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首页> 外文期刊>ACS applied materials & interfaces >Mimicking the Endothelium: Dual Action Heparinized Nitric Oxide Releasing Surface
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Mimicking the Endothelium: Dual Action Heparinized Nitric Oxide Releasing Surface

机译：模仿内皮：双作用肝素化一氧化氮释放表面

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The management of thrombosis and bacterial infection is critical to ensure the functionality of medical devices. While administration of anticoagulants is the current antithrombotic clinical practice, a variety of complications, such as uncontrolled hemorrhages or heparin-induced thrombocytopenia, can occur. Additionally, infection rates remain a costly and deadly complication associated with use of these medical devices. It has been hypothesized that if a synthetic surface could mimic the biochemical mechanisms of the endothelium of blood vessels, thrombosis could be reduced, anticoagulant use could be avoided, and infection could be prevented. Herein, the interfacial biochemical effects of the endothelium were mimicked by altering the surface of medical grade silicone rubber (SR). Surface modification was accomplished via heparin surface immobilization (Hep) and the inclusion of a nitric oxide (NO) donor into the SR polymeric matrix to achieve synergistic effects (Hep-NO-SR). An in vitro bacteria adhesion study revealed that Hep-NO-SR exhibited a 99.46 +/- 0.17% reduction in viable bacteria adhesion compared to SR. An in vitro platelet study revealed Hep-NO-SR reduced platelet adhesion by 84.12 +/- 6.19% compared to SR, while not generating a cytotoxic response against fibroblast cells. In a 4 h extracorporeal circuit model without systemic anticoagulation, all Hep-NO-SR samples were able to maintain baseline platelet count and device patency; whereas 66% of SR samples clotted within the first 2 h of study. Results indicate that Hep-NO-SR creates a more hemocompatible and antibacterial surface by mimicking two key biochemical functions of the native endothelium.
机译：血栓形成和细菌感染的管理对于确保医疗器械的功能至关重要。虽然抗凝血剂的给药是目前的抗血栓形成临床实践，但可能发生各种并发症，例如不受控制的出血或肝素诱导的血小板减少症。此外，感染率仍然是与使用这些医疗设备相关的昂贵和致命的复杂性。已经假设，如果合成表面可以模拟血管内皮的生化机制，则可以降低血栓形成，可以避免抗凝血用途，并且可以防止感染。这里，通过改变医用级硅橡胶（Sr）的表面来模拟内皮的界面生物化学效果。通过肝素表面固定化（HEP）完成表面改性，并将一氧化氮（NO）供体包含到SR聚合物基质中以达到协同作用（HEP-NO-SR）。体外细菌粘附性研究表明，与Sr相比，HEP-No-SR在活性细菌的粘附性降低99.46 +/- 0.17％。体外血小板研究表明，与Sr相比，血小板粘附降低了血小板粘附，同时不会产生针对成纤维细胞的细胞毒性反应。在一个4小时的体外电路模型没有系统性抗凝凝血的情况下，所有HEP-No-SR样品都能够保持基线血小板计数和器件通畅;而66％的SR样品在研究的前2小时内凝结。结果表明，通过模拟天然内皮的两个关键生物化学功能，HEP-No-SR通过模拟了两个关键的生物化学功能来产生更血液相处和抗菌表面。

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