Postischemic lung injury has not been well defined experimentally or clinically prior to the onset of successful pulmonary allotransplantation. A variety of pulmonary disorders, such as Acute Respiratory Distress Syndrome (ARDS), however, are considered to be related to postischemic changes. In the past ten years, lung transplantation has evolved as an effective treatment of endstage pulmonary disease. Safe preservation methods to prolong the ischemic tolerance of donor organs are very much in demand. It has been repeatedly shown that the efficacy of donor organ protection for transplantation is limited when confined to the use of cold preservation solutions for flushing and storage. Accordingly, more recent studies have focused on reperfusion modalities and their implications for postischemic functional and metabolic recovery. 152 The optimum method for reperfusion of the lung after global ischemia, however, still has to be defined. This is particularly true for lung transplantation, where the early postoperative organ function may be transiently but critically impaired.3 Attempts to prevent this temporary functional derangement, which has been referred to as the reimplantation response, concentrated on minimizing injury during preservation of the lung before transplantation, rather than during the initial phase of reperfusion.4 This study focuses on the effects of the calcium channel blockers nifedipine and diltiazem, administered in the early phase of postischemic reperfusion. This period is known to be most susceptible for calcium influx into cells, as the capacity to sequester calcium is severely impaired.5 We used a rabbit model applying 2 h of normothermic ischemia of the left lung. Thereafter, oxygenation and pulmonary hemodynamics as well as extravascular fluid accumulation as an estimate of pulmonary edema formation were investigated.