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以高胆固醇饮食喂养的新西兰兔为实验对象 ,观测蛋白激酶C抑制剂 (H 7)及蛋白激酶C激动剂 (PMA) ,对乙酰胆碱 (acetylcholine,Ach)诱导的离体胸主动脉舒张反应的影响 ,及其对血栓素A2 和前列环素代谢产物生成的影响 ,探讨蛋白激酶C激活在高胆固醇血症引起的动脉内皮依赖性血管舒张功能障碍中的作用。结果显示 :H 7可显著改善高胆固醇组动脉条乙酰胆碱诱导的舒张功能障碍 ,并可显著减少有内皮高胆固醇组动脉条血栓素B2 的生成 ;PMA可显著抑制普通饮食组动脉条乙酰胆碱诱导的舒张功能 ,并可显著增加有内皮普通饮食组动脉条血栓素B2 的生成量 ;H 7及PMA对 2组动脉条 6 酮 前列腺素F1a的生成量均无显著影响。提示高胆固醇血症可激活动脉内皮蛋白激酶C ,增加内皮血管收缩性前列腺素类物质血栓素A2 的生成 ,进而引起动脉内皮依赖性舒张功能障碍。
To investigate the effects of protein kinase C inhibitor (H7) and protein kinase C agonist (PMA) on acetylcholine (Ach) -induced thoracic aortic relaxation in New Zealand rabbits fed high cholesterol diet , And its impact on the production of thromboxane A2 and prostacyclin metabolites, and to explore the role of protein kinase C activation in arterial endothelium-dependent vasodilatation dysfunction induced by hypercholesterolemia. The results showed that: H 7 can significantly improve acetylcholine-induced diastolic dysfunction in hypercholesterolemic rats and significantly reduce the formation of thromboxane B2 in endothelial hypercholesterolemia group; PMA can significantly inhibit acetylcholine-induced diastolic Function, and could significantly increase the formation of aortic endothelium thromboxane B2; H 7 and PMA had no significant effect on the formation of 6 keto prostaglandin F1a. Tip hypercholesterolemia can activate arterial endothelial protein kinase C, increased endothelial vasoconstrictive prostaglandin thromboxane A2 generation, and then cause endothelium-dependent dilatation of the artery dysfunction.