Yokoyama M, Sakamoto S, Kawashima S, Okada T, Fukuzaki H
Cardiovasc Res. 1985 Apr;19(4):237-48. doi: 10.1093/cvr/19.4.237.
Experiments were designed to determine the contribution of active vasomotor tone of a large coronary artery during a preexisting coronary stenosis to the production of myocardial ischaemia. The quantitative relations between ergonovine dose and systemic and coronary haemodynamic and electrocardiographic responses during various degrees of coronary stenosis were evaluated in 55 anaesthetised open-chest dogs. In the absence of coronary stenosis, intracoronary infusion of ergonovine (0.04 to 4 micrograms X min-1) had no systemic or coronary haemodynamic effects. In dogs with coronary stenosis created with intraluminal microballoon occluder, ergonovine produced marked decreases in coronary blood flow and distal coronary pressure followed by a decline in left ventricular dP/dt and ST-elevation in epicardial electrogram in the presence of moderate (28 +/- 1.1 mmHg in pressure gradient) and severe (41 +/- 1.4 mmHg), but not mild (15 +/- 0.9 mmHg) stenosis. These detrimental effects of ergonovine were dependent on its dose as well as the severity of preexisting coronary stenosis. Interventions such as aspirin pretreatment or endothelial denudation did not attenuate the coronary vasomotor response or ergonovine, but pretreatment with nifedipine (3 micrograms X kg-1 iv) prevented this response. Intravenous injection of ergonovine (4 to 15 micrograms X kg-1) in doses relevant to clinical usage during intraluminal obstruction resulted in similar changes in coronary haemodynamics as those of intracoronary ergonovine. In contrast, in dogs with various degrees of coronary stenosis produced with an externally applied constrictor device, ergonovine did not affect systemic and coronary haemodynamics. These experiments demonstrate that normal vasomotion superimposed on moderate and severe pliable coronary stenosis can cause transient myocardial ischaemia, which helps to clarify the conditions to produce myocardial ischaemia according to geometric theory.
设计实验以确定在预先存在冠状动脉狭窄的情况下，大冠状动脉的活性血管运动张力对心肌缺血产生的作用。在55只麻醉开胸犬中评估了不同程度冠状动脉狭窄时麦角新碱剂量与全身和冠状动脉血流动力学及心电图反应之间的定量关系。在无冠状动脉狭窄时，冠状动脉内输注麦角新碱（0.04至4微克×分钟-1）对全身或冠状动脉血流动力学无影响。在用腔内微球囊封堵器造成冠状动脉狭窄的犬中，在存在中度（压力梯度为28±1.1 mmHg）和重度（41±1.4 mmHg）而非轻度（15±0.9 mmHg）狭窄的情况下，麦角新碱可使冠状动脉血流和冠状动脉远端压力显著降低，随后左心室dp/dt下降，心外膜心电图ST段抬高。麦角新碱的这些有害作用取决于其剂量以及预先存在的冠状动脉狭窄的严重程度。阿司匹林预处理或内皮剥脱等干预措施并未减弱冠状动脉血管运动反应或麦角新碱的作用，但硝苯地平（3微克×千克-1静脉注射）预处理可预防这种反应。在腔内阻塞期间静脉注射与临床使用相关剂量的麦角新碱（4至15微克×千克-1）导致冠状动脉血流动力学变化与冠状动脉内注射麦角新碱相似。相比之下，在用外部施加的收缩装置造成不同程度冠状动脉狭窄的犬中，麦角新碱不影响全身和冠状动脉血流动力学。这些实验表明，叠加在中度和重度柔韧性冠状动脉狭窄上的正常血管运动可导致短暂性心肌缺血，这有助于根据几何理论阐明产生心肌缺血的条件。
