Direct effects of various catecholamines on liver circulation in dogs

Abstract

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.

Impact of hypoxic hepatitis on mortality in the intensive care unit

“…The principal response of the hepatic vascular bed to catecholamines is vasoconstriction [21,22]. Norepinephrine and epinephrine divert blood flow away from the mesenteric circulation and decrease microcirculatory blood flow in the gastrointestinal tract despite increased perfusion pressure and increased systemic blood flow in experimental sepsis [23].…”

Effect of Intraarterial, Intraportal or Combined Norepinephrine Infusion on Hemorrhage at Experimental Liver Trauma in the Rat

“…Intraportal in jection of NE using the above canine model, caused a dose-dependent increase in hepatic portal vascular resistance [11]. Hepatic ar terial vasoconstriction in dogs was also pro duced by intraportal NE, while arterial injec tion of the compound provoked simulta neous portal vasoconstriction [5,6]. Ri chardson and Withrington [13] postulated that the observed phenomenon was due to an intrahepatic effect of NE at the level of presinusoidal sphincters.…”

Compensated Cardiogenic Shock: A Subset with Damage Limited to Liver and Kidneys

“…A favorable outcome was observed in those patients who were administered intra venous dopamine at low dose, presumably because of the ability of this agent to selec tively dilate the hepatic and renal vascular beds. This effect is unique to low doses, while higher concentrations of dopamine cause splanchnic vasoconstriction by adren ergic mechanisms [13][14][15], Since the syn drome of specific organic failure in the ab sence of hypotension is relatively uncom mon, it is not possible to do a randomized study. However, by comparing and matching groups of treated and nontreated patients, low dosage of dopamine appeared to benefit the treated group, whereas those without therapy appeared to do poorly.…”