Ingemansson R, Budrikis A, Bolys R, Sjöberg T, Steen S
Department of Cardiothoracic Surgery, University Hospital, Lund, Sweden.
Ann Thorac Surg. 1997 Oct;64(4):1075-81. doi: 10.1016/s0003-4975(97)00821-7.
The aim of this study was to investigate how much perfusion pressure an artery can tolerate without significant loss of endothelium-dependent relaxation (EDR) and vascular contractility.
The abdominal aortas of 396 Sprague-Dawley rats were used. One hundred twenty aortas were flush-perfused for 1 or 5 minutes with cold St. Thomas' Hospital cardioplegic (STHC) solution or with the same solution but modified by the addition of 3.5% dextran 40. Three perfusion pressures were tested: 50, 100, and 150 mm Hg. Two hundred eighty vessels were subjected to pressures of 50, 150, or 300 mm Hg using saline or STHC solution at 22 degrees C or STHC solution at 4 degrees C, for 10 or 60 seconds. The vessels were investigated in organ baths. Contractility was tested with the thromboxane analogue U-46619, acetylcholine was used to investigate EDR, and papaverine to elicit endothelium-independent relaxation.
Flush-perfusion with cold STHC solution for 5 minutes at a perfusion pressure of 50 or 100 mm Hg affected neither contractility nor EDR. Vessels exposed to a flush-perfusion pressure of 150 mm Hg for 1 or 5 minutes lost 39% (p < 0.001) and 53% (p < 0.001) of their contractility, respectively. Flush-perfusion at 150 mm Hg for 1 minute did not affect EDR, whereas 5 minutes' perfusion caused a reduction of 7% (p < 0.05). A repetition of these experiments using STHC solution with 3.5% dextran 40 added gave no significantly different results. The impairment in contractility and EDR seen after perfusion at 150 mm Hg for 5 minutes disappeared after transplantation and reperfusion for 7 days. The vessels could be distended with saline or STHC solution at a pressure of 150 mm Hg without affecting contractility at 22 degrees C. At 4 degrees C, however, this pressure was harmful to contractility. Distention at a pressure of 300 mm Hg almost abolished contractility and 7 days after transplantation there had not yet been any recovery of contractility, but 30 days after transplantation the grafts had regained their normal contractility.
Cold STHC solution, with or without dextran 40, can be used with a perfusion pressure of 100 but not 150 mm Hg without impairing EDR or vascular smooth muscle function.
本研究的目的是探究动脉在不显著丧失内皮依赖性舒张功能（EDR）和血管收缩性的情况下能够耐受多大的灌注压力。
使用396只Sprague-Dawley大鼠的腹主动脉。120条主动脉分别用冷圣托马斯医院心脏停搏液（STHC）溶液或添加3.5%右旋糖酐40的相同溶液进行1分钟或5分钟的冲洗灌注。测试了三种灌注压力：50、100和150毫米汞柱。280条血管在22℃下使用生理盐水或STHC溶液或在4℃下使用STHC溶液，分别施加50、150或300毫米汞柱的压力，持续10秒或60秒。在器官浴槽中对血管进行研究。用血栓素类似物U-46619测试收缩性，用乙酰胆碱研究EDR，用罂粟碱引发非内皮依赖性舒张。
在50或100毫米汞柱的灌注压力下，用冷STHC溶液冲洗灌注5分钟对收缩性和EDR均无影响。暴露于150毫米汞柱冲洗灌注压力1分钟和5分钟的血管，其收缩性分别丧失39%（p<0.001）和53%（p<0.001）。150毫米汞柱冲洗灌注1分钟不影响EDR，而5分钟灌注导致EDR降低7%（p<0.05）。使用添加3.5%右旋糖酐40的STHC溶液重复这些实验，结果无显著差异。150毫米汞柱灌注5分钟后观察到的收缩性和EDR损伤在移植和再灌注7天后消失。在22℃下，血管可以用150毫米汞柱的生理盐水或STHC溶液扩张而不影响收缩性。然而，在4℃下，这种压力对收缩性有害。300毫米汞柱压力下的扩张几乎消除了收缩性，移植7天后收缩性尚未恢复，但移植30天后移植物恢复了正常收缩性。
含或不含右旋糖酐40的冷STHC溶液在灌注压力为100毫米汞柱而非150毫米汞柱时使用，不会损害EDR或血管平滑肌功能。
