Incomplete biochemical adaptation of vein grafts to the arterial environment in terms of prostacyclin production.
Incomplete biochemical adaptation of vein grafts to the arterial environment in terms of prostacyclin production.
复制标题
就前列环素的产生而言，静脉移植物对动脉环境的生化适应不完全。
DOI：
10.1067/mva.1987.avs0060496
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发表时间：
1987
影响因子：
4.3
通讯作者：
Miller,DC
中科院分区：
文献类型：
--
作者：
Cahill,PD;Brown,BA;Handen,CE;Kosek,JC;Miller,DC
血管移植物的生化（或功能）适应性最近得到了证实。我们重新研究了这种生化“动脉化”过程的一个方面：犬静脉动脉自体移植物产生前列环素（PGI2），以及这种生物合成途径对底物增强的最大刺激的反应性。将4个逆行自体移植物（股静脉）插入8只狗的颈动脉和股动脉。12周后，移植物被移除，用放射免疫法测定在基础和刺激（27 μmol/L花生四烯酸[AA]）状态下6-酮- pgf1 α（PGI2的稳定代谢物）的管腔表面生成量。将自体静脉移植物与对照原生动、静脉的pgi2生成量进行比较。我们证实，在基础条件下（5.8±0.4[±SEM] vs. 2.7±0.5,p < 0.001）和刺激条件下（8.8±0.8 vs. 5.5±0.4,p = 0.002），对照动脉的pgi2产量（以纳克/毫升计）均大于静脉；此外，与基础pgi2生成相比，AA刺激显著增加了原生动脉和静脉的pgi2生成。在基础条件下，移植物pgi2产量（6.3±1.6 ng/ml）与基础动脉水平无显著差异（p = 0.8），但高于基础静脉水平（p = 0.05）。然而，与原生动脉和静脉相比，AA对底物增强的静脉移植物流动表面没有明显的反应：基础（6.3±1.6 ng/ml） vs刺激（5.9±0.9 ng/ml） （p = 0.8）。这些观察结果证实，犬自体静脉动脉移植物经历了生化“动脉化”；然而，这个过程似乎是一个不完整的过程。12周后，血管内皮pgi2的生成增加到动脉水平，但与正常静脉和动脉相比，移植物内皮对底物增强的反应性有显著差异。需要进一步的工作来阐明这种生理反应减弱的确切机制，并研究移植超过3个月的移植物的反应。(J VASCSURG1987; 6:496 - 503)。
Biochemical (or functional) adaptation of venoarterial grafts has been demonstrated recently. We reexamined one aspect of this biochemical “arterialization” process: prostacyclin (PGI2) production by canine venoarterial autologous grafts and the responsiveness of this biosynthetic pathway to maximal stimulation with substrate enhancement. Four reversed autologous grafts (femoral vein) were interposed into both carotid and femoral arteries in eight dogs. After 12 weeks, the grafts were removed, and radioimmunoassay was used to determine luminal surface production of 6-keto-PGF1α(the stable metabolite of PGI2) in both the basal and stimulated (27 μmol/L arachidonic acid [AA]) states. PGI2production by the venous autologous grafts was compared with that of control native artery and vein. We confirmed that PGI2production (measured in nanograms per milliliter) by control artery was greater than vein under both basal conditions (5.8 ± 0.4 [±SEM] vs. 2.7 ± 0.5, p < 0.001) and stimulated conditions (8.8 ± 0.8 vs. 5.5 ± 0.4, p = 0.002); moreover, AA stimulation significantly increased PGI2production in both native artery and vein compared with basal PGI2production. Under basal conditions, graft PGI2production (6.3 ± 1.6 ng/ml) was not significantly different than basal arterial levels (p = 0.8) but was higher than basal venous levels (p = 0.05). However, in marked contrast to both native artery and vein, the vein graft flow surface showed no significant response to substrate enhancement with AA: basal (6.3 ± 1.6 ng/ml) vs. stimulated (5.9 ± 0.9 ng/ml) (p = 0.8). These observations confirm that canine venoarterial autologous grafts undergo biochemical “arterialization”; however, this process appears to be an incomplete one. Vein graft endothelial PGI2production increased to arterial levels after 12 weeks, but there was a marked difference in the responsiveness of the graft endothelium to substrate enhancement compared with both normal veins and arteries. Further work is necessary to elucidate the exact mechanisms responsible for this blunted physiologic response and to investigate the response of grafts implanted for longer than 3 months. (J VASCSURG1987;6:496-503.)