Liver Blood Flow and Oxygen Consumption during Metabolic Acidosis and Alkalosis in the Greyhound

1981 ◽  
Vol 60 (4) ◽  
pp. 355-361 ◽  
Author(s):  
R. L. Hughes ◽  
R. T. Mathie ◽  
W. Fitch ◽  
D. Campbell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Portal Venous Blood Flow ◽  
Arterial Blood ◽  
Portal Venous Blood

1. Hepatic arterial and portal venous blood flow and hepatic oxygen consumption were measured in two groups of greyhounds anaesthetized with pentobarbitone. Flows were measured with electromagnetic flowmeters. 2. In the first group the effects of metabolic acidosis produced by the infusion of a molar solution of lactic acid were studied. In the second group the effects of metabolic alkalosis produced by the infusion of a molar solution of sodium bicarbonate were studied. 3. In the acidotic group hepatic arterial blood flow decreased from 35.2 to 9.6 ml min− 100 g− of liver whereas portal venous blood flow increased from 94.2 to 126.1 ml min− 100 g− of liver. Total liver blood flow was unchanged. Hepatic oxygen consumption increased, but not significantly, while hepatic venous oxygen content decreased significantly. Hepatic arterial resistance increased from 1.18 to 2.77 mmHg min− ml− while peripheral resistance was virtually unchanged. Portal venous pressure increased from 7.08 to 11.6 mmHg. 4. In the alkalotic group portal venous blood flow increased from 112 to 137 ml min− 100 g− of liver. Hepatic arterial blood flow increased, but not significantly. Total liver blood flow increased from 151 to 185, ml min− 100 mg− of liver. There were no significant changes in hepatic oxygen consumption. 5. It is concluded that metabolic acidosis reduces the supply of oxygen to the liver owing to the reduction in hepatic arterial blood flow and is therefore potentially harmful, whereas metabolic alkalosis probably has no biologically significant effect on liver blood flow.

Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound

1979 ◽  
Vol 47 (2) ◽  
pp. 290-295 ◽  
Author(s):  
R. L. Hughes ◽  
R. T. Mathie ◽  
W. Fitch ◽  
D. Campbell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Airway Pressure ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Intermittent Positive Pressure Breathing

Pentobarbital-anesthetized greyhounds were passively hyperventilated using intermittent positive-pressure breathing (IPPV) and the effects of raised airway pressure, accompanied by hypocapnia and then by normocapnia, on liver blood flow and oxygen consumption were studied. Electromagnetic flowmeters were used to measure hepatic arterial, portal venous, and splenic venous blood flow. Studies were carried out at three levels of raised airway pressure, both at normocapnia and hypocapnia. It was found that hypocapnic hyperventilation produced a decrease in portal venous and hepatic arterial blood flow. Normocapnic hyperventilation resulted in a restoration of portal venous blood flow but with a further decrease in hepatic arterial blood flow. A decrease in oxygen consumption with hypocapnia, returning to control values with normocapnia, was seen. It is suggested that the reduction in liver blood flow and oxygen consumption seen with passive hyperventilation is chiefly an effect of hypocapnia and is largely reversed by restoration of normocapnia.

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

2001 ◽  
Vol 280 (5) ◽  
pp. G819-G827 ◽  
Author(s):  
S. M. Jakob ◽  
J. J. Tenhunen ◽  
S. Laitinen ◽  
A. Heino ◽  
E. Alhava ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Tamponade ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Hepatic Function ◽  
Arterial Blood Flow ◽  
Cellular Damage ◽  
Aortic Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml · kg−1 · min−1 for 1 h (short-term tamponade) and further to 30 ml · kg−1 · min−1 for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 ± 3 (baseline) to 6 ± 4 ml · kg−1 · min−1 (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 ± 1 (baseline) to 1 ± 1 ml · kg−1 · min−1 (prolonged tamponade; P = 0.050) and increased from 2 ± 1 to 4 ± 2 ml · kg−1 · min−1in controls ( P = 0.002). The change in hepatic arterial conductance (Δ C ha) during acute portal vein occlusion decreased from 0.1 ± 0.05 (baseline) to 0 ± 0.01 ml · kg−1 · min−1 · mmHg−1(prolonged tamponade; P = 0.043). In controls, Δ C ha did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

