An experimental study on the disorders of hepatic hemodynamics and changes of plasma histamine in dogs with fulminant hepatic failure.

Abstract

The model of fulminant hepatic failure induced by acetaminophen was established in dogs to observe the changes of hepatic hemodynamics and plasma histamine levels in portal vein (PV), hepatic vein (HV), abdominal aorta (AA) and inferior vena cava (ICV). The results showed that the portal vein resistance (PVR) was elevated and portal venous blood flow (PVF) was decreased; hepatic artery resistance (HAR) was decreased and the hepatic artery blood flow (HAF), portal venous pressure (PVP), wedged hepatic venous pressure (WHVP) and inferior vena cava pressure (ICVP) had no changes. The histamine of the PV, HV, ICV and AA were all elevated after formation of fulminant hepatic failure. And the increasing wave of the HV was the highest. The increased histamine in HV may be mediated by H1 receptor causing the contraction of hepatic venulae, resulting liver sinusoid congestion, increasing PVR and decreasing PVF which exacerbate the liver cell damage. Moreover, the more severe liver damage, the more histamine was released, and a vicious circle may ensue. Our results also suggest the possibility of using H1 receptor antagonist to treat the disturbance of liver hemodynamics in severe acute liver damage. The increased histamine in systematic circulation as a vasodilator may lower blood pressure and accelerate heart beats. The increase of plasma histamine may play an important role in the changes of hepatic and systemic hemodynamics in fulminant hepatic failure.