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Results for “LIVER CIRCULATION”

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At least 37 records · Page 2Linked to original sources
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↗
PubMed1979

[New aspects of liver circulation: effects and consequences for the portocaval shunt therapy in liver cirrhosis].

Hepatic circulation, which is of essential importance in supplying the liver cells with oxygen and substrates needed for securing metabolic homeostasis of the organism, is characterized by well-regulated mechanisms of intrahepatic arterial, portal and hepatovenous interaction. Furthermore, the hepatic circulation is integrated in the systemic and splanchnic hemodynamic as interposed in a high, or respectively low, pressure system. Beside these hemodynamic mechanisms there are also specific morphologic features in the hepatic vascular bed responsible for regulating liver blood flow. For hepatic nutritions and trophics, and for the metabolic homeostasis of the organism, portal blood is of greater importance than arterial. In porto-caval shunt surgery it is recommended that any remaining portal flow to the liver be preserved to the greatest extent possible.

Homeostasis↗
PubMed1988

[An experimental study of PGE1 infusion into the liver circulation].

The present study was performed to determine the effects of PGE1 on the liver circulations. Adult mongrel dogs were used for this experimental study. Following the continuous infusion of PGE1 to the hepatic artery (HA) and portal vein (PV), the change of hepatic arterial flow (HAF) and portal venous flow (PVF) was measured by the electromagnetic flow meter, and hepatic tissue flow (HTF) by the hydrogen clearance meter. Hepatic enzymes were also measured at the same time. A single infusion of saline was done for the control. HAF and HTF increased significantly by the continuous infusion of over 0.5ng/Kg/min of PGE1 to HA. PVF and HTF also showed an increase by the continuous infusion of 100ng/Kg/min of PGE1 to PV. Compared with the control group, lactate acid and pyruvate acid levels remained low in the PGE1 infused group. The optimum dose of PGE1 to HA was thought to be 1.0-2.0ng/Kg/min. The results of experimental studies suggest that the direct infusion of PGE1 to the liver may prevent the ischemic change of hepatic metabolism during and after the surgical interventions.

Alprostadil↗
PubMed1995

The selective effects of dopamine and dobutamine on liver circulation in the dog.

The selective effects od dopamine and dobutamine in various doses on liver circulation were studied in 12 mongrel dogs. Dopamine increased portal flow but decreased hepatic arterial flow markedly as infusion rate of dopamine increased. Dopamine 3 micrograms/kg/min infusion rate produced vasodilation in mesenteric vascular bed and the portal flow ratio to cardiac output was significantly increased. Dobutamine increased both portal and hepatic arterial flows at the 5 and 10 micrograms/kg/min dobutamine infusion rates, and decreased hepatic arterial flow at the 15 micrograms/kg/min dobutamine infusion rate. Both dopamine and dobutamine increased total liver flows, however, total liver flow ratio to cardiac output was not increased. Pressure gradient of portal system was not changed during dopamine and dobutamine infusion, since both portal venous pressure and hepatic venous pressure were avariant from control values. These findings suggest that congestive hyperemia was not occurred in intrahepatic portal vascular system when portal flows were increased during dopamine and dobutamine infusion. The results of this study demonstrate that both dopamine and dobutamine did not produce selective increases in total liver blood flow. In addition, both agents should be safe to use to the normal liver patient; total liver blood flow did not decrease and intrahepatic congestive hyperemia was not occurred when portal flow was increased.

Animals↗
PubMed1985

[Determination of liver circulation with radionuclides. I. Modification of 99mTc-MMS accumulation in the liver using drugs].

The rate constant of liver uptake of 99mTc-labelled millimicrospheres is taken to be a measure of nutritive RES blood supply. Animal experiments were used to determine whether this constant--similar to that of other colloids--is affected by drugs such as heparin or corticosteroids which alter RES function. In rabbits, the scatter of k between individuals is quite large, with a standard deviation of 27%, whereas the scatter within an individual appears to be acceptable (8%). Heparin does not change the value of k significantly, whereas prednisolone in a dose of 40 mg/kg BW--a dose that is normal in bolus therapy--reduces k significantly by 21%. If k is determined during such therapy, its reduction may be due to the pharmacological effect and must not be interpreted as a rejection phenomenon.

Animals↗
PubMedDate not supplied

D-sorbitol plasma disappearance rate: an index to evaluate changes in liver circulation.

The hepatic clearance of D-sorbitol was proven to be a reliable parameter for evaluating the functional liver plasma flow. Twenty-five normal subjects and 50 cirrhotic patients were studied in order to assess if the measure of the plasma disappearance rate of sorbitol can be used as a simpler procedure to evaluate changes in liver perfusion and to predict modifications of drug bioavailability due to circulatory events. The plasma disappearance rate was calculated between 10 and 20 min after intravenous administration of a 2-g dose because in this time interval plasma levels were in the optimum range for the chemical assay, and the plasma concentration/time curve fitted a decreasing exponential function. Plasma disappearance rate values were found to correlate significantly (r = 0.666, p less than 0.001) with sorbitol hepatic clearance, as calculated after the 2-h test. The test had a good day-to-day reproducibility both in normal subjects and cirrhotic patients. In 5 patients submitted to surgical side-to-side portacaval shunt, decreases of plasma disappearance rate and sorbitol hepatic clearance showed no significant difference. Mean values (+/- SD) of D-sorbitol plasma disappearance rate were 0.048 +/- 0.014 min-1 in cirrhotic patients, and 0.081 +/- 0.014 min-1 in normal subjects (p less than 0.001).

Blood Flow Velocity↗