means ± SE) performed intense (100 ± 6 watts) two-legged knee-extensor exercise for 2 min in normoxia (NOR) and hypoxia [fractional inspired oxygen concentration (FiO2) = 0.13; HYP]. Thigh V̇o2 was measured by frequent arterial and venous blood sampling and blood flow measurements. In arterial blood, oxygen content was reduced ( P < 0.05) from 191 ± 5 ml O2/l in NOR to 180 ± 5 ml O2/l in HYP, and oxygen pressure was reduced ( P < 0.001) from 111 ± 4 mmHg in NOR to 63 ± 4 mmHg in HYP. Thigh blood flow was the same in NOR and HYP, and thigh oxygen delivery was consequently reduced ( P < 0.05) in HYP, but femoral arterial-venous oxygen difference and thigh V̇o2 were similar in NOR and HYP. In addition, muscle lactate release was the same in NOR and HYP, and muscle lactate accumulation during the first 25 s of exercise determined from muscle biopsy sampling was also similar (0.35 ± 0.07 and 0.36 ± 0.07 mmol·kg dry wt−1·s−1 in NOR and HYP). Thus the increase in thigh V̇o2 was not attenuated at the onset of intense knee-extensor exercise despite a reduction in oxygen delivery and pressure.

Catecholamine and serotonin concentrations in fetal guinea-pig brain: relation to regional cerebral blood flow and oxygen delivery in the growth-restricted fetus

1996 ◽  
Vol 8 (3) ◽  
pp. 355 ◽  
Author(s):  
A Jensen ◽  
HJ Klonne ◽  
A Detmer ◽  
AM Carter
Keyword(s):  
Blood Flow ◽  
Guinea Pig ◽  
Oxygen Delivery ◽  
Oxygen Supply ◽  
Tissue Concentrations ◽  
Blood Flows ◽  
Arterial Blood ◽  
Tissue Po2 ◽  
The Brain ◽  
Neurotransmitter Metabolism

To test the hypothesis that intrauterine growth restriction (IUGR) would lead to altered neurotransmitter metabolism in the brain because of poorer oxygenation, blood flows and tissue concentrations of noradrenaline, dopamine, serotonin and their metabolites were measured in 14 parts of the brain of guinea-pig fetuses at 61-64 days' gestation. Eight fetuses with IUGR induced by uterine artery ligation were compared with 8 controls. Regional brain blood flows were determined by the microsphere method and tissue concentrations of monoamines by HPLC with electrochemical detection. The oxygen content of preductal arterial blood was significantly lower in IUGR fetuses than in controls (2.3 +/- 0.6 v. 3.5 +/- 0.5 mM; P < 0.001). Although this was compensated by increases in blood flow to many areas of the brain, significant decreases occurred in oxygen delivery to the temporal and occipital cortex, hippocampus and cerebellum of IUGR fetuses. In contrast, oxygen delivery to brainstem areas was maintained. Noradrenaline concentrations were closely similar in brains from the two groups, except for an increase in the caudate nucleus of IUGR fetuses. Dopamine concentrations were significantly elevated in brainstem areas. Concentrations of 3,4-dihydroxyphenylglycol (DOPEG), a noradrenaline metabolite, and 3,4-dihydroxyphenylacetic acid (DOPAC), a dopamine metabolite, showed a similar pattern of increase in brains of IUGR fetuses, possibly resulting from increased synthesis of noradrenaline and dopamine rather than from decreased degradation. Concentrations of serotonin were significantly higher in frontal and temporal cortex of IUGR fetuses, and the serotonin metabolite 5-HIAA increased significantly in cortical areas. Changes in neurotransmitter metabolism could not be related to oxygen supply, since serotonin concentrations increased in the forebrain, despite reduced oxygen delivery and the known dependence of tryptophan-5-hydroxylase on tissue PO2, and dopamine levels were elevated in the brainstem, where the oxygen supply was maintained.

Glucagon increases hepatic oxygen supply-demand ratio in pigs

1987 ◽  
Vol 252 (5) ◽  
pp. G648-G653
Author(s):  
S. Gelman ◽  
E. Dillard ◽  
D. A. Parks
Keyword(s):  
Blood Flow ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Young Pigs ◽  
Hepatic Venous Blood ◽  
Pentobarbital Sodium Anesthesia

The present study was performed on eight young pigs to test the hypothesis that glucagon increases hepatic oxygen supply to a greater extent than hepatic oxygen uptake, providing a better hepatic oxygen supply-demand relationship. The experiments were performed under pentobarbital sodium anesthesia and controlled ventilation. Splanchnic blood flow was studied using radioactive microspheres. Glucagon was administered in doses of 1 and 5 micrograms X kg-1 X min-1. During glucagon infusion, hepatic arterial blood flow substantially increased, splenic and pancreatic blood flows increased moderately, while stomach and intestinal blood flows, as well as portal blood flow did not change significantly. Shunting of both 9- and 15-micron spheres through preportal tissues did not change significantly. Oxygen content in arterial or portal venous blood did not change significantly, while it increased in hepatic venous blood by 30%. There were no differences in the effects between the doses of glucagon administered. There was no correlation found between changes in hepatic oxygen supply and cardiac output or blood pressure. The changes observed during glucagon administration resulted in an increase in oxygen delivery to the liver and hepatic oxygen supply-uptake ratio.

