ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Long-term outcomes of aortic grafts after 2-week storage in a rat model of orthotopic aortic transplantation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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9 authors.
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Abstract
Vascular allografts represent a potential alternative to autologous grafts when suitable vessels are unavailable. However, current preservation methods, particularly cryopreservation, lead to substantial endothelial damage and poor clinical outcomes. This study evaluated the long-term efficacy of an N-acetylhistidine-buffered, potassium-chloride-enriched and amino-acid-fortified solution augmented with iron chelators, as an advanced preservation solution (NTK-Chel), compared to histidine-tryptophan-ketoglutarate (HTK) and normal saline for vascular graft storage. Abdominal aortae from male Wistar rats (n = 75) were stored for 2 weeks at 4 °C in NTK-Chel (n = 24), HTK (n = 26), or normal saline (n = 25), then transplanted orthotopically. Grafts were harvested at 8, 16, and 26 weeks post-transplantation for vascular function testing and histological analysis. Upon explantation, smooth muscle contractility was severely impaired in all preservation solutions at 8, 16, and 26 weeks post-transplantation. At 8 weeks, only NTK-Chel-preserved grafts demonstrated detectable contractile responses to KCl, though these did not meet criteria for comprehensive vasomotor testing. By 16 and 26 weeks, all grafts had lost measurable contractility. The NTK-Chel group was associated with significantly reduced intimal hyperplasia compared to HTK and normal saline, particularly at 8 and 26 weeks. However, progressive smooth muscle cell loss occurred in all groups, with NTK-Chel showing only delayed rather than prevented degeneration. While NTK-Chel resulted in significantly less intimal hyperplasia compared to conventional solutions, prolonged cold storage combined with transplantation-associated remodeling ultimately compromises long-term vasomotor function regardless of preservation strategy.
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