The Clearance of 133Xenon from the Liver Intraportal Injection in Man

1965 ◽  
Vol 05 (03) ◽  
pp. 241-245 ◽  
Author(s):  
K.-F. Aronsen ◽  
B. Ericsson ◽  
A. Fajgelj ◽  
S.-E. Lindell
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Scintillation Detectors ◽  
Disappearance Rate ◽  
Simultaneous Measurements

Summary 133Xe dissolved in saline was injected into the portal vein in man. Hepatic blood flow was calculated from the disappearance rate of 133Xe recorded with scintillation detectors placed over the liver. The results are discussed and related to simultaneous measurements of the pressure in the portal vein.

Rapid Infusion of Hydroxyethyl Starch 70/0.5 but not Acetate Ringer’s Solution Decreases the Plasma Concentration of Propofol during Target-controlled Infusion

2016 ◽  
Vol 125 (2) ◽  
pp. 304-312 ◽  
Author(s):  
Sayako Itakura ◽  
Kenichi Masui ◽  
Tomiei Kazama
Keyword(s):  
Blood Flow ◽  
Plasma Concentration ◽  
Indocyanine Green ◽  
Blood Volume ◽  
Hydroxyethyl Starch ◽  
Hepatic Blood Flow ◽  
Disappearance Rate ◽  
Rapid Infusion ◽  
Ringer’S Solution ◽  
Target Controlled Infusion

Abstract Background Rapid fluid infusion resulting in increased hepatic blood flow may decrease the propofol plasma concentration (Cp) because propofol is a high hepatic extraction drug. The authors investigated the effects of rapid colloid and crystalloid infusions on the propofol Cp during target-controlled infusion. Methods Thirty-six patients were randomly assigned to 1 of 3 interventions (12 patients per group). At least 30 min after the start of propofol infusion, patients received either a 6% hydroxyethyl starch (HES) solution at 24 ml·kg−1·h−1 or acetated Ringer’s solution at 24 or 2 ml·kg−1·h−1 during the first 20 min. In all groups, acetated Ringer’s solution was infused at 2 ml·kg−1·h−1 during the next 20 min. The propofol Cp was measured every 2.5 min as the primary outcome. Cardiac output, blood volume, and indocyanine green disappearance rate were determined using a pulse dye densitogram analyzer before and after the start of fluid administration. Effective hepatic blood flow was calculated as the blood volume multiplied by the indocyanine green disappearance rate. Results The rapid HES infusion significantly decreased the propofol Cp by 22 to 37%, compared to the Cp at 0 min, whereas the rapid or maintenance infusion of acetate Ringer’s solution did not decrease the propofol Cp. Rapid HES infusion, but not acetate Ringer’s solution infusion, increased the effective hepatic blood flow. Conclusions Rapid HES infusion increased the effective hepatic blood flow, resulting in a decreased propofol Cp during target-controlled infusion. Rapid HES infusion should be used cautiously as it may decrease the depth of anesthesia.

Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits

1998 ◽  
Vol 274 (3) ◽  
pp. H777-H785 ◽  
Author(s):  
Carl F. Rothe ◽  
Roberto Maass-Moreno
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Inferior Vena ◽  
Liver Volume ◽  
Liver Lobe ◽  
Inferior Vena Caval ◽  
Total Hepatic Blood Flow ◽  
Constant Rate ◽  
Increased Blood Flow

Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 ± 15 (SD) μm vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.

Hepatic blood flow in experimental hemorrhagic shock

1962 ◽  
Vol 202 (1) ◽  
pp. 7-11 ◽  
Author(s):  
Edward D. Frank ◽  
Howard A. Frank ◽  
Stanley W. Jacob ◽  
Jacob Fine
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Hepatic Blood Flow ◽  
Marked Reduction ◽  
Blood Replacement ◽  
Transient Improvement ◽  
Experimental Hemorrhagic Shock

In dogs in hemorrhagic shock, the blood flow and oxygenation of the liver were measured with a catheter in a hepatic vein. There is a marked reduction in hepatic blood flow and oxygenation throughout hemorrhagic shock. There is transient improvement following blood replacement and additional transfusions. Arterial shunts into the portal vein may restore hepatic oxygenation to preshock levels. Norepinephrine does not increase hepatic blood flow even though arterial pressure is restored to normal. Dibenamine pretreatment sustains the hepatic flow to some extent during hypovolemia; antibiotic pretreated animals do not differ from controls.