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.

Regional oxygen delivery in oxygen supply-dependent states

1990 ◽  
Vol 16 (S2) ◽  
pp. S169-S171 ◽  
Author(s):  
M. R. Pinsky ◽  
R. Schlichtig
Keyword(s):  
Oxygen Delivery ◽  
Oxygen Supply

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Development of dependence on oxygen in embryo salamanders

1979 ◽  
Vol 236 (5) ◽  
pp. R282-R291
Author(s):  
E. F. Adolph
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Oxygen Pressure ◽  
Oxygen Delivery ◽  
Survival Times ◽  
Stages Of Development ◽  
Heart Rates ◽  
Species Survival ◽  
Critical Oxygen

Survival times in anoxia and hypoxia were measured at various stages of development in Ambystoma embryos and larvae of two species. Survival times in anoxia at 20 degrees C shifted from more than 30 h at 2 days after fertilization to 20 h at 10 days of age, to only 4--2 h at 14 days of age. In hypoxia (oxygen pressure equivalent to 3.8% oxygen) similar shifts of survival times appeared about 7 days of age later. During anoxia heart rates decreased, less at younger stages than at older. At older stages the heart stopped beating, sometimes irreversibly. In hypoxia also, hearts at all stages whether in situ or isolated decreased their rates of beat. Oxygen uptakes of larvae diminished in oxygen pressures even as high as 11% oxygen. This critical oxygen pressure did not change between early stages without blood flow and later stages with blood flow. Oxygen uptake was probably not limited by oxygen delivery but presumably by properties of cellular masses. No oxygen debts were paid off. Some parallel changes of tolerances to anoxia in embryo birds and mammals are noted.

Right ventricular oxygen supply/demand balance in exercising dogs

2001 ◽  
Vol 281 (2) ◽  
pp. H823-H830 ◽  
Author(s):  
Bradley J. Hart ◽  
Xiaoming Bian ◽  
Patricia A. Gwirtz ◽  
Srinath Setty ◽  
H. Fred Downey
Keyword(s):  
Right Ventricular ◽  
Oxygen Supply ◽  
Venous Blood ◽  
Oxygen Demand ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
Conscious Animal ◽  
Flow Reserve ◽  
Exercise Induced

This is the first investigation of right ventricular (RV) myocardial oxygen supply/demand balance in a conscious animal. A novel technique developed in our laboratory was used to collect right coronary (RC) venous blood samples from seven instrumented, conscious dogs at rest and during graded treadmill exercise. Contributions of the RV oxygen extraction reserve and the RC flow reserve to exercise-induced increases in RV oxygen demand were measured. Strenuous exercise caused a 269% increase in RV oxygen consumption. Expanded arteriovenous oxygen content difference (A-VΔO2) provided 58% of this increase in oxygen demand, and increased RC blood flow (RCBF) provided 42%. At less strenuous exercise, expanded A-VΔO2 provided 60–80% of the required oxygen, and increases in RCBF were small and driven by increased aortic pressure. RC resistance fell only at strenuous exercise after the extraction reserve had been mobilized. Thus RC resistance was unaffected by large decreases in RC venous Po 2 until an apparent threshold at 20 mmHg was reached. Comparisons of RV findings with published left ventricular data from exercising dogs demonstrated that increased O2 demand of the left ventricle is met primarily by increasing coronary flow, whereas increased O2extraction makes a greater contribution to RV O2 supply.

Effect of stimulation of hepatic nerves on hepatic O2 uptake and blood flow

1977 ◽  
Vol 232 (6) ◽  
pp. H652-H656
Author(s):  
W. W. Lautt
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Venous Blood ◽  
Neurogenic Vasoconstriction ◽  
Pressure Changes ◽  
Hepatic Nerves ◽  
Stimulation Of

Acute denervation of the liver did not result in changes of oxygen uptake or hemodynamics in the intact liver of the cat. Stimulation of the hepatic nerves resulted in a marked reduction of vascular conductance of the hepatic artery and portal vein (intrahepatic) resulting in almost complete cessation of arterial flow and increased portal blood pressure. The hepatic artery showed a more complete escape from the neurogenic vasoconstriction than did the portal vein. During the stable "escape phase" oxygen delivery was 86% of control, but hepatic extraction of oxygen increased so that oxygen uptake was not altered from control values. The return of oxygen consumption to normal during nerve stimulation suggests that redistribution of hepatic blood flow did not occur. In spite of arterial and portal venous blood pressure changes and changes in gut conductance, oxygen extraction of the gut did not change.

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