title: Functional significance of hepatic arterial flow reserve in patients with cirrhosis.
abstract: In cirrhosis, hepatic arterial vasodilatation occurs in response to reduced portal venous blood flow. However, although the hepatic arterial flow reserve is high in patients with cirrhosis, its impact on hepatic function is unknown. This study investigated the effect of adenosine-induced hepatic arterial vasodilatation on different markers of liver function. In 20 patients with cirrhosis (Child-Pugh class A/B/C: n = 2/7/11) adenosine (2-30 microg x min(-1) x kg body wt(-1)) was infused into the hepatic artery and hepatic arterial average peak flow velocities (APV), pulsatility indices (PI), and blood flow volumes (HABF) were measured using digital angiography and intravascular Doppler sonography. Indocyanine green (ICG), lidocaine, and galactose were administered intravenously in doses of 0.5, 1.0, and 500 mg/kg body weight in the presence of adenosine-induced hepatic arterial vasodilatation and, on a separate study day, without adenosine. ICG disappearance, galactose elimination capacity (GEC), and formation of the lidocaine metabolite monoethylglycinxylidide (MEGX) were assessed. Adenosine markedly increased APV and HABF and markedly decreased PI. Serum MEGX concentrations were 63.7 +/- 18.2 (median, 62; range, 36-107) and 99.0 +/- 46.3 (82.5; 49-198) ng/mL in the absence and presence of adenosine infusion, respectively (P =.001). Adenosine-induced changes in MEGX concentrations were correlated inversely to changes in APV (r = -0.5, P =.02) and PI (r = -0.55, P =.01) and were more marked in Child-Pugh class C compared with Child-Pugh class A patients (57.4 +/- 49.9 [44; -14 to 140] vs. 8.4 +/- 16.5 [13; -11 to 35] ng/mL, P <.01). In conclusion, hepatic arterial vasodilatation provides substantial functional benefit in patients with cirrhosis. The effect does not depend directly on hepatic arterial macroperfusion and is observed preferentially in patients with decompensated disease.
authors.affiliation: First Department of Medicine, Martin-Luther-University Halle-Wittenberg, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Zipprich
authors.forename: Norbert
authors.initials: N
authors.lastname: Steudel
authors.forename: Curd
authors.initials: C
authors.lastname: Behrmann
authors.forename: Frank
authors.initials: F
authors.lastname: Meiss
authors.forename: Ursula
authors.initials: U
authors.lastname: Sziegoleit
authors.forename: Wolfgang E
authors.initials: WE
authors.lastname: Fleig
authors.forename: Gerhard
authors.initials: G
authors.lastname: Kleber
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects; D001810:Blood Volume / Q000187:drug effects; D004396:Coloring Agents / Q000493:pharmacokinetics; D005260:Female; D005690:Galactose / Q000378:metabolism; D006499:Hepatic Artery / Q000503:physiopathology*; D006801:Humans; D007208:Indocyanine Green / Q000493:pharmacokinetics; D008012:Lidocaine / Q000031:analogs & derivatives* / Q000097:blood / Q000378:metabolism; D008103:Liver Cirrhosis / Q000145:classification / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D011674:Pulse; D012039:Regional Blood Flow / Q000187:drug effects; D012720:Severity of Illness Index; D014664:Vasodilation
chemical_list: D004396:Coloring Agents; D008012:Lidocaine; C001173:monoethylglycinexylidide; D007208:Indocyanine Green; D000241:Adenosine; D005690:Galactose