Hepatic vascular response to epinephrine

1961 ◽  
Vol 201 (1) ◽  
pp. 58-62 ◽  
Author(s):  
William C. Shoemaker ◽  
L. Newton Turk ◽  
Francis D. Moore
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Hepatic Blood Flow ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Portal Vein Pressure ◽  
Pronounced Increase ◽  
Epinephrine Administration ◽  
Arterial Blood

Hepatic hemodynamic events were measured before and after epinephrine administration in unanesthetized dogs in which the hepatic vessels had been previously catheterized. Comparisons were made of the response after a single intravenous injection at various doses and after a constant infusion of epinephrine; comparisons were also made between portal vein and femoral vein injections. After femoral venous injection of epinephrine (1–10 µg/kg) there was a marked increase in hepatic blood flow, roughly increasing with the size of the dose. With doses of 25 µg/kg or more, an initial increase in hepatic blood flow was followed by a decreased flow; in some instances death ensued. Epinephrine injected into the femoral vein produced a rise in the arterial blood pressure, followed by a rise in the portal vein pressure, portal-hepatic venous pressure gradient, and mechanical impedance across the hepatic venous bed. When injected into the portal vein under comparable conditions, epinephrine produced little or no change in hepatic blood flow or arterial pressure, but did produce a more rapid and pronounced increase in portal vein pressure, portal-hepatic pressure gradient and hepatic venous impedance.

Hepatic vascular response to norepinephrine

1962 ◽  
Vol 202 (6) ◽  
pp. 1175-1178 ◽  
Author(s):  
L. Newton Turk ◽  
William C. Shoemaker
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Pressure Gradient ◽  
Arterial Blood Pressure ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Hepatic Venous Pressure Gradient ◽  
Portal Venous Pressure ◽  
Arterial Blood ◽  
Venous Resistance

Norepinephrine injected into the femoral vein or inferior vena cava in doses ranging from 1 to 10 µg/kg produced a prompt and definite decrease in hepatic blood flow; this response was, in general, more pronounced with increasing doses. Femoral venous injections also produced a prompt increase in arterial blood pressure followed by a decreased portal venous pressure and portal-hepatic venous pressure gradient. The calculated hepatic venous resistance increased, reaching a maximum at about 60 sec after injection. When the identical doses were injected into the portal vein in the same animals under comparable conditions, the arterial blood pressure and hepatic blood flow responses were delayed in time and attenuated in amount. However, within 10–15 sec of injection the portal venous pressure and portal-hepatic venous pressure gradient increased. The calculated hepatic venous resistance increased more rapidly after intraportal norepinephrine injection.

Effects of nifedipine on hepatic venous pressure gradient and portal vein blood flow in patients with cirrhosis

1995 ◽  
Vol 10 (2) ◽  
pp. 198-204 ◽  
Author(s):  
KAZUHIRO OTA ◽  
HIROSHI SHIJO ◽  
HIROSHI KOKAWA ◽  
KATSUHIKO KUBARA ◽  
TETSUHIRO KIM ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Venous Pressure ◽  
Hepatic Venous Pressure Gradient

Increase of portal vein pressure gradient after hepatectomy predicts post-operative liver dysfunction

2020 ◽  
Author(s):  
Nan Xiao ◽  
Xiao-long Li ◽  
Xiao-dong Zhu ◽  
Cheng huang ◽  
Ying-hao Shen ◽  
...  
Keyword(s):  
Liver Resection ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Venous Pressure ◽  
Multivariable Analysis ◽  
Central Vein ◽  
Roc Curve Analysis ◽  
Portal Vein Pressure ◽  
Mortality And Morbidity ◽  
The Impact

