花生四烯酸受环氧化酶作用产生的化合物在血管内皮上形成前列腺素I₂（PGI₂)，同样的化合物在血小板里却形成血栓素（TXA₂)。两种化合物的血管活性作用正相反，前者使血管舒张，而后者使之收缩。PGI₂还有抑制血小板凝聚的作用。若能增加PGI₂的活性，抑制TXA₂的生成，就能改善冠脉缺血状态及预防随着缺血伴发的心律失常。

　　阿司匹林、潘生丁、磺酰吡唑酮（Sulfinpyrazone,Auturane小板凝)、消炎痛有抑制环氧化酶的作用，所以用以抗血小板凝集治疗。表5-9是几种大系列的观察报告。阿司匹林lg反而增加了病死率和猝死率。小剂量阿司匹林可以选择性地抑制TXA₂而不影响PGI₂的合成，有减少病死率和猝死率的效果。磺酰比唑酮试验组，共1558例心梗后25～35天患者，24个月随访时间，与对照组比较，猝死率在用药组中减少43%（P<0.05)。这种差别在6个月以内尤为明显，而此时期正是心梗的高危阶段。

表5-9 抑制血小板药物在心肌梗死后的预防作用

　　^* 有统计学意义。

　　（选自Gelman & Mehta: Suddun Cardiac Death,ed by Mark E Josephson,F A Davis Co.,Philadelphia,1985,P.65)

　　心得安有改变血小板功能的作用，抑制ADP、肾上腺素、胶原、血栓素造成的血小板凝集。其机制不清楚，可能与血小板结合改变膜的性能，对促凝集物质不敏感。临床尚无心得安等β受体阻滞剂抑制血小板的研究报道。

　　参考文献

　　[1] Kennel WB & Thomas HE,Jr.:Sudden coronary death:the Framimgham study.Ann NY Acad Sci 1982；382: 3～21

　　[2] Kulbertus HE & Wellens HJJ(eds):Sudden Death.Martinus Nijhoff Pub,Boston/London,1980

　　[3] Liberthson RR, et al: Pathophysiologic observations in prehospital ventricular fibrillation and sudden cardiac death.Circulation 1974；48:796

　　[4] Schwartz PJ & Stone HL:The role of the autonomic nervous system in sudden cardic death. Ann NY Acad Sci 1982；382:162

　　[5] Morganroth J & Moore EN(eds): Sudden Cardiac Death and Congestive Heart Failure:Diagnosis and Treatment.Martinus nijhoff Pub,Boston,1983,p 46,64,& 95

　　[6] Perper JA,et al:Arterjosclerosis of coronary arteries in sudden, unexpected death.Circulation 1975；51:27～33

　　[7] Moss AJ: clinical significance of ventricualr arrhythmias in patients with and without coronary artery disease. Prog Cardiovasc Dis 1980；23:33

　　[8] Lown B & Wolf M: Approaches to sudden death from coronary heart disease. Circulation 1971,48:130～142

　　[9] Problete PF,et al :Detective of ventricular ectopy in patients with coronary heart disease and normal subjects by exercise testing and ambulatory electrocardiography.Chest 1978；74:402

　　[10] Furberg CD,et al :Secondary prevention after myocardial infarction: a review of long-term trials.Prog Cardiovasc Dis 1982；24:331～352

　　[11] Hamer A,et al:Prediction of sudden death by electrophysiologic studies in high risk patients surviving acute mvocardial infarction.Amer J Cardiol 1982；50:223

　　[12] Roy D et al:Clinical Characterjstics and long-term follow-up in 119 survivors of cardiac arrest:relation to inducibility at electrophysiologic gic testing.Amer J Cardiol 1983；52:969～974

　　[13] Ru skin JN,et al:Electrophysiologic testing in survivors of prehospital cardiac arrest:therapy and long-term follow-up.Amer J Cardiol 1982；49:958

　　[14] Folts JD, et al:Blood flow reductions in stenosed canine coronary arteries.Vasospasm or platelet aggregation? Circulation 1982；65:248

　　[15] Bassan M et al.:Improved prognosis during long-term treatment with beta-blockers after myocardial infarction:analysis of randomized trial and pooling on results.Heart and Lung 1984；13:164～168

　　[16] Lombardi F,et al.:Relationship between sympathetic neural activity,coronary dynamics,and vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.Amer Heart J 1983；105:958～965

　　[17] Mehta J & Mehta P:Effects of propranolol therapy on platelet release and prostaglandin generatio in patients with coronary heart disease. Circulation 1982；66:1294

　　[18] 洪昭光，等：北京地区心血管病人群监测1984年基线研究，中华心血管病杂志1988；16：4～7

　　[19] 范伟，等：针刺“内关”对缺血性室性心律失常的实验电生理研究，中华心血管病杂志1987；15：285～288

上一页  [1] [2] [3]  下一页