Zambetis M, Grossman H J
Department of Pathology, University of Melbourne, Parkville, Victoria, Australia.
Br J Exp Pathol. 1988 Feb;69(1):81-90.
The isolated perfused rat superior mesenteric artery preparation was used to determine whether endothelium-dependent vasodilatation occurs in this vessel, and to test whether impairment of this function may contribute to post-ischaemic mesenteric vasospasm. It was found that vessels preconstricted with noradrenaline responded to optimal concentrations of acetylcholine (3 X 10(-5) M), ADP (2 X 10(-5) M) and to isolated homologous platelets (500,000/mm3) with an 84%, 85% and 37% decrease in mean perfusion resistance, respectively. In preparations treated with collagenase to denude the vessels of endothelium there was a significantly diminished response to acetylcholine and ADP (24% & 23% decrease in resistance, respectively). Platelets, on the other hand, caused a further 34% increase in resistance. A model of mesenteric ischaemia was produced by interrupting perfusate flow through the preparation for intervals of 1 to 4 h. This was associated with morphological evidence of endothelial cell damage and with a progressive decline in the responsiveness to acetylcholine and ADP. After 1 h there was also a significant reduction in the response to platelets. With intervals of ischaemia longer than 2 h platelets caused only further constriction which could be inhibited by the serotonin antagonist, methysergide. This study suggests that an altered response of the endothelium to platelet-derived vasoactive substances may contribute to the post-ischaemic vasospasm encountered during reperfusion.
采用离体灌注大鼠肠系膜上动脉标本，以确定该血管是否存在内皮依赖性血管舒张，并检测该功能受损是否可能导致缺血后肠系膜血管痉挛。结果发现，用去甲肾上腺素预收缩的血管对最佳浓度的乙酰胆碱（3×10⁻⁵M）、二磷酸腺苷（2×10⁻⁵M）及分离的同源血小板（500,000/mm³）有反应，平均灌注阻力分别降低84%、85%和37%。在用胶原酶处理以剥脱血管内皮的标本中，对乙酰胆碱和二磷酸腺苷的反应明显减弱（阻力分别降低24%和23%）。另一方面，血小板使阻力进一步增加34%。通过中断灌注液流经标本1至4小时建立肠系膜缺血模型。这与内皮细胞损伤的形态学证据以及对乙酰胆碱和二磷酸腺苷反应性的逐渐下降有关。缺血1小时后，对血小板的反应也显著降低。缺血时间超过2小时后，血小板仅引起进一步收缩，可被5-羟色胺拮抗剂麦角酰二乙胺抑制。本研究提示，内皮对血小板衍生的血管活性物质反应改变可能是再灌注期间缺血后血管痉挛的原因之一。