Abstract Background Post-hepatectomy liver failure (PHLF) is an important cause of mortality and morbidity. Whether Child–Pugh A Patients with varying degrees of cirrhosis are good candidates for hepatectomy is disputed. The purpose of this study was to analyse the impact of portal venous pressure gradient (PVPG) variation during surgery on PHLF. Methods PVPG, the pressure gradient between the portal vein and central vein, was measured in consecutive patients before and after liver resection. The optimal cut-off of PVGP to predict PHLF was determined by receiver operating characteristic (ROC) curve analysis. Risk factors for PHLF were subjected to univariable and multivariable analysis. Results Sixty Child-Pugh A patients were recruited. The mean PVPG was increased from 5.17 ± 4.78 millimeters of Mercury (mmHg) to 6.37 ± 4.44 mmHg after liver resection. The optimal cut-off value of PVPG increments to predict PHLF was 1.5 mmHg. Multivariable analysis showed prothrombin time (PT), post-hepatectomy PVPG increments of 1.5 mmHg or greater, and resected liver segments of 3 or more to be independent predictors of PHLF. Conclusions Acute PVPG increase after hepatectomy is associated with a higher risk of PHLF in Child-Pugh A patients.

scholarly journals Increase of Portal Vein Pressure Gradient After Hepatectomy Predicts Post-operative Liver Dysfunction

2021 ◽  
pp. 155335062110186
Author(s):  
Nan Xiao ◽  
Xiao-Long Li ◽  
Xiao-Dong Zhu ◽  
Cheng Huang ◽  
Ying-Hao Shen ◽  
...  
Keyword(s):  
Liver Resection ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Characteristic Curve ◽  
Venous Pressure ◽  
Multivariable Analysis ◽  
Central Vein ◽  
Optimal Cutoff ◽  
Portal Vein Pressure ◽  
The Impact

Background. Post-hepatectomy liver failure (PHLF) is an important cause of mortality and morbidity. Whether Child–Pugh A patients with varying degrees of cirrhosis are good candidates for hepatectomy is disputed. The purpose of this study was to analyze the impact of portal venous pressure gradient (PVPG) variation during surgery on PHLF. Methods. PVPG, the pressure gradient between the portal vein and central vein, was measured in consecutive patients before and after liver resection. The optimal cutoff of PVPG to predict PHLF was determined by receiver operating characteristic curve analysis. Risk factors for PHLF were subjected to univariate and multivariable analysis. Results. Sixty Child–Pugh A patients were recruited. The mean PVPG was increased from 5.17 ± 4.78 mm of mercury (mmHg) to 6.37 ± 4.44 mmHg after liver resection. The optimal cutoff value of PVPG increments to predict PHLF was 1.5 mmHg. Multivariable analysis showed prothrombin time (PT), post-hepatectomy PVPG increments of 1.5 mmHg or greater, and resected liver segments of 3 or more to be independent predictors of PHLF. Conclusions. Acute PVPG increase after hepatectomy is associated with a higher risk of PHLF in Child–Pugh A patients.

Hemodynamic Effects And Changes Of Blood Flow Distribution By Dextran 70, Dihydroergotamin (DHE) And Their Combination

1981 ◽  
Author(s):  
B Lindblad ◽  
D Bergqviat
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Flow Distribution ◽  
Tissue Blood Flow ◽  
Blood Flow Distribution ◽  
Arterial Blood ◽  
Dextran 70 ◽  
The Central Nervous System

Dextran 70 and DHE are both effective in reducing the risk for postoperative thromboembolic complications. As they at least in part have different mechanisms of action it is important to analyse if their combination potentiates the prophylactic effect. Therefore it is necessary to study the effect on hemodynamics and tissue blood flow, a problem which is delt with in this report.MATERIAL AND METHODS: In 18 dogs the following parameters were followed: cardiac output, heart rate, arterial blood pressure, central venous pressure, pulmonary artery pressure, left atrium pressure and volume blood flow in the femoral vein. Blood flow distribution was determined by the radioactive microsphere technique.RESULTS: Dextran 70 gave an increase of cardiac output and femoral vein flow. Other hemodynamic parameters were mainly unaffected. Total peripheral resistance decreased. DHE increased arterial blood pressure, central venous pressure and pulmonary arterial pressure. Cardiac output and femoral vein flow were unchanged.Tissue blood flow increased in general slightly after infusion of dextran 70. No significant change in blood flow distribution was seen. DHE reduced pancreatic and thyroid blood flow and increased tissue blood flow to the central nervous system. The blood flow to other organs including the heart was unaffected. The combination of dextran 70 and DHE influenced hemodynamic parameters and flow distribution in an additative way.CONCLUSIONS: From this experimental study it is concluded that it is possible to combine dextran and DHE without inducing a circulatory overload. DHE increased tissue blood flow to the central nervous system.

