Nifedipine Has No Effect on Liver Blood Flow or Portal Venous Pressure

InPharma ◽  
1988 ◽  
Vol 641 (1) ◽  
pp. 16-16
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Liver Blood Flow ◽  
Portal Venous Pressure

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.

Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers

2004 ◽  
Vol 286 (1) ◽  
pp. H121-H130 ◽  
Author(s):  
Chiaki Kamikado ◽  
Toshishige Shibamoto ◽  
Minoru Hongo ◽  
Shozo Koyama
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Regression Line ◽  
Venous Occlusion ◽  
Portal Venous Pressure ◽  
Venous Resistance ◽  
Four Levels ◽  
Rat Livers ◽  
Line Analysis

We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.

Derecruitment in cat liver: extension of undistributed parallel tube model to effects of low hepatic blood flow on ethanol uptake

1989 ◽  
Vol 67 (10) ◽  
pp. 1225-1231 ◽  
Author(s):  
C. V. Greenway ◽  
L. Bass
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Liver Blood Flow ◽  
Hepatic Uptake ◽  
Tube Model ◽  
Low Flows ◽  
Wide Range ◽  
Parallel Tube ◽  
Parallel Tube Model

Previous studies showed two deviations from the predictions of the undistributed parallel tube model for hepatic uptake of substrates: a small deviation at high flows and a large deviation at low flows. We have examined whether these deviations could be described by a single correction factor. In cats anesthetized with pentobarbital, a hepatic venous long-circuit technique with an extracorporeal reservoir was used to vary portal flow and hepatic venous pressure, and allow repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cat's blood volume. Hepatic uptake of ethanol was measured over a wide range of blood flows and when intrahepatic pressure was increased at low flows. This uptake could be described by the parallel tube model with a correction for hepatic blood flow: [Formula: see text]. In 22 cats, [Formula: see text], k = 0.021 ± 0.0015 when flow (F) was in millilitres per minute per 100 g liver, and Km = 150 ± 20 μM when ĉ is the log mean sinusoidal concentration. (1 − e−kF) represents the proportion of sinusoids perfused and metabolically active. A dynamic interpretation of this proportion is related to intermittency (derecruitment) of sinusoidal flow. Half the sinusoids were perfused at a flow of 33 mL/(min∙100 g liver) and the liver was essentially completely perfused (> 95%) at the normal flow of 150 mL/(min∙100 g liver). Derecruitment was not changed by raising hepatic venous pressure, and it was not related to hepatic venous resistance.Key words: liver circulation, ethanol metabolism, liver blood flow, sinusoidal perfusion, portal pressure.

The effect of pitressin on esophageal blood flow of the dog

1991 ◽  
Vol 69 (12) ◽  
pp. 1810-1813 ◽  
Author(s):  
S. F. White ◽  
P. K. Dinda ◽  
I. T. Beck
Keyword(s):  
Blood Flow ◽  
Lower Esophageal Sphincter ◽  
Intravenous Infusion ◽  
Striated Muscle ◽  
Partial Agonist ◽  
Venous Pressure ◽  
The Body ◽  
Portal Venous Pressure ◽  
Squamous Mucosa ◽  
Esophageal Sphincter

In a previous study on canine esophagus, we reported that intravenous infusion of isoproterenol caused mucosal (i.e., mucosal + submucosal) vasodilation only in the lower esophageal sphincter (but not in the body) and muscularis vasodilation only in the body (not in the lower esophageal sphincter). In the present study, we have investigated in dogs whether these esophageal tissues also exhibit a similar difference in their vasoconstrictory response to intravenous infusion of pitressin. All measurements were made before (basal) and after infusion of 0.02 U pitressin∙min−1∙kg−1 for 15 min. Pitressin significantly decreased portal venous pressure and blood flow, and increased vascular resistance of all tissues of the esophagus. This vasoconstriction of the tissues, however, was higher in the squamous mucosa of the body than in the columnar mucosa of the lower esophageal sphincter. In contrast, it was higher in the smooth muscle of the lower esophageal sphincter than in the striated muscle of the body. These data together with those of our previous report on isoproterenol demonstrate that pitressin causes a pronounced vasoconstriction in those esophageal tissues where isoproterenol had no effect. Conversely, pitressin causes least vasoconstriction in those tissues where isoproterenol produced a significant vasodilation. These differences could be the result of partial agonist actions or differences in receptor density or in receptor-effector coupling mechanism.Key words: microspheres, portal venous pressure, esophageal body, lower esophageal sphincter.

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.

