Grossman H J, Zambetis M
Department of Pathology, University of Melbourne, Parkville, Vic., Australia.
Br J Exp Pathol. 1989 Oct;70(5):515-23.
The purpose of this study was to investigate the possible role of leucocytes in the pathogenesis of reperfusion-induced vasospasm of ischaemic mesenteric arteries. Scanning electron microscopy of the rat superior mesenteric artery (SMA) after 30 min of ischaemia in vivo revealed adherence of leucocytes to the vessel wall. Isolated SMA preparations were perfused with Krebs-Henseleit buffer containing noradrenaline. Infusion of homologous leucocytes resuspended in perfusate (3 x 10(6) cells/ml) into these preconstricted preparations caused a fall in resistance of 29 +/- 2%. Removal of the endothelium by collagenase treatment abolished this response. Indeed, leucocyte infusion caused an increase in resistance of 39 +/- 8% under these circumstances. Following 30 min of normothermic ischaemia, leucocyte infusion caused a transient vasodilatation of 31 +/- 4% followed by an increase of 38 +/- 11% in the perfusion resistance of isolated SMA preparations. In each case, a similar response was obtained to infusion of the cell-free supernatant. These results suggest that leucocyte activation occurs in vivo during reperfusion of the SMA after as little as 30 min of ischaemia, and that activated leucocytes can release humoral vasoactive factors which evoke an endothelium-dependent vasodilator response in normal vessels but a predominantly vasoconstrictor response following brief intervals of ischaemia.
本研究的目的是探讨白细胞在缺血性肠系膜动脉再灌注诱导的血管痉挛发病机制中可能发挥的作用。对大鼠肠系膜上动脉(SMA)进行30分钟体内缺血后的扫描电子显微镜检查显示白细胞粘附于血管壁。将分离的SMA制剂用含去甲肾上腺素的Krebs-Henseleit缓冲液灌注。将重悬于灌注液中的同源白细胞(3×10⁶个细胞/ml)注入这些预先收缩的制剂中,导致阻力下降29±2%。用胶原酶处理去除内皮可消除这种反应。实际上,在这些情况下,白细胞注入导致阻力增加39±8%。在常温缺血30分钟后,白细胞注入导致分离的SMA制剂短暂血管扩张31±4%,随后灌注阻力增加38±11%。在每种情况下,对无细胞上清液的注入都获得了类似的反应。这些结果表明,在缺血仅30分钟后SMA再灌注期间,体内发生白细胞活化,并且活化的白细胞可释放体液血管活性因子,这些因子在正常血管中引发内皮依赖性血管舒张反应,但在短暂缺血后主要引发血管收缩反应。