Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis

1994 ◽  
Vol 39 (11) ◽  
pp. 2439-2444 ◽  
Author(s):  
Tadashi Iwao ◽  
Atsushi Toyonaga ◽  
Motoki Ikegami ◽  
Michihiro Sumino ◽  
Kazuhiko Oho ◽  
...  
Keyword(s):  
Drug Administration ◽  
Venous Pressure ◽  
Vasoactive Drug ◽  
Portal Venous Pressure ◽  
Wedged Hepatic Venous Pressure

scholarly journals Discrepancy Between Wedged Hepatic Venous Pressure and Portal Venous Pressure After Acute Propranolol Administration in Patients With Alcoholic Cirrhosis

1984 ◽  
Vol 86 (6) ◽  
pp. 1400-1403 ◽  
Author(s):  
Dominique Valla ◽  
Eric Bercoff ◽  
Yves Menu ◽  
Christian Bataille ◽  
Didier Lebrec
Keyword(s):  
Venous Pressure ◽  
Alcoholic Cirrhosis ◽  
Portal Venous Pressure ◽  
Propranolol Administration ◽  
Wedged Hepatic Venous Pressure

scholarly journals The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 276-282 ◽  
Author(s):  
X Li ◽  
I S Benjamin ◽  
B Alexander
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Steady State ◽  
Portal Vein ◽  
Rat Liver ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
The Relationship ◽  
Wedged Hepatic Venous Pressure

Background—Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.Aims—To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.Methods—Different sized microspheres were sequentially injected into the portal vein of male Wistar rats.Results—Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 μm diameter microspheres, respectively. Sequential injection of 15, 40, and 80 μm diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 × 105 80 μm microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p>0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 μm microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 μm microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow.Conclusion—It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

scholarly journals Comparison of Free Portal Venous Pressure and Wedged Hepatic Venous Pressure in Patients with Cirrhosis of the Liver

1970 ◽  
Vol 59 (3) ◽  
pp. 372-375 ◽  
Author(s):  
André Viallet ◽  
Jean-Gil Joly ◽  
Denis Marleau ◽  
Pierre Lavoie
Keyword(s):  
Venous Pressure ◽  
Cirrhosis Of The Liver ◽  
Portal Venous Pressure ◽  
Wedged Hepatic Venous Pressure

Serum concentrations of laminin and aminoterminal propeptide of type III procollagen in relation to the portal venous pressure of fibrotic liver diseases

1986 ◽  
Vol 161 (3) ◽  
pp. 249-258 ◽  
Author(s):  
Axel M. Gressner ◽  
Wolfgang Tittor ◽  
Anne Negwer ◽  
Karl-Heinz Pick-Kober
Keyword(s):  
Liver Diseases ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Serum Concentrations ◽  
Fibrotic Liver ◽  
Type Iii ◽  
Type Iii Procollagen

Portal venous pressure in “pipestem” fibrosis of the liver due to schistosomiasis

1959 ◽  
Vol 27 (5) ◽  
pp. 807-810 ◽  
Author(s):  
Arthur H. Aufses ◽  
Fenton Schaffner ◽  
William S. Rosenthal ◽  
Bernard E. Herman
Keyword(s):  
Venous Pressure ◽  
Portal Venous Pressure

scholarly journals Measurement of portal venous pressure prior to major liver resections: hospital based experience

HPB ◽  
2018 ◽  
Vol 20 ◽  
pp. S476
Author(s):  
H. Bari ◽  
F. Hanif ◽  
S.A. Akbar ◽  
U. Farooq
Keyword(s):  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Liver Resections

Is Portal Venous Pressure Modulation Still Indicated for All Recipients in Living Donor Liver Transplantation?

2018 ◽  
Vol 24 (11) ◽  
pp. 1578-1588 ◽  
Author(s):  
Siyuan Yao ◽  
Toshimi Kaido ◽  
Ryuji Uozumi ◽  
Shintaro Yagi ◽  
Yosuke Miyachi ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Living Donor ◽  
Living Donor Liver Transplantation ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Donor Liver ◽  
Donor Liver Transplantation ◽  
Pressure Modulation

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 818-824 ◽  
Author(s):  
C. Risoe ◽  
C. Hall ◽  
O. A. Smiseth
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Central Blood Volume ◽  
Positive End Expiratory Pressure ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Blood Volumes

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

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