Departments of Surgery, Pathology and Medicine Washington University School of Medicine St. Louis Missouri 63110 USA.
Mediators Inflamm. 1994;3(5):393-5. doi: 10.1155/S0962935194000554.
The object of this study was to characterize the synthesis and metabolism of platelet activating factor (PAF) by intestinal mucosa subjected to ischaemia-reperfusion injury. Canine intestinal mucosa produced 16:0-PAF, 18:0-PAF, and high levels of the corresponding lyso- PAF metabolites. Three h of intestinal ischaemia and ischaemia followed by 1 h of reperfusion did not affect the synthesis or metabolism of PAF by intestinal mucosa. Intestinal mucosa elaborated a factor that rapidly hydrolyzes PAF to lyso-PAF. The observed hydrolysis rate was not altered by ischaemia or ischaemia and reperfusion. In conclusion, this study suggests that intestinal mucosa produces PAF and rapidly hydrolyzes PAF. The PAF synthesis and metabolism rates of intestinal mucosa is not altered by ischaemia reperfusion in this model under the imposed conditions.
本研究旨在探讨肠黏膜在缺血再灌注损伤时血小板活化因子(PAF)的合成和代谢特征。犬肠黏膜可产生 16:0-PAF、18:0-PAF 和高浓度相应的溶酶体 PAF 代谢产物。3 小时肠缺血和缺血后继 1 小时再灌注并不影响肠黏膜的 PAF 合成或代谢。肠黏膜可产生一种快速水解 PAF 为溶酶体 PAF 的因子。观察到的水解速率不受缺血或缺血再灌注的影响。总之,本研究提示肠黏膜可产生 PAF 并快速水解 PAF。在本模型中,在施加的条件下,缺血再灌注并不改变肠黏膜的 PAF 合成和代谢速率。