Native Collaterals in the Development of Collateral Circulation After Chronic Coronary Stenosis in Mongrel Dogs

Native Collaterals in the Development of Collateral Circulation After Chronic Coronary Stenosis in Mongrel Dogs
复制标题

杂种犬慢性冠状动脉狭窄后侧支循环发育中的原生络脉

DOI:
--
复制
发表时间:
1982
期刊:
影响因子:
37.8
通讯作者:
W. Kubler
W. Kubler
中科院分区:
医学1区
文献类型:
--
作者:
F. Schwarz;H. Wagner;M. Sesto;M. Hofmann;W. Schaper;W. Kubler

文献摘要

被引文献

相似文献

在 17 只杂种犬中研究了天然侧支循环对左冠状动脉回旋支 (LCx) 慢性狭窄的反应。狭窄限制了 LCx 的反应性充血,而不影响静息血流。通过示踪微球技术测量局部心肌血流量。在开胸制剂中植入固定 LCx 狭窄之前和之后 5 周,在左前降支最大反应性充血期间测定流向 LCx 的冠状动脉侧支血流量。狭窄植入后5周通过LCx结扎测试络脉的保护作用。通过硝基蓝四唑染色确定急性心肌梗塞的存在。 11 只狗患有心肌梗塞(A 组),但 6 只狗在尸检时未显示出梗塞证据(B 组)。在 A 组中,LCx 床的侧支血流和最小冠状动脉阻力在 LCx 狭窄后几乎没有变化,分别从 12 至 15 ml/min/100 g 和 10.5 至 10.0 mm Hg/ml/min/100 g(均 p > 0.05)。相比之下,B 组的侧支流量从 22 增加至 102 ml/min/100 g (p < 0.05),LCx 床的最小冠状动脉阻力从 4.8 降至 1.4 mm Hg/ml/min/100 g (p < 0.01)。与 B 组相比,A 组具有较低的天然侧支流量 (p < 0.05) 和较高的 LCx 床天然最小冠状动脉阻力 (p < 0.05)。梗阻后 LCx 压力与血流数据密切相关。 A 组和 B 组的 LCx 风险区域大小相当,分别占左心室总量的 36.4% 和 39.0% (p > 0.05)。记录了侧支循环对慢性狭窄的两种反应:A 组缺乏侧支生长,但 B 组有显着的侧支生长。侧支循环的自然变化是不同反应的主要决定因素,这对主冠状动脉狭窄很重要。
The response of native collateral circulation to chronic stenosis of the left circumflex coronary artery (LCx) was studied in 17 mongrel dogs. Stenosis restricted reactive hyperemia of the LCx without affecting resting flow. Regional myocardial blood flow was measured by the tracer microsphere technique. Coronary collateral blood flow to the LCx was determined during maximal reactive hyperemia of the left anterior descending branch before and 5 weeks after implantation of a fixed LCx stenosis in the open‐chest preparation. The protective effect of collaterals was tested by LCx ligation 5 weeks after implantation of stenosis. Presence of acute myocardial infarction was determined by nitroblue tetrazolium staining. Eleven dogs had a myocardial infarction (group A), but six dogs showed no evidence of infarction at autopsy (group B). In group A, collateral flow and minimal coronary resistance of the LCx bed changed little after LCx stenosis, from 12 to 15 ml/min/100 g and from 10.5 to 10.0 mm Hg/ml/min/100 g, respectively (both p > 0.05). In contrast, collateral flow in group B increased from 22 to 102 ml/min/100 g (p < 0.05), and minimal coronary resistance of the LCx bed decreased from 4.8 to 1.4 mm Hg/ml/min/100 g (p < 0.01). Group A had lower native collateral flow (p < 0.05) and higher native minimal coronary resistance of the LCx bed than group B (p < 0.05). Postobstructive LCx pressure correlated well with blood flow data. The LCx risk region was of comparable size in groups A and B, 36.4% vs 39.0% of total left ventricle (p > 0.05). Two responses of collateral circulation to chronic stenosis were documented: lack of collateral growth in group A, but significant collateral growth in group B. The natural variation of collateral circulation was the major determinant of the different responses that were important with stenosis of a major coronary artery.