Adenosine A2A receptor activation reduces inflammation and preserves pulmonary function in an in vivo model of lung transplantation.

作者: T. Brett Reece , Peter I. Ellman , Thomas S. Maxey , Ivan K. Crosby , Patrick S. Warren

DOI: 10.1016/J.JTCVS.2004.11.042

关键词:

摘要: Background Reperfusion injury continues to significantly affect patients undergoing lung transplantation. Isolated models have demonstrated that adenosine A 2A receptor activation preserves function while decreasing inflammation. We hypothesized by ATL-146e during the initial reperfusion period pulmonary and attenuates inflammation in a porcine model of Methods Mature pig lungs preserved with Viaspan (Barr Laboratories, Pomona, NY) underwent 6 hours cold ischemia before transplantation 4 reperfusion. Animals were treated (ATL group, n=7) without (IR (0.05 μg kg −1 · min administered intravenously for 3 hours). With occlusion opposite artery, animal was maintained final 30 minutes on allograft alone. Recipient physiology monitored tissue evaluation edema (wet-to-dry weight ratio), myeloperoxidase assay, tumor necrosis factor α means enzyme-linked immunosorbent assay. Results When ATL group compared IR had better partial pressure carbon dioxide (43.8 ± 4.1 vs 68.9 6.3 mm Hg, P = .04). ATL-146e-treated lower wet-to-dry ratios (5.9 0.39 7.3 0.38, −5 1.2 × 10 1.3 −4 4.0 ΔOD mg , .03), trend toward decreased levels (57 12 96 15 pg/mL, .06). The less histology. Conclusion Adenosine early attenuated this similar compounds could play significant role improving outcomes

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