BIOCHEMICAL (FUNCTIONAL) ADAPTATION OF ARTERIALIZED VEIN GRAFTS
BIOCHEMICAL (FUNCTIONAL) ADAPTATION OF ARTERIALIZED VEIN GRAFTS
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DOI：
10.1097/00000658-198604000-00001
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发表时间：
1986-04-01
影响因子：
9
通讯作者：
MILLER, DC
中科院分区：
文献类型：
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作者：
HENDERSON, VJ;MITCHELL, RS;MILLER, DC
将犬静脉自体移植物插入29只犬的股动脉和颈动脉位置;在术后3个时间间隔（1-2周、4-6周和8-10周）收获移植物，用于光学和扫描电子（SEM）显微镜检查和管腔表面前列环素（PGI 2）生产。正常静脉和动脉作为对照。氚标记的6-k-PGF 1 α的放射免疫测定，PGI 2的稳定代谢物，在基础和花生四烯酸刺激条件下使用流动表面模板孵育室进行。使用SEM，自体移植物在所有时间间隔显示正常的内皮细胞（EC）表面;相反，同种异体移植物在1-2周时表现出广泛的EC损失，并在10- 1-2周时逐渐修复（因此EC表面与对照静脉或自体移植物的EC表面几乎无法区分）。对照动脉中的PGI 2生成显著高于静脉（p = 0.0001）。在1-2周和4-6周，自体移植物和同种异体移植物中的PGI 2管腔产生与对照静脉没有显著差异;然而，在基础和刺激条件下，10- 1 - 2周后的PGI 2产生与正常动脉水平相同（并且显著[p < 0.0044]高于静脉水平）。虽然负责这种功能性（生化）“动脉化”过程的机制仍然是复杂的，增加的生物合成和/或释放的PGI 2的内皮细胞，急性期炎症细胞（同种异体移植物）介导的白细胞介素-1或肌内膜细胞似乎最有可能。进一步阐明这些PGI 2的来源是必要的，但这些数据首次证明，静脉移植物放置在动脉循环进行完整的功能适应（除了众所周知的形态学变化）。
Canine venous autografts were interposed in the femoral and carotid arterial positions in 29 dogs; grafts were harvested at three postoperative intervals (1-2 weeks, 4-6 weeks, and 8-10 weeks) for light and scanning electron (SEM) microscopy and lumenal surface prostacyclin (PGI2) production. Normal veins and arteries were used as controls. Radioimmunoassay for tritiated 6-k-PGF1.alpha., the stable metabolite of PGI2, was performed using a flow surface template incubation chamber during basal and arachidonic acid stimulated conditions. Using SEM, the autografts revealed normal endothelial cell (EC) surfaces at all time intervals; conversely, allografts exhibited extensive EC loss at 1-2 weeks with gradual reparation by 10-12 weeks (such that the EC surface was virtually indistinguishable from that of control veins or autografts). PGI2 production was significantly greater in control arteries than veins (p = 0.0001). At 1-2 weeks and 4-6 weeks, lumenal production of PGI2 in both the autografts and allografts was not significantly different from control vein; however, PGI2 production after 10-12 weeks was identical to normal arterial levels (and significantly [p < 0.0044] higher than venous levels) in both basal and stimulated conditions. Although the mechanisms responsible for this functional (biochemical) "arterialization" process remain conjectural, increased biosynthesis and/or release of PGI2 by endothelial cells, acute phase inflammatory cells (allografts) mediated by interleukin-1 or myointimal cells seems most likely. Further elucidation of these sources of PGI2 is necessary, but these data demonstrate for the first time that venous grafts placed in the arterial circulation undergo complete functional adaptation (in addition to the well known morphological changes).