Bishop S P, White F C, Bloor C M
Circ Res. 1976 May;38(5):429-38. doi: 10.1161/01.res.38.5.429.
Regional myocardial blood flow was studied in the conscious dog at periods of 5 minutes to 4 days after occlusion of a major branch of the left coronary artery. Dogs were instrumented with aortic electromagnetic flow probes, occlusive cuffs on either the anterior descending or circumflex branch of the left coronary artery, and a left atrial Silastic catheter for injection of microspheres (15 +/- 5 mum) labeled with either 85Sr, 141Ce, or 51Cr. Microspheres were injected into 25 fully conscious dogs during three of the following time periods: control preocclusion and 0.1, 2, 6, 24, or 96 hours postocclusion. In the conscious dog, before occlusion, the endocardial half of the left ventricular myocardium received 28% more blood flow than the epicardial half. After sudden occlusion of a coronary artery branch, there was a marked reduction in blood flow as well as an alteration in distribution of blood flow within the ischemic tissue; blood flow was most severly reduced in the subendocardial center of the ischemic region, less so in the epicardial ischemic region, and least reduced in the marginal region of the infarct. Blood flow was increased to the nonischemic tissue. There was no change in this pattern of reduced blood flow by 6 hours postocclusion, but by 24 hours, flow was moderately increased to all areas except the central subendocardial core, and was further increased at 96 hours. Blood flow to the endocardial half of the left ventricular myocardium averaged 63 ml/100 g per min during the control period, was reduced to 12-18 ml/100 g per min at 0.1-6 hours in the ischemic region, increased to 29 ml/100 g per min at 24 hours, and to 48 ml/100 g per min by 96 hours. These findings indicate that there is a reversal of the flow ratio within ischemic myocardium with relative under-perfusion of the endocardial half of the wall, which is not corrected by 4 days. There is a modest increase of collateral blood flow to ischemic tissue by 24 hours and this increase is considerably augmented by 96 hours, apparently as a result of the growth and enlargement of collateral vessels.
在清醒犬身上,于左冠状动脉主要分支闭塞后5分钟至4天的不同时段,对局部心肌血流进行了研究。给犬安装主动脉电磁血流探头、左冠状动脉前降支或左旋支上的闭塞袖带,以及用于注射标记有85Sr、141Ce或51Cr的微球(15±5μm)的左心房硅橡胶导管。在以下三个时间段之一,向25只完全清醒的犬注射微球:对照性闭塞前以及闭塞后0.1、2、6、24或96小时。在清醒犬身上,闭塞前,左心室心肌的心内膜侧所接受的血流量比心外膜侧多28%。冠状动脉分支突然闭塞后,血流量显著减少,且缺血组织内的血流分布发生改变;缺血区域的心内膜下中心血流量减少最为严重,心外膜缺血区域次之,梗死边缘区域减少最少。非缺血组织的血流量增加。闭塞后6小时,这种血流量减少的模式没有变化,但到24小时时,除心内膜下中心核心区域外,所有区域的血流量适度增加,96小时时进一步增加。在对照期,左心室心肌心内膜侧的血流量平均为63ml/100g每分钟,在缺血区域,0.1 - 6小时时降至12 - 18ml/100g每分钟,24小时时增至29ml/100g每分钟,96小时时增至48ml/100g每分钟。这些发现表明,缺血心肌内的血流比率发生了逆转,即心壁的心内膜侧相对灌注不足,且4天内未得到纠正。到24小时时,缺血组织的侧支血流量适度增加,96小时时这种增加显著增强,这显然是侧支血管生长和扩张的结果。