Effects of nonshunting operations on portal venous pressure and hepatic blood flow

1987 ◽  
Vol 153 (3) ◽  
pp. 295-298 ◽  
Author(s):  
Seiji Kawasaki ◽  
Akio Kidokoro ◽  
Mitsuo Sugiura ◽  
Kensho Sanjo ◽  
Yasuo Idezuki
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Portal Venous Pressure

The Risk Of Surgery In Patients With Liver Disease 1: Epidemiology, Pathophysiology, And Pre-Operative Evaluation

2018 ◽  
Author(s):  
Adrian Reuben
Keyword(s):  
Blood Flow ◽  
Liver Disease ◽  
Liver Function ◽  
Large Scale ◽  
Venous Pressure ◽  
Liver Blood Flow ◽  
Disease Patient ◽  
Case Series ◽  
Kidney Injury ◽  
Operative Evaluation

The results of retrospective large scale registry and cohort studies, and small case series, substantiate the common perception that operating on a liver disease patient is risky.  The preexisting physiological derangements of liver disease may be exacerbated by the trauma of surgery and its complications, which contributes strongly to the aforementioned surgical risks, especially (but not exclusively) in cirrhotics.  Perturbations in liver blood flow and oxygenation may be exaggerated by anesthesia, surgery itself, blood loss, and other operative complications. Cirrhotics are especially susceptible to acute and chronic kidney injury.  Malnutrition is common in cirrhosis, which compromises wound healing and recovery from surgery. In cirrhosis, elimination of infection is impaired and its systemic effects are deleterious. The metabolic and immunological stresses of surgery may lead to liver function deterioration, even in stable cirrhotics. Presented here is the pre-operative evaluation of liver disease patients, including the use of predictive indices, new dynamic tests of liver function, and modestly invasive assessment of portal hypertension.  This review contains 9 figures, 6 tables and 52 references Keywords: acute-on-chronic liver failure, Child-Turcotte-Pugh, cirrhosis, coagulopathy, infection, hepatic venous pressure gradient, liver blood flow, model for end-stage liver disease, systemic inflammatory response syndrome, thrombocytopenia   

The Risk Of Surgery In Patients With Liver Disease 1: Epidemiology, Pathophysiology, And Pre-Operative Evaluation

2018 ◽  
Author(s):  
Adrian Reuben
Keyword(s):  
Blood Flow ◽  
Liver Disease ◽  
Liver Function ◽  
Large Scale ◽  
Venous Pressure ◽  
Liver Blood Flow ◽  
Disease Patient ◽  
Case Series ◽  
Kidney Injury ◽  
Operative Evaluation

The results of retrospective large scale registry and cohort studies, and small case series, substantiate the common perception that operating on a liver disease patient is risky.  The preexisting physiological derangements of liver disease may be exacerbated by the trauma of surgery and its complications, which contributes strongly to the aforementioned surgical risks, especially (but not exclusively) in cirrhotics.  Perturbations in liver blood flow and oxygenation may be exaggerated by anesthesia, surgery itself, blood loss, and other operative complications. Cirrhotics are especially susceptible to acute and chronic kidney injury.  Malnutrition is common in cirrhosis, which compromises wound healing and recovery from surgery. In cirrhosis, elimination of infection is impaired and its systemic effects are deleterious. The metabolic and immunological stresses of surgery may lead to liver function deterioration, even in stable cirrhotics. Presented here is the pre-operative evaluation of liver disease patients, including the use of predictive indices, new dynamic tests of liver function, and modestly invasive assessment of portal hypertension.  This review contains 9 figures, 6 tables and 52 references Keywords: acute-on-chronic liver failure, Child-Turcotte-Pugh, cirrhosis, coagulopathy, infection, hepatic venous pressure gradient, liver blood flow, model for end-stage liver disease, systemic inflammatory response syndrome, thrombocytopenia   

scholarly journals Measurement of portal vascular resistance in patients with chronic liver diseases by simultaneous measurement of portal blood flow and portal venous pressure.

Kanzo ◽  
1985 ◽  
Vol 26 (4) ◽  
pp. 485-492
Author(s):  
Fuminori MORIYASU ◽  
Osamu NISHIDA ◽  
Nobuyuki BAN ◽  
Takefumi NAKAMURA ◽  
Yasunari SOH ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Simultaneous Measurement ◽  
Liver Diseases ◽  
Venous Pressure ◽  
Portal Blood Flow ◽  
Chronic Liver ◽  
Portal Blood ◽  
Portal Venous Pressure ◽  
Chronic Liver Diseases

Effects of glucagon and somatostatin on portal venous pressure and gastric mucosal blood flow

1998 ◽  
Vol 114 ◽  
pp. A313
Author(s):  
CP Tsui ◽  
JY Sung ◽  
FW Leung
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Portal Venous Pressure
Sign in / Sign up

Export Citation Format

Share Document