Control of hepatic arterial blood flow: independence from liver metabolic activity

1980 ◽  
Vol 239 (4) ◽  
pp. H559-H559 ◽  
Author(s):  
W. Wayne Lautt
Keyword(s):  
Blood Flow ◽  
Metabolic Activity ◽  
Hepatic Blood Flow ◽  
Venous Blood ◽  
Arterial Blood Flow ◽  
Hepatic Veins ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow

This investigation tested the hypothesis that hepatic arterial blood flow is not dependent on hepatic metabolism, but rather is controlled in a manner that tends to maintain total hepatic blood flow constant. Cats anesthetized with pentobarbital sodium received SKF 525 A or 2,4-dinitrophenol (DNP), respectively, to inhibit or stimulate metabolism. Blood flows and oxygen uptake of the liver and gut were determined by use of a hepatic venous long circuit and noncannulating electromagnetic recording of hepatic arterial blood flow. In both sets of experiments the hepatic arterial blood flow. In both sets of experiments the hepatic artery constricted sufficiently to offset elevated portal venous blood flow, thereby maintaining total hepatic blood flow constant. The reduced hepatic arterial conductance occurred with DNP despite elevated metabolic rate and reduced oxygen in the portal and hepatic veins. Altered gut metabolism correlated with altered vascular conductance in the gut; hepatic arterial conductance changes did not correlate with changes in liver metabolic activity. The data confirmed the hypothesis. It is suggested that for hormonal homeostatis it is essential that total hepatic blood flow be regulated because hepatic clearance is flow dependent.

Direct effects of various catecholamines on liver circulation in dogs

1976 ◽  
Vol 230 (5) ◽  
pp. 1394-1399 ◽  
Author(s):  
LJ Hirsch ◽  
T Ayabe ◽  
G Glick
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Venous Blood ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Pressure ◽  
Beta Receptor ◽  
Liver Sinusoids ◽  
Arterial Blood ◽  
Portal Venous Blood

As measured by electromagnetic blood flow transducers, direct infusion of epinephrine, norepinephrine, and dopamine into the portal vein (PV) produced a 40-50% decrease in hepatic arterial (HA) blood flow; isoproterenol increased HA flow by about 69%. No changes in PV flow or pressure were observed. Direct HA infusion of the vasoconstrictors decreased HA flow by amounts comparable to those occurring after PV infusion. However, HA infusion of isoproterenol increased HA flow only 15% suggesting a difference in beta-receptor population in the two vessels. When infused directly into the superior mesenteric artery (SMA), epinephrine and norepinephrine reduced SMA flow by about 45% and PV flow by 20-25%; HA flow increased 6-8%. Infusion of isoproterenol and dopamine into SMA increased SMA flow by 115% and 206% and PV flow by 60% and 70%, respectively, whereas HA flow decreased by 25% and 50%. Portal vein pressure increased less than 3 mmHg. Alpha- and beta-receptor blockade of the liver did not change significantly the alterations in hepatic arterial blood flow that were secondary to changes in portal venous blood flow. It is likely that regulation of hepatic arterial flow resides in mechanisms located within the liver sinusoids.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Insufflation profile and body position influence portal venous blood flow during pneumoperitoneum

2003 ◽  
Vol 17 (12) ◽  
pp. 1951-1957 ◽  
Author(s):  
C. -G. Schmedt ◽  
O. Heupel ◽  
V. Riemer ◽  
C. N. Gutt
Keyword(s):  
Blood Flow ◽  
Body Position ◽  
Venous Blood ◽  
Venous Blood Flow ◽  
Portal Venous Blood Flow ◽  
Portal Venous Blood
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