Graft preservation with heparinized blood/saline solution induces severe graft dysfunction

Vascular grafts are often stored in cold physiological saline/heparinized blood preservation solution. Until now, only in vitro studies investigated the effect of the aforementioned preservation solutions on endothelial function. The main goal of our study was to compare the storage effect of physiological saline and heparinized blood after short-time cold storage and warm reperfusion in a rat model of aortic transplantation.

Aortic abdominal transplantations (n = 6-8/group) were performed in Lewis rats. The donor aortic arches were placed in cold physiological saline and heparinized blood solutions and stored for 2 h. After the 2 h ischaemia, the aortic arches were transplanted into the abdominal aorta of the recipient. Two, 24 h or 1 week after transplantation, implanted grafts were harvested. Endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) vasorelaxation were investigated in organ bath experiments. DNA strand breaks were assessed by transferase-mediated dUTP nick-end labelling-method and mRNA expression by quantitative real-time polymerase chain reaction. In addition, the expression of CD-31 was also investigated by immunochemistry.

Severely impaired endothelial function and integrity of grafts were shown after 2 and 24 h reperfusion in both groups (maximal vasorelaxation control: 94 ± 1%, heparinized blood: 27 ± 4 and 17 ± 3%, saline 34 ± 5% and 28 ± 5%; CD-31 positive area control: 96 ± 1% blood: 38 ± 8% and 41 ± 6%, saline: 35 ± 12% and 41 ± 7%, respectively P < 0.05). After 1 week, endothelial function and integrity were partially recovered (maximal vasorelaxation: heparinized blood: 46 ± 4%, saline: 46 ± 2%, CD-31 positive area blood: 35 ± 4%; saline: 56 ± 5%, P < 0.05). In addition, mRNA levels of Bax, Bcl-2 and caspase-3 were significantly altered and DNA stand breaks were observed.

Storage with the generally used physiological saline and heparinized blood solutions is unable to protect the endothelium against cold ischaemia and warm reperfusion injury. A similar weak preservation effect was observed.