In contrast to traditional static cold preservation of donor livers, normothermic machine perfusion may reduce preservation injury, improve graft viability and potentially allows ex vivo assessment of graft viability before transplantation. We have studied the feasibility of normothermic machine perfusion in four discarded human donor livers. Normothermic machine perfusion consisted of pressure and temperature controlled pulsatile perfusion of the hepatic artery and continuous portal perfusion for 6 h. Two hollow fiber membrane oxygenators provided oxygenation of the perfusion fluid. Biochemical markers in the perfusion fluid reflected minimal hepatic injury and improving function. Lactate levels decreased to normal values, reflecting active metabolism by the liver (mean lactate 10.0 ± 2.3 mmol/L at 30 min to 2.3 ± 1.2 mmol/L at 6 h). Bile production was observed throughout the 6 h perfusion period (mean rate 8.16 ± 0.65 g/h after the first hour). Histological examination before and after 6 h of perfusion showed well-preserved liver morphology without signs of additional hepatocellular ischemia, biliary injury or sinusoidal damage. In conclusion, this study shows that normothermic machine perfusion of human donor livers is technically feasible. It allows assessment of graft viability before transplantation, which opens new avenues for organ selection, therapeutic interventions and preconditioning.
After partial liver resection, a low platelet count is an independent predictor of delayed postoperative liver function recovery and is associated with increased risk of postoperative mortality. These clinical findings are in accordance with the accumulating evidence from experimental studies, indicating that platelets play a critical role in liver regeneration.
A blunted or absent rise in PCs in critically ill patients is associated with increased mortality. deltaPC/deltat is a readily available and simple parameter to improve assessment of critically ill patients.
We thank Niccoli et al for their letter, which interestingly suggested that intracoronary administration of abciximab may exert its action in patients with ST-segment elevation myocardial infarction through facilitation of reversible no reflow. Our study was designed to detect a difference in electrocardiographic and angiographic measures of immediate myocardial reperfusion after primary percutaneous coronary intervention, markers that are frequently used in medium-sized randomized studies and show strong correlation with clinical outcome. 1,2 In this regard, we did not include recovery of myocardial perfusion at a later time point as a prespecified end point. It is not our center's routine clinical practice to reevaluate the initial angiographic result and recovery of myocardial perfusion in the infarct-related artery before discharge, either by repeat angiography or by cardiac magnetic resonance imaging. Because the infarct-related artery may have been filmed in additional revascularization procedures only in highly selected cases, we believe that analysis of this small, nonprespecified subset of patients would not produce meaningful results. In fact, an early study has indicated that intracoronary administration of abciximab significantly reduced the primary end point of microvascular obstruction on cardiac magnetic resonance 2 days after primary percutaneous coronary intervention compared with intravenous administration. 3 Therefore, we agree with Niccoli et al that facilitation of reversible no reflow is one of the plausible mechanisms of action of intracoronary abciximab, a hypothesis that may be further tested in ongoing randomized studies on intracoronary versus intravenous abciximab administration that include cardiac magnetic resonance end points. 4 Rationale and design of the INFUSE-AMI study: a 2ϫ2 factorial, randomized, multicenter, single-blind evaluation of intracoronary abciximab infusion and aspiration thrombectomy in patients undergoing percutaneous coronary intervention for anterior ST-segment elevation myocardial infarction.
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