Interference of angiotensin II and enalapril with hepatic blood flow regulation

2014 ◽  
Vol 307 (6) ◽  
pp. G655-G663 ◽  
Author(s):  
Adriano J. Pereira ◽  
Victor Jeger ◽  
René Fahrner ◽  
Siamak Djafarzadeh ◽  
Michael Lensch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Flow Regulation ◽  
Arterial Perfusion ◽  
Arterial Blood ◽  
Blood Flow Regulation

Acute reduction of portal vein blood flow ( Qpv) increases hepatic arterial perfusion ( Qha) [the hepatic arterial buffer response (HABR)]. Angiotensin II (AT-II) reduces Qpv, but its effect on HABR is not known. We explored interactions of AT-II and enalapril with hepatic blood flow regulation. Twenty healthy anesthetized pigs were randomized to receive AT-II ( n = 8) from 5 to 61 ng/kg per min, enalapril ( n = 8) from 3 to 24 μg/kg per h, or saline ( n = 4). HABR was assessed by occluding portal vein and expressed as 1) ratio between changes in Qha and Qpv, 2) hepatic arterial conductance ( Cha). AT-II infusion increased mean arterial blood pressure from 74 (66–77) mmHg to 116 (109–130) mmHg (median, IQR; P < 0.0001) and decreased cardiac output, Qpv, and renal artery flow (−24%, −28% and −45%, respectively). The fraction of cardiac output of Qha, carotid, and femoral flows increased. With enalapril, blood pressure decreased, whereas cardiac output was maintained with flow redistribution favoring hepatic and renal arteries. In AT-II group, d Qha/d Qpv increased from 0.06 (0.03, 0.17) to 0.24 (0.13, 0.31) ( P = 0.002), but Cha during acute portal vein occlusion decreased from 4.3 (1.6, 6.6) to 2.9 (1.2, 3.7) ml/mmHg ( P = 0.003). Both variables remained unchanged in the enalapril group and in controls. AT-II infusion reduces portal flow in parallel with cardiac output and induces a dose-dependent redistribution of flow, favoring brain, hepatic artery, and peripheral tissues at the expense of renal perfusion. During HABR, AT-II decreases Cha but increases Qha compensation, likely as result of increased hepatic arterial perfusion pressure. Enalapril had no effect on HABR.

scholarly journals Assessment of hemodynamic parameters of hepatic and visceral blood flow in decompensated liver cirrhosis

2021 ◽  
Vol 23 (3) ◽  
pp. 363-369
Author(s):  
A. S. Tugushev ◽  
O. S. Cherkovska ◽  
D. I. Mikhantiev
Keyword(s):  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Natural Course ◽  
Arterial Blood Flow ◽  
Hemodynamic Parameters ◽  
Decompensated Liver Cirrhosis ◽  
Arterial Blood

