Mellow C G, Knight K R, Angel M F, O'Brien B M
Microsurgery Research Centre, St. Vincent's Hospital, Melbourne, Australia.
Plast Reconstr Surg. 1990 Aug;86(2):329-34. doi: 10.1097/00006534-199008000-00023.
The harmful effects of the no-reflow phenomenon on skin flaps were modified by using the thromboxane synthetase inhibitor UK-38,485. Sprague-Dawley rats (N = 134) were subjected to either 3 or 5 hours of secondary venous occlusion occurring 24 hours after a primary ischemic episode of 1 1/2 hours. Within each time period, rats received either saline or UK-38,485 at the primary ischemic episode and/or at the secondary ischemic episode. Flaps treated with UK-38,485 in relation to the period of secondary ischemia had a higher survival rate than control ischemic flaps (p less than 0.01). Those treated only at the end of the primary ischemic episode but prior to the secondary ischemic episode had improved survival rates, but these were not statistically significant. These effects may be explained by the lower thromboxane:prostacyclin ratios at the time of revascularization. The possible interrelationship of the prostanoids with free-radical mechanisms in the no-reflow phenomenon is also discussed.
通过使用血栓素合成酶抑制剂UK - 38,485，可减轻无再流现象对皮瓣的有害影响。将134只Sprague - Dawley大鼠在经历1.5小时的初次缺血发作24小时后，进行3或5小时的二次静脉闭塞。在每个时间段内，大鼠在初次缺血发作和/或二次缺血发作时接受生理盐水或UK - 38,485。与继发性缺血期相关的用UK - 38,485处理的皮瓣，其存活率高于对照缺血皮瓣（p小于0.01）。仅在初次缺血发作结束但在二次缺血发作之前接受处理的皮瓣，其存活率有所提高，但无统计学意义。这些作用可能是由于血管再通时血栓素与前列环素的比例较低所致。还讨论了前列腺素与无再流现象中自由基机制之间可能的相互关系。
