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.

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

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.

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.

Measurement of hepatic blood flow after severe hemorrhage: lack of restoration despite adequate resuscitation

1992 ◽  
Vol 262 (1) ◽  
pp. G92-G98 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
J. Burkhardt ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hemorrhagic Shock ◽  
Hepatic Blood Flow ◽  
Microvascular Blood Flow ◽  
Midline Laparotomy ◽  
Doppler Flowmetry ◽  
Severe Hemorrhage ◽  
Icg Clearance

Although Ringer lactate (RL) is routinely used for resuscitation, it is not known whether the volume of RL that restores cardiac output after severe hemorrhagic shock also restores the depressed effective hepatic blood flow (EHBF). To study this, a 5-cm midline laparotomy was performed in rats (i.e., trauma induced), and the animals were then bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximum bleedout volume was returned in the form of RL. Animals were then resuscitated with four or five times the volume of maximum bleedout with RL. EHBF was determined during hemorrhage and at various intervals thereafter by an in vivo indocyanine green (ICG) clearance technique and corrected by the appropriate hepatic extraction ratio for ICG. Cardiac output was determined by ICG dilution, and hepatic microvascular blood flow (HMBF) was measured with laser Doppler flowmetry. In addition, hepatic blood flow was assessed by using radioactive microspheres. Results indicate that resuscitation markedly improved but did not restore the depressed EHBF after trauma and hemorrhagic shock despite the fact that cardiac output was restored. Similar changes in EHBF, HMBF, and hepatic blood flow as determined by microspheres were observed, suggesting that the in vivo ICG clearance is a reliable method to assess effective hepatic perfusion. Thus the lack of restoration of EHBF may be responsible for the subsequent hepatocellular dysfunction after trauma and severe hemorrhage.

Regulation of hepatic blood flow during resuscitation from hemorrhagic shock: role of NO and endothelins

1997 ◽  
Vol 272 (6) ◽  
pp. H2736-H2745 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
G. F. Noldge-Schomburg ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Receptor Antagonist ◽  
Hepatic Blood Flow ◽  
Vehicle Group ◽  
Venous Flow ◽  
Systemic Hemodynamic ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

We determined the role of nitric oxide (NO) and endothelins (ETs) in the regulation of hepatic blood flow during resuscitation from hemorrhagic shock (HS) in anesthetized rats. Volume resuscitation restored systemic hemodynamics and increased hepatic arterial and portal venous flow above baseline in the vehicle group. Presence of N omega-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg) during resuscitation increased systemic vascular resistance (SVR) above baseline, prevented the restoration of hepatic arterial flow, and abolished portal hyperemia. Although the ETA+B-receptor antagonist bosentan (10 mg/kg) did not alter the systemic hemodynamic response, it abolished the hepatic arterial and portal hyperemia. The ETA-receptor antagonist BQ-610 (150 micrograms/kg) reduced SVR below baseline, allowed hepatic arterial hyperemia to occur, and further enhanced the portal venous hyperemia. This indicates that 1) NO reduces SVR and acts to preserve hepatic blood flow during resuscitation from HS; 2) ETA-receptor-mediated vasoconstriction counteracts the systemic and portal hemodynamic effects of NO; and 3) simultaneous ETB-receptor stimulation enhances blood flow to the liver and may serve to modulate the ETA-receptor-mediated vasoconstrictive effects of ETs.

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.

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