González Fx

Intrahepatic biliary lesions after orthotopic liver transplantation

Abstract Intrahepatic biliary lesions (IBL) are rare (2–9 %) after orthotopic liver transplantation (OLT). The aim was to evaluate the incidence, etiology and outcome. In nine years, a total 532 OLTs were performed in 481 patients. Twenty-four patients developed IBL. Eight were due to HAT, seven to ABOI, three to CDR and six to PI. The time until diagnosis of HAT is longest in patients (14 ± 6) with IBL. ABOI is another cause of IBL. CDR is a rare cause of IBL, however when it takes place, patients must undergo Rtx. Finally, PI is a relevant cause of IBL. In order to suppress the incidence of IBL we should consider 1) the systematic use of Doppler-Ultrasound; 2) emergency reoperation of patients with HAT, 3) avoid ABOI in OLT; 4) Rtx in cases of CDR, and 5) OLT should still be performed as an emergency procedure.

Evaluation of Ischemic Injury during Liver Procurement from Non-Heart-Beating Donors

The aim of this study was to assess liver viability after different periods of cardiac arrest and the predictive value of two markers of ischemia-reperfusion injury. Methods: A pig liver transplantation model of non-heart-beating donors was studied. Four donor groups were designed; three groups were submitted to different periods of cardiac arrest (20, 30 and 40 min), and the fourth group served as the control group (without cardiac arrest). In the non-heart-beating donor groups, normothermic recirculation was established 30 min prior to total body cooling. Aminotransferase, α-glutathione-S-transferase, and hyaluronic acid determinations as well as liver biopsies, were serially performed. Results: Although hepatocellular function could be preserved after 40 min of cardiac arrest, histological lesions at 5 days were considered irreversible due to the presence of a necrotic biliary tract. An overall significant relationship was found between the time period of cardiac arrest (20, 30 or 40 min) and the levels of hyaluronic acid (p = 0.004) or α-glutathione-S-transferase (p = 0.01) obtained during liver procurement and transplantation. Conclusions: The period of cardiac arrest is the determinant factor of liver viability after liver transplantation from non-heart-beating donors. As early markers of endothelial or hepatocellular damage, hyaluronic acid or α-glutathione-S-transferase levels may help to evaluate the ischemic injury of a potential donor.

L-Arginine reduces liver and biliary tract damage after liver transplantation from non-heart-beating donor pigs

Background. To evaluate whether l-arginine reduces liver and biliary tract damage after transplantation from non heart-beating donor pigs. Methods. Twenty-five animals received an allograft from non-heart-beating donors. After 40 min of cardiac arrest, normothermic recirculation was run for 30 min. The animals were randomly treated with l-arginine (400 mg·kg−1 during normothermic recirculation) or saline (control group). Then, the animals were cooled and their livers were transplanted after 6 hr of cold ischemia. The animals were killed on the 5th day, liver damage was assessed on wedged liver biopsies by a semiquantitative analysis and by morphometric analysis of the necrotic areas, and biliary tract damage by histological examination of the explanted liver. Results. Seventeen animals survived the study period. The histological parameters assessed (sinusoidal congestion and dilatation, sinusoidal infiltration by polymorphonuclear cells and lymphocytes, endothelitis, dissociation of liver cell plates, and centrilobular necrosis) were significantly worse in the control group. The necrotic area affected 15.9±14.5% of the liver biopsies in the control group and 3.7±3.1% in the l-arginine group (P <0.05). Six of eight animal in the control group and only one of eight survivors in the l-arginine group developed ischemic cholangitis (P <0.01). l-Arginine administration was associated with higher portal blood flow (676.9±149.46 vs. 475.2±205.6 ml·min·m−2;P <0.05), higher hepatic hialuronic acid extraction at normothermic recirculation (38.8±53.7% vs. −4.2±18.2%;P <0.05) and after reperfusion (28.6±55.5% vs. −10.9±15.5%;P <0.05) and lower levels of &agr;-glutation-S-transferase at reperfusion (1325±1098% respect to baseline vs. 6488±5612%;P <0.02). Conclusions. l-Arginine administration during liver procurement from non heart beating donors prevents liver and biliary tract damage.

Prostacyclin, thromboxane and oxygen free radicals and postoperative liver function in human liver transplantation

The aim of this prospective study is to evaluate prostanoid (prostacyclin and thromboxane) and lipid peroxide levels at the portal and hepatic veins, and their relation to immediate postoperative liver function. Nineteen patients with liver cirrhosis undergoing orthotopic liver transplantation were prospectively studied. Blood samples were obtained within 5 min and 1 and 2 hr after reperfusion of the new liver, through a catheter placed at the portal vein in the recipient and another at the left hepatic vein in the donor liver. Plasma prostacyclin and thromboxane were analyzed by HPLC and RIA. The formation of lipid peroxides was determined and expressed in terms of thiobarbituric acid-reacting substances. Immediate postoperative liver function was evaluated using the transaminase levels within the first 48 hr and the early postoperative graft function score, as described previously. After reperfusion, only determinations at 5 min were related with liver function. Either prostacyclin (R = -0.61, P = 0.004) levels at the hepatic vein or prostacyclin production (subtraction between hepatic and portal vein levels) (R = -0.47, P = 0.04) correlated significantly with the early postoperative graft function score. Besides, there was a significant relationship between lipid peroxide production as measured by thiobarbituric acid-reacting substances and a worse early postoperative graft function score (R = 0.61, P = .005). These results suggest that prostacyclin released after liver grafting attenuates preservation and reperfusion damage of the liver, supporting the hypothesis that there is an imbalance of prostanoids within the microvasculature in patients with a compromised postoperative liver function. Our results agree with the involvement of some degree of lipid peroxidation products in the damage of hepatocytes during anoxia and reperfusion.