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At least 19 recordsLinked to original sources
PubMed1994

An experimental study on the disturbance of liver circulation and the change of hemorrheology in dogs with acute liver damage.

The changes of hepatic hemodynamics and hemorrheology were investigated in dogs with acute liver damage induced by acetaminophen. There were remarkable disturbance in liver circulation and hemorrheological abnormality occurring in both slight and severe liver damage. The study indicated that the degree of disturbance in liver circulation as well as in hemorheological change is positively correlated with the severity of liver damage. For example, marked increase in blood viscosity linked with elevated fibrinogen level appeared in slight liver damage, whereas reduced blood viscosity associated with decreased plasma fibrinogen level and hematocrit occurred in severe liver damage. This study also revealed that the increase of portal venous resistance (PVR) and the disturbance of liver circulation in slight liver damage were chiefly related to the increase of blood viscosity and the increase of PVR in severe liver damage was mainly associated with the reduction of the radius of portal vein.

Acetaminophen↗
PubMedDate not supplied

Pathophysiology of liver circulation with an overview of medical and invasive treatments.

Liver hemodynamics is characterized by a dual venous and portal blood supply whose physiologic variations are particularly evident during digestion. In the normal subject portal blood flow is laminar with the left liver receiving the blood from the small intestine while the left liver is supplied by the blood from the spleen and colon. In pathologic conditions increased arterial blood flow accompanies the decreased portal flow. Portal hypertension in its various forms is the most frequent and important circulatory alteration in chronic liver disease; besides the "organic" obstacles to the hepatic blood flow there are the dynamic mechanisms which regulate the vascular resistance in the microcirculation Therapies which impact on liver circulation are surgical, of interventional radiology and medical, used in the prevention and cure of complications of portal hypertension.

Hepatic Artery↗
PubMed1979

Liver circulation and oxygen metabolism during short time ligation and the hepatic artery in the dog.

The changes of liver circulation and liver oxygen metabolism during and after one hour hepatic artery ligation (HAL) were studied in eight mongrel dogs. At the end of the HAL period total hepatic blood flow (THBF) was reduced from 115.6 +/- 5.5 ml/min . 100 g liver tissue to 68.0 +/- 3.7 ml/min . 100 g or 59% of the initial value. The portal venous blood flow was reduced from 83.1 +/- 3.4 to 58.8 +/- 3.7 ml/min . 100 or 82% of the initial value and the liver oxygen consumption was reduced from 4.1 +/- 0.2 ml/min . 100 g to 3.1 +/- 0.3 ml/min . 100 g or 76% of the initial value. The changes in portal venous blood flow and liver oxygen consumption were reversible following reopening of the hepatic artery. The clinical importance of a reduced portal venous blood flow and liver oxygen consumption following HAL and the possibilities to increase the portal venous blood flow are discussed.

Animals↗
PubMed1994

Effect of modifying nitric oxide pathway on liver circulation in a rabbit endotoxin shock model.

The role of nitric oxide (NO) inhibition on liver circulation during sepsis is unknown. To answer this question, we studied the effects of L-arginine (the substrate for the NO synthase), linsidomine (a direct NO donor), and N omega-nitro-L-arginine (an NO inhibitor) on the liver circulation in anesthetized rabbits previously injected with endotoxin (Escherichia coli, Salmonella enteridis, and Salmonella minnesota, 400 micrograms each). After endotoxin administration, and without fluid resuscitation, rabbits showed a hypodynamic shock with decrease in mean arterial pressure (MAP) and aortic blood flow velocity. Portal vein blood flow velocity decreased, whereas hepatic artery blood flow velocity increased. Saline or treatments were injected, 75 min after endotoxin administration. In saline-treated rabbits, MAP, aortic and portal vein blood flow velocities remained steady but hepatic artery blood flow velocity decreased. Only N omega-nitro-L-arginine (7.5 mg/kg, intravenously) significantly increased MAP compared to saline treatment. However, aortic, portal vein, and hepatic artery blood flow velocities were lower in rabbits treated with N omega-nitro-L-arginine than in saline-treated rabbits. L-Arginine (600 mg/kg, intravenously) increased aortic blood flow and portal vein blood flow velocity with no change on hepatic artery blood flow velocity. In contrast, linsidomine (1 mg) increased both hepatic flows. These results show that NO inhibition after endotoxin injection reduces systemic and liver flows, while NO release from linsidomine improves them. These findings question the usefulness of NO inhibition during septic shock, particularly as hepatic failure frequently occurs in the evolution of the disease.

Animals↗