Leong L, Sturm M, Taylor R
Department of Medicine, University of Western Australia, Perth.
J Lipid Mediat. 1991 Nov;4(3):277-87.
While it has been postulated that lyso-PAF and PAF might contribute to structural and functional damage in myocardial ischaemia, there has been no clear evidence for the accumulation of these bioactive compounds in ischaemic myocardium. In open chest, anaesthetised dogs, the proximal left anterior descending coronary artery was ligated and myocardial samples from the central ischaemic and normal areas assayed for lyso-PAF, free arachidonic acid and PLA2 activity. Ischaemic myocardium contained 50 +/- 29% (SD) more lyso-PAF than non-ischaemic myocardium after 20 min ischemia (P less than 0.002; N = 8) and 53 +/- 39% more after 60 min (P less than 0.01; N = 8) but there was no difference after 10 min (N = 8). Free arachidonic acid significantly increased in ischaemic myocardium after 60 min (122 +/- 136%; P less than 0.05) while no increase in PLA2 activity was found in-vitro. Since lyso-phospholipids themselves damage cell membranes and, additionally, lyso-PAF is the precursor of PAF which has potent effects on platelets, leukocytes and small vessels, the increase in lyso-PAF in ischaemic myocardium could contribute to myocardial damage.
虽然有人推测溶血血小板活化因子(lyso-PAF)和血小板活化因子(PAF)可能在心肌缺血的结构和功能损伤中起作用,但尚无明确证据表明这些生物活性化合物在缺血心肌中蓄积。在开胸、麻醉的犬中,结扎左冠状动脉前降支近端,测定中心缺血区和正常区心肌样本中的溶血血小板活化因子、游离花生四烯酸和磷脂酶A2(PLA2)活性。缺血20分钟后,缺血心肌中的溶血血小板活化因子含量比非缺血心肌高50±29%(标准差)(P<0.002;N=8),60分钟后高53±39%(P<0.01;N=8),但10分钟后无差异(N=8)。缺血60分钟后,缺血心肌中的游离花生四烯酸显著增加(122±136%;P<0.05),而体外未发现PLA2活性增加。由于溶血磷脂本身会损伤细胞膜,此外,溶血血小板活化因子是血小板活化因子的前体,对血小板、白细胞和小血管有强大作用,缺血心肌中溶血血小板活化因子的增加可能导致心肌损伤。