The aim. To assess the hemodynamic parameters of the hepatic and visceral blood flow in patients with compensated and decompensated liver cirrhosis. Materials and methods. 290 patients with liver cirrhosis were examined: 206 had gastrointestinal bleeding, 84 had diuretic-resistant ascites. Ultrasonic scanning, Doppler sonography, esophagogastroduodenoscopy, angiography, radioisotope scintigraphy were performed to assess blood flow in the portal, splenic and superior mesenteric veins and in the hepatic, splenic and superior mesenteric arteries. Results. Change in the hepatic microcirculatory blood flow in the natural course of liver cirrhosis was characterized by decreased portal and increased arterial blood flow, “arterialization” of hepatic blood flow based on scintigraphy. Decompensation of the disease was associated with progressive reduction in both portal and arterial hepatic blood flow, which were correlated with the severity of functional liver disorders regardless of the complication nature. The portal blood flow in the natural course of liver cirrhosis was characterized by 3.5–4.5 times increased volume of visceral blood. Decompensation of the disease was accompanied by a decrease in blood flow in the portal vein as compared to the splenic and superior mesenteric veins by 1.8–2.2 and 1.5–2.7 times, respectively. Arterial blood flow in the natural course of liver cirrhosis was characterized by a relatively increased hepatic arterial flow. The ultrasound criterion of hepatic blood flow “arterialization” was an increase in hepatic-splenic arterial index, which can be used as a sign to differentiate between different forms of portal hypertension. Decompensation of the disease was characterized by an average of 8.2 % decreased arterial blood flow in the hepatic artery compared to the splenic artery in dynamics. Prognostically unfavorable signs were the progression of splenomegaly degree, the increase in the portal vein diameter with the decreased velocity characterizing the increase in congestive index by 2.4–2.6 times, the decrease in the hepatic artery diameter and velocity in it over time.Conclusions. The hepatic and visceral blood flow characteristics should be considered when choosing method of conservative, surgical or minimally invasive treatment of liver cirrhosis complications. Based on the hepatic hemodynamic characteristics, the mismatch between portal perfusion (reduced) and visceral blood flow (increased) is the essence of portal hypertension in liver cirrhosis. Accordingly, the criterion of treatment effectiveness in decompensated liver cirrhosis should be improved portal liver perfusion and (or) reduced volume of visceral 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.

Effect of Propranolol on Hepatic Blood Flow in Normal and Portal Hypertensive Rats

1982 ◽  
Vol 63 (1) ◽  
pp. 29-32 ◽  
Author(s):  
P. Hillon ◽  
L. Blanchet ◽  
D. Lebrec
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Stenosis ◽  
Vein Stenosis

1. The effects of propranolol on heart rate, arterial pressure, portal venous pressure and fractional hepatic blood flow were studied in rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats. The effect of propranolol on cardiac output was also studied in normal rats. 2. In rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats, propranolol decreased heart rate and portal venous pressure significantly and did not alter arterial pressure. Propranolol decreased fractional hepatic blood flow significantly in rats with hepatic artery ligature, but did not change hepatic blood flow in rats with portal vein stenosis or in sham-operated rats. 3. We conclude therefore that: (a) propranolol decreases portal venous pressure in rats; (b) this decrease in portal venous pressure results in a reduction in portal blood flow which is related, in part, to a reduction in cardiac output; (c) propranolol does not alter hepatic blood flow in normal rats or in rats with portal hypertension.

scholarly journals Long-Term Hemodynamic Effects of Portocaval Shunt and Sugiura Procedure in Patients with Cirrhosis

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 209-213 ◽  
Author(s):  
Corinne Vons ◽  
Antoine Hadengue ◽  
Claude Smadja ◽  
Dominique Franco ◽  
Didier Lebrec
Keyword(s):  
Blood Flow ◽  
Cardiac Index ◽  
Pressure Gradient ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Hepatic Venous Pressure Gradient ◽  
Portocaval Shunt ◽  
Portal Systemic Shunt ◽  
Sugiura Procedure

Systemic and splanchnic hemodynamics were studied before and six months after a portal systemic shunt (n=6) or a Sugiura procedure (n=9) in 15 patients with cirrhosis and a past history of variceal bleeding. Hepatic blood flow was estimated by hepatic extraction and clearance of continuous indocyanine green infusion. Azygos blood flow was measured with a continuous thermodilution catheter. After portocaval shunt, the cardiac index increased significantly from 4.0±1.4 to 5.4±0.8 l/min m2 (p<0.05), the hepatic venous pressure gradient and hepatic blood flow were significantly decreased from 21±3 to 13±5 mm Hg (p<0.05) and from 1.20±0.35 to 0.37±0.16 l/min (p<0.05) respectively. The decrease in azygos blood flow was not significant (0.51±0.31 vs 0.25±0.33 l/min; p=0.1). After Sugiura procedure, there was no significant change in cardiac index, hepatic venous pressure gradient, hepatic blood flow or azygos blood flow. This is the first study to show the long-term maintenance of splanchnic and systemic hemodynamics in patients with cirrhosis after Sugiura procedure. The absence of long-term hemodynamic alterations could explain the absence of encephalopathy after this procedure.

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