Hypercholesterolemia Enhances Thromboembolism in Arterioles but Not Venules: Complete Reversal by l-Arginine

M. Broeders, G. Tangelder, D. Slaaf, R. Reneman, M. O. oude Egbrink
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引用次数: 15

Abstract

We investigated in vivo the effect of cholesterol diet–induced hypercholesterolemia (HC) on thromboembolism in nonatherosclerotic rabbit mesenteric arterioles and venules (diameter 21 to 45 &mgr;m). After mechanical vessel wall injury, the ensuing thromboembolic reaction was studied by intravital videomicroscopy. A dramatic prolongation of embolization duration (median >600 seconds) was observed in the arterioles of the HC group compared with the arterioles of a normal chow–fed (NC) control group (142 seconds, P <0.0001); concomitantly, relative thrombus height increased (thrombus height/vessel diameter was 68% for the HC group and 58% for the NC group;P <0.05). By contrast, in venules, cholesterol did not affect embolization duration (42 seconds for HC group, 34 seconds for NC group) and thrombus height (66% for HC group, 64% for NC group). Furthermore, the role of endothelial NO synthesis was studied. In arterioles, stimulation of endogenous NO synthesis through mesenteric superfusion of l-arginine (1 mmol/L) completely reversed cholesterol-enhanced embolization (152 seconds) but did not influence thrombus height (63%). l-Arginine had no effect in venules of the HC group (51 seconds) and nor in the arterioles and venules of the NC group (177 seconds for arterioles, 43 seconds for venules). This study indicates that hypercholesterolemia selectively enhances thrombus formation and embolization in arterioles but not in venules and that stimulation of endogenous NO production antagonizes this enhancement of arteriolar thromboembolism.
高胆固醇血症增强小动脉血栓栓塞,而不是小静脉:精氨酸完全逆转
我们在体内研究了胆固醇饮食诱导的高胆固醇血症(HC)对非动脉粥样硬化兔子肠系膜小动脉和小静脉(直径21至45微米)血栓栓塞的影响。机械血管壁损伤后,通过活体视频显微镜观察血栓栓塞反应。HC组小动脉栓塞时间显著延长(中位值>600秒),与正常周喂(NC)对照组相比(142秒,P <0.0001);同时,血栓相对高度升高(HC组血栓高度/血管直径为68%,NC组为58%,P <0.05)。相比之下,在小静脉中,胆固醇不影响栓塞时间(HC组42秒,NC组34秒)和血栓高度(HC组66%,NC组64%)。进一步研究了内皮细胞NO合成的作用。在小动脉中,通过肠系膜灌注L -精氨酸(1 mmol/L)刺激内源性NO合成完全逆转胆固醇增强栓塞(152秒),但不影响血栓高度(63%)。l-精氨酸对HC组的小静脉(51秒)和NC组的小动脉和小静脉(小动脉177秒,小静脉43秒)没有影响。该研究表明,高胆固醇血症选择性地促进小动脉血栓形成和栓塞,而不是小静脉血栓形成和栓塞,刺激内源性NO的产生可拮抗小动脉血栓栓塞的增强。
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