Submitted on January 28, 2008
Accepted on June 2, 2008
Reactive hyperemia in the human liver
Helmut G. Hinghofer-Szalkay1*, Nandu Goswami2, Andreas Roessler3, Erik Konrad Grasser3, and Daniel Schneditz4
1 Physiology, Medical University Graz, Graz, Austria, Austria; Institute of Adaptive and Spaceflight Physiology, Graz, Austria
2 Physiology, Medical University Graz, Graz, Austria, Austria
3 Physiology, Medical University, Graz, Steiermark, Austria
4 Graz, Austria; Physiology, Medical University Graz, Graz, Austria, Austria
* To whom correspondence should be addressed. E-mail: helmut.hinghofer{at}meduni-graz.at.
Aim. We tested whether hepatic blood flow is altered following central hypovolemia caused by simulated orthostatic stress. Procedures and methods. 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. Results. Plasma volume decreased during LBNP (-10%) as did cardiac output (-15%) while heart rate (+14%) and peripheral resistance (+17%) increased, as expected. Based on ICG elimination, hepatic perfusion decreased from 1.67±0.32 (pre-LBNP control) to 1.33±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/mmHg, p<0.0001). Conclusion. 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 will quantify the intensity of this response in relation to stimulus duration and magnitude, and clarify its mechanism.
