Einfluss der portalvenösen und simultanen Transplantatreperfusion auf die Mikrozirkulation nach Leber-Lebendtransplantation

Abstract

In clinical liver transplantation portal reperfusion is preferentially performed before arterial reconstruction to reduce the anhepatic period. Experimental and clinical data have raised doubts upon this concept. However, visualization and quantitative analysis of sinusoidal perfusion comparing simultaneous arterial/portal with portal/delayed arterialization reperfusion are missing up to now. Therefore, the present study aimed to analyze sinusoidal perfusion during sequential and simultaneous graft reperfusion in patients undergoing living-donor liver transplantation (n = 21). Microvascular observation was performed using the orthogonal polarization spectral (OPS)-imaging technique. Baseline microcirculation was assessed in donor livers directly following laparotomy. In group 1 (n = 14) the reperfusion was performed sequentially compared to group 2 (n = 7) with simultaneous arterial/portal reperfusion. Sinusoidal perfusion was analyzed 5 and 30 min following rearterialization. The mean cold ischemia time was 72 ± 33 min in group 1 and 100 ± 36 min in group 2 (p = 0.1). The mean portal clamping time was 41 ± 16 min in group 1 and 57 ± 11 min in group 2 (p = 0.07). Quantification of the microcirculatory parameters was performed off-line by using a computer-assisted image analysis system as were the sinusoidal diameter (D), red blood cell velocity (RBCV), sinusoidal volumetric blood flow (BVs), functional sinusoidal density (FSD), and inter-sinusoidal distance (ISD). Deteriorations of sinusoidal perfusion were significantly less pronounced in group 2. Typically, manifestation of red blood cell sludging and sinusoidal perfusion stasis was observed in group 1. In group 2 the FSD was significantly increased compared to group 1. In contrast, the RBCV, D, and BVs in group 1 were significantly higher compared to group 2, indicating a reactive post-ischemic hyperemia. Delayed arterialization, i.e. portal reperfusion may cause rapid graft rewarming without adequate oxygenation, resulting in warm ischemia, which may lead to the more pronounced post-ischemic reaction. The lack of vis a tergo during initial reperfusion, when sinusoids have to be cleared of hepatocellular blebs and endothelial cells detached during cold storage, may be responsible for sinusoidal no-reflow phenomenon, particularly in areas receiving predominantly arterial inflow and could explain the improvement of FSD following simultaneous reperfusion.