Arterial pressure suffices to increase liver stiffness

Introduction: Elevated liver stiffness (LS) is not only observed in patients with liver cirrhosis but also in response to pressure changes such as liver congestion, inflammation or food intake. We here study in real-time pressure and LS in response to adrenergic stimulation.

Materials and Methods: LS was measured in 25 male Wistar rats using transient elastography (Microfibroscan, Echosens, Paris) during single i.v. injections of epinephrine (0.05 mg), norepinephrine (4 µg), dobutamine (50 – 150 mg) and sodium chloride (1 – 4 mL). Pressures in abdominal aorta, caval and portal vein were invasively measured in real-time using the Powerlab device (AD Instruments, New Zealand).

Results: Baseline LS values in all rats were comparable to those in humans with a mean of 3.8 ± 0.5 kPa (n = 25). Epinephrine and norepinephrine drastically increased mean arterial pressure (MAP) from 82.5 to 172.6 and 155.6 mmHg, respectively, while LS almost doubled from 4.1 to 7.5 kPa. In the same time, central venous pressure (CVP) remained unchanged while portal pressure slightly increased from 9.1 to 10.3 and 13.7 mmHg. Surprisingly, real-time monitoring clearly demonstrated that LS immediately increased with arterial pressure elevation while portal pressure followed with a latency of 8 seconds. In confirmation, LS was highly correlated with arterial (r = 0.799, P < 0.01) and portal pressures (r = 0.599, P < 0.01) but not with CVP. Dobutamine and volume up to 4 mL challenge failed to increase LS.

Conclusion: Arterial pressure elevation suffices to increase LS independent of the central venous pressure and prior to the portal pressure. Thus, hepatic arterial perfusion and sinusoidal pressure are a novel important modulator of LS e.g. during inflammation or food intake.