King R C, Binns O A, Kanithanon R C, Parrino P E, Reece T B, Maliszewskyj J D, Shockey K S, Tribble C G, Kron I L
Department of Surgery, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
Ann Thorac Surg. 1997 Sep;64(3):795-800. doi: 10.1016/s0003-4975(97)00595-x.
We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4 degrees C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20% whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia.
We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4 degrees C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients.
The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 +/- 65.1 versus 145.3 +/- 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 +/- 48.4 versus 70.7 +/- 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 +/- 0.96 versus 55.52 +/- 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 +/- 1,291 versus 67,594 +/- 9,467 dynes.s.cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups.
Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.
我们之前已经表明,在一个离体的、全血灌注的兔肺模型中,于4℃进行18小时冷缺血后,细胞外保存液能提供更好的肺保护。我们还报道,在同一模型中,向低钾右旋糖酐溶液(BLPD)中添加20%全血相比单独使用低钾右旋糖酐(LPD)并无明显优势。我们当前的研究旨在证明血液在低温缺血24至48小时期间缓冲细胞外保存液的重要性。
我们使用一个离体的、全血灌注、通气的兔肺模型研究了三组肺。用Euro - Collins液、LPD或BLPD溶液冲洗肺,然后在4℃低温保存24、36或48小时后再灌注。连续测量肺动脉压、肺血管阻力、左心房压、潮气量和动态气道顺应性。使用新鲜的、非再循环的静脉血来测定单通道肺静脉到动脉的氧梯度。
24小时Euro - Collins组因立即再灌注失败而未能完成。36小时LPD组的氧合明显优于36小时BLPD组(分别为363.3±65.1与145.3±40.3 mmHg;p = 0.015)。与48小时BLPD组相比,48小时LPD组在氧合方面也有显著改善(肺静脉 - 动脉氧差分别为239.4±48.4与70.7±19.5 mmHg;p = 0.012)。与48小时BLPD组相比,48小时LPD组在肺动脉压(分别为34.72±0.96与55.52±7.37 mmHg;p = 0.031)和肺血管阻力(分别为39,737±1,291与67,594±9,467达因·秒·厘米⁻⁵;p = 0.027)方面也有显著改善。三个LPD组之间无显著差异。
在48小时冷缺血后,细胞外溶液在离体兔肺模型中能提供更好的肺保存。当与36至48小时的缺血期相结合时,向细胞外保存溶液中添加血液会降低肺功能。