EFFECT OF FUROSEMIDE ON MESENTERIC ARTERIAL BLOOD FLOW AND HEPATIC PORTAL VENOUS BLOOD FLOW

Abstracts ◽  
1978 ◽  
pp. 63
Author(s):  
H.E. Williamson ◽  
G.R. Gaffney ◽  
L.K. Betzer
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Venous Blood Flow ◽  
Arterial Blood ◽  
Portal Venous Blood ◽  
Hepatic Portal

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.

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

Portal and splanchnic haemodynamics in patients with advanced post-hepatitic cirrhosis and in healthy adults

1998 ◽  
Vol 39 (2) ◽  
pp. 152-156
Author(s):  
H. Dinç ◽  
A. Sari ◽  
H. Resit Gümele ◽  
N. Cihanyurdu ◽  
A. Baki
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Venous Blood ◽  
Resistive Index ◽  
Venous Blood Flow ◽  
Blood Flows ◽  
Portal Venous Blood Flow ◽  
Portal Venous Blood ◽  
The Mean ◽  
Duplex Doppler

Purpose: to assess portal and splanchnic haemodynamics, and splanchnic vascular resistance in patients with advanced post-hepatitic cirrhosis and in healthy volunteers, by means of duplex Doppler ultrasound (US) Material and Methods: the duplex Doppler US examination was performed in 16 patients with cirrhosis and in 24 healthy volunteers. We investigated vessel diameters, mean flow velocities, and mean blood flows in the portal vein, the superior mesenteric artery (SMA), and the splenic artery (SA), and measured the resistive index values of SMA and SA Results: the mean portal venous blood flow in patients with cirrhosis (829 ± 264 ml/min) was not statistically different from those in the volunteers (734 ± 194 ml/min). the ratio of the SMA and SA blood flows (621 ml/min) to the portal venous blood flow (734 ml/min) was 0.85 in the control subjects. the mean portal venous blood flow (1261 ml/min) and the portal venous velocity (14.6 cm/s) were higher in the patients with recanalized para-umbilical veins than in the volunteers and in the patients without recanalized para-umbilical veins. the SMA and SA blood flows were significantly increased in patients with cirrhosis compared with volunteers. Splanchnic inflow (the sum of the SMA and SA blood flows) was higher than the portal blood flow in patients with cirrhosis except in the subjects with recanalized para-umbilical veins. SMA and SA resistive index values were significantly higher in these patients than in the volunteers Conclusion: Splanchnic blood flow and splanchnic vascular impedance increased significantly in patients with advanced post-hepatitic cirrhosis. Splanchnic inflow must not exceed portal venous blood flow in patients with recanalized para-umbilical veins. Portal vein velocity and portal venous blood flow measurements alone are not useful parameters for discriminating patients with cirrhosis from healthy subjects

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