Urabe N, Fujisawa T, Saitoh Y, Takeda T, Sekine Y, Yamaguchi Y, Kimizuka G, Terano T
Department of Surgery, Institute of Pulmonary Cancer Research, Chiba University Medical School, Japan.
Transplantation. 1994 Jan;57(2):194-8. doi: 10.1097/00007890-199401001-00006.
The release of prostaglandin I2 (PGI2) from the vasculature is thought to reflect damage to the vessels. Basal and bradykinin (BK)-stimulated release of PGI2 from isolated dog lungs after 6-hr preservation were investigated to evaluate lung damage after preservation. Maximal PGI2 release induced by BK decreased significantly after preservation at 24 degrees C (room temperature), but not after hypothermic preservation at 4 degrees C, although basal PGI2 release without BK stimulation did not change in either group of lungs after preservation. The function of allotransplanted lungs assessed by arterial oxygen tension was impaired by preservation at room temperature but not by hypothermic preservation. No differences were observed by light microscopy in either group in the pulmonary tissues, including the pulmonary artery, after preservation. In summary, damage to the lung after preservation may be reflected by the maximal PGI2 release from the lung after BK infusion. Therefore the maximal PGI2 releasing capacity induced by BK may be a useful biochemical parameter for estimating the viability of preserved lungs.
血管中前列腺素I2（PGI2）的释放被认为反映了血管的损伤。研究了保存6小时后，从离体犬肺中基础状态下以及缓激肽（BK）刺激下PGI2的释放情况，以评估保存后的肺损伤。24℃（室温）保存后，BK诱导的最大PGI2释放显著降低，但4℃低温保存后未降低，尽管在两组保存后的肺中，无BK刺激时的基础PGI2释放均未改变。通过动脉血氧分压评估的同种异体移植肺功能在室温保存后受损，但低温保存后未受损。保存后，两组肺组织（包括肺动脉）在光学显微镜下均未观察到差异。总之，保存后肺的损伤可能通过BK注入后肺中最大PGI2释放来反映。因此，BK诱导的最大PGI2释放能力可能是评估保存肺活力的一个有用的生化参数。
