Hinghofer-Szalkay Helmut G, Goswami Nandu, Rössler Andreas, Grasser Erik, Schneditz Daniel
Institute of Physiology, Center for Physiological Medicine, Medical Univ. Graz, Harrachgasse 21, A-8010 Graz, Austria.
Am J Physiol Gastrointest Liver Physiol. 2008 Aug;295(2):G332-7. doi: 10.1152/ajpgi.00042.2008. Epub 2008 Jun 5.
We tested whether hepatic blood flow is altered following central hypovolemia caused by simulated orthostatic stress. After 30 min of supine rest, hemodynamic, plasma density, and indocyanine green (ICG) clearance responses were determined during and after release of a 15-min 40 mmHg lower body negative pressure (LBNP) stimulus. Plasma density shifts and the time course of plasma ICG concentration were used to assess intravascular volume and hepatic perfusion changes. Plasma volume decreased during LBNP (-10%) as did cardiac output (-15%), whereas heart rate (+14%) and peripheral resistance (+17%) increased, as expected. On the basis of ICG elimination, hepatic perfusion decreased from 1.67 +/- 0.32 (pre-LBNP control) to 1.29 +/- 0.26 l/min (-22%) during LBNP. Immediately after LBNP release, we found hepatic perfusion 25% above control levels (to 2.08 +/- 0.48 l/min, P = 0.0001). Hepatic vascular conductance after LBNP was also significantly higher than during pre-LBNP control (21.4 +/- 5.4 vs. 17.1 +/- 3.1 ml.min(-1).mmHg(-1), P < 0.0001). This indicates autoregulatory vasodilatation in response to relative ischemia during a stimulus that has cardiovascular effects similar to normal orthostasis. We present evidence for physiological post-LBNP reactive hyperemia in the human liver. Further studies are needed to quantify the intensity of this response in relation to stimulus duration and magnitude, and clarify its mechanism.
我们测试了模拟直立位应激导致中心性血容量减少后肝血流量是否发生改变。在仰卧休息30分钟后，在施加15分钟40 mmHg的下体负压（LBNP）刺激期间及刺激解除后，测定血流动力学、血浆密度和吲哚菁绿（ICG）清除率反应。利用血浆密度变化和血浆ICG浓度的时间进程来评估血管内容量和肝脏灌注变化。正如预期的那样，LBNP期间血浆容量下降（-10%），心输出量也下降（-15%），而心率上升（+14%），外周阻力增加（+17%）。基于ICG清除率，LBNP期间肝脏灌注从1.67±0.32（LBNP前对照）降至1.29±0.26 l/min（-22%）。LBNP解除后立即发现肝脏灌注比对照水平高25%（至2.08±0.48 l/min，P = 0.0001）。LBNP后的肝血管传导率也显著高于LBNP前对照期间（21.4±5.4对17.1±3.1 ml·min⁻¹·mmHg⁻¹，P < 0.0001）。这表明在一种具有与正常直立位相似心血管效应的刺激过程中，肝脏对相对缺血产生了自动调节性血管舒张。我们提供了人体肝脏LBNP后生理性反应性充血的证据。需要进一步研究来量化这种反应的强度与刺激持续时间和幅度的关系，并阐明其机制。
