Pathophysiological Events Related to Coronary Spasm and Provocation of Intramural Hemorrhage at the Spastic Site.

1. 通过原位血管造影研究了球囊损伤后自发性冠状动脉收缩的机制。选取46头哥廷根小型猪，饲喂高胆固醇饲粮1个月，随机分为3组；ⅰ组18头猪静脉滴注肝素500单位，ⅱ组7头猪同时滴注肝素500单位和酮丝素1 mg/kg，ⅲ组21头猪滴注肝素3000单位。在这些预处理之后，通过2F栓子切除导管机械剥离左前降支和/或旋冠状动脉。ⅰ组猪在剥脱部位出现自发性冠状动脉收缩，在伤后6分钟达到峰值，在30分钟内恢复到对照组状态。最大冠状动脉狭窄程度由I组的56<正负>5%显著降低至II组的26<正负>7%和III组的30<正负>5%。这些结果提示脱落区血小板聚集对自发性冠状动脉狭窄的发生起关键作用。研究了冠状动脉痉挛在器质性冠状动脉狭窄进展、壁内出血和/或急性心肌梗死中的作用。本研究用20头高胆固醇日粮饲养5个月的哥廷根小型猪，研究了冠状动脉痉挛在器质性冠状动脉狭窄进展和/或急性心肌梗死演变中的作用。4周、5周取左冠状动脉分支2次剥取，2月、3月取x线照射2次。第2次x射线照射2个月后，将猪随机分为2种冠状动脉痉挛刺激。A组10头猪，每5分钟在冠状动脉内注射5次10杯/千克血清素，引起严重冠状动脉痉挛。剥脱部位冠状动脉收缩程度分别为87<正负> 4,89 <正负>5和89<正负>5%，分别为3,18和28分钟。在B组，通过增加血清素的剂量从0.1到10马克杯/公斤血清素，冠状动脉收缩逐渐增加。3、8、13、18 min时冠状动脉收缩程度分别为27.6% <正- bbb60,43 <正- bbb55,57 <正- >3,85 <正- >5%。通过5次重复注射10杯/千克血清素（B1组），10头猪中有4头的冠状动脉持续收缩25分钟。另外6头猪作为B2组，通过24次重复注射10杯/千克血清素来维持持续收缩120分钟。B2组猪静脉注射尿激酶60万单位。A组和B组分别有9头和3头猪出现痉挛部位内出血（p<0.01）。7头猪经血管造影或组织学检查证实冠脉狭窄进展与壁内出血有关。在B2组中，尽管同时使用溶栓剂治疗，仍有5头猪引起急性心肌梗死。这些结果提示：1)痉挛加速越快，壁内出血发生的频率越高；2)壁内出血增加了冠状动脉狭窄的程度；3)延长的冠状动脉痉挛导致急性心肌梗死的演变

1. Spontaneous Coronary Constriction Following Mechanical Denudation of the Coronary Artery Mechanisms of spontaneous coronary constriction following balloon injury were studied in situ angiographically. Forty six Gottingen miniature pigs were fed cholesterol rich diet for a month and were randomly allotted to 3 groups; 18 pigs in group I were given 500 units heparin intravenously, 7 in group II both 500 units heparin and 1 mg/kg ketanserin and 21 in group III 3000 units heparin. After these pretreatments, the left anterior descending and/or circumflex coronary arteries were mechanically denuded by a 2F embolectomy catheter. Spontaneous coronary constriction was noted in pigs in group I at the area denuded, which was at its peak level 6 minutes after the injury and was reverted to the control state within 30 minutes. The maximum level of coronary constriction was significantly attenuated from 56<plus-minus>5% in group I to 26<plus-minus>7% and 30<plus-minus>5% in groups II and III, res … More pectively. These results suggest the critical role of the platelet aggregation at the denuded area for the genesis of spontaneous coronary constri2. Pathogenetic Effects of Coronary Spasm on Progression of Stenosis, Intramural Hemorrhage and/or Acute Myocardial Infarction The role of coronary spasm in the progression of organic coronary stenosis and/or the evolution of acute myocardial infarction was studied in 20 Gottingen miniature pigs fed cholesterol rich diet for 5 months. A branch of the left coronary artery was denuded twice 4 and 5 weeks and were X-irradiated twice 2 and 3 months after the cholesterol feeding. Two months after the 2nd X-irradiation, pigs were randomly allotted to 2 types of provocation of coronary spasm. In 10 pigs in group A, abrupt onset of severe coronary spasm was provoked by 5 intracoronary injections of 10 mug/kg serotonin every 5 minutes. The extent of coronary constriction at the denuded sites was 87<plus-minus>4, 89<plus-minus>5 and 89<plus-minus>5% at 3, 18 and 28 minutes. In group B, stepwise increases of coronary constriction were produced by increasing doses of serotonin from 0.1 to 10 mug/kg serotonin. The extent of coronary constriction was 27<plus-minus>6, 43<plus-minus>5, 57<plus-minus>3, and 85<plus-minus>5 % at 3, 8, 13, and 18 min. The sustained level of coronary constriction was maintained for 25 minutes in 4 of 10 pigs by 5 repetitive injections of 10 mug/kg serotonin (group B1). In other 6 pigs as group B2, sustained constriction was maintained for 120 minutes by 24 repeated injections of 10 mug/kg serotonin. Urokinase was given 600,000units intravenously to pigs in group B2. Intramural hemorrhage was noted at the spastic site in 9 pigs in group A and 3 in group B (p<0.01). Progression of coronary stenosis was confirmed angiographically or histologically in 7 pigs, which was related to the presence of intramural hemorrhage. Acute myocardial infarction was provoked in 5 pigs in group B2, despite the concomitant treatment with a thrombolytic agent. These results suggest that 1) the faster the acceleration of spasm is provoked, the more frequent the occurrence of intramural hemorrhage is noted, 2) intramural hemorrhage augments the extent coronary stenosis and 3) prolonged coronary spasm results in evolution of acute myocardi Less