Changes Porto-hepatic Blood Flow in Patients with Cirrhosis of the Liver, Combined with Chronic Bronchitis

2016 ◽  
pp. 129-132
Author(s):  
Nataliia Virstyuk ◽  
Iryna Kobitovych ◽  
Olha Gerasymchuk
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Chronic Bronchitis ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Blood Flow Velocity ◽  
Splenic Artery ◽  
Splenic Vein ◽  
Resistance Index ◽  
Healthy Individuals

The objective: study the features of porto1hepatic blood flow in patients with alcoholic liver cirrhosis (ALC) in conjunction with chronic bronchitis (CB) according to Doppler ultrasound. Patients and methods. The study involved 60 patients who were hospitalized, 20 ALC patients in stage B according to Child-Pugh without CB (Ist group), 20 ALC patients in stage B according to Child-Pugh combined with CB in the acute phase (IInd group), 20 patients exacerbation of chronic bronchitis, for which there was no evidence of digestive system diseases (IIIrd group). All patients underwent a complex ultrasonic research techniques scanning in B-mode, the VD-mode, color duplex scanning using «Hitachi EUB 7000» ultrasonic scanner connected to the Doppler flourimetr was visualized main arterial and venous vessels of hepatic and splenic pools. Results. Changes porto-hepatic blood flow were most pronounced in patients with ALC in combination with CB when compared with patients of groups I and III (p<0,05) according to the obtained Doppler indices: diameter of the hepatic artery was 5,55±0,19 mm, portal vein – 12,60±0,17 mm, where increased by 159,12% and 53,56%, respectively (p<0,05) higher than those in healthy individuals. The diameter of the splenic artery and splenic vein at the ALC for combination with CB significantly increased compared with control on 31,13% and 35,67%, respectively (p<0,05). Linear and volumetric blood flow rate in portal vein decreased in this group of patients, 60,24% and 22,68%, respectively (p<0,05) compared with healthy individuals, the linear velocity of blood flow in the splenic vein also significantly slowed down compared to the control on 41,06% (p<0,05), and the volumetric blood flow velocity v. lienalis grew by 155,80% (p<0,05). Among the characteristics of the arterial blood flow hepato-splenic system Gosling pulsatility index (PI) and Pursello resistance index (RI) of hepatic artery also Pursello resistance index (RI) of splenic artery significantly grew in ALC patients in combination with CB 147,20%, 65,49% and 32,31%, respectively (p<0,05) compared with the control group. Maximal systolic velocity of blood flow in the hepatic artery of patients – grew by 8,95% (p<0,05). End diastolic blood flow velocity in the hepatic artery tended to decrease on 13,36% (p<0,05) compared with healthy individuals. Conclusion. Violation of porto-hepatic blood flow in patients with ALC is characterized by its redistribution in the veins of the portal system in the direction of the spleen with a decrease in the average linear and the volumetric velocity in the portal and hepatic veins, increasing the resistance index in the interlobar arteries.

BEDSIDE ARTERIAL HEPATIC BLOOD FLOW (AHBF) AND PORTAL VEIN BLOOD FLOW (PVBF) OF HUMAN LIVER TRANSPLANT

1988 ◽  
Vol 69 (3A) ◽  
pp. A175-A175
Author(s):  
C GATECEL ◽  
P DUPUY ◽  
M D FRATACCI ◽  
Y OZIER ◽  
D PAYEN MD ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Liver Transplant ◽  
Hepatic Blood Flow ◽  
Human Liver

EFFECTS OF ISOFLURANE VS HALOTHANE ON HUMAN ARTERIAL HEPATIC BLOOD FLOW (AHBF) AND PORTAL VEIN BLOOD FLOW (PVBF) AFTER SURGICAL STRESS

1988 ◽  
Vol 69 (3A) ◽  
pp. A77-A77 ◽  
Author(s):  
D PAYEN ◽  
C GATECEL ◽  
P DUPUY ◽  
J J CARACO ◽  
F RICHE ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Surgical Stress

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.

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.

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