Vallance S R, Randall D C, Yingling J D
Department of Physiology and Biophysics, University of Kentucky College of Medicine, Lexington 40536-0084.
Int J Cardiol. 1990 Mar;26(3):291-302. doi: 10.1016/0167-5273(90)90085-j.
The effect of neurogenic coronary vasomotor tone upon contraction in ischemic myocardium was investigated in awake, mongrel dogs. The animals were chronically instrumented with a hydraulic occluder around the left circumflex coronary artery; a small catheter was also implanted within the vessel. Ultra-sound crystal pairs were placed distal to the occluder in myocardium perfused by the left circumflex artery. Pacing electrodes were sutured onto the right ventricular conus. During the experiment (n = 6) the occluder was inflated to stenose the vessel; the imposition of cardiac pacing (210/min) in conjunction with this stenosis resulted in depressed contraction of the myocardium distal to the occluder as assessed by the ultra-sound crystals: Segmental shortening decreased to 45.4 +/- 5.4% of unpaced control. Phentolamine, an alpha-antagonist, was then infused into the left circumflex catheter for ten minutes (0.1 mg/min) and the experiment repeated. After the alpha-blockade the combination of coronary stenosis and heart rate pacing decreased segmental shortening to only 84.6 +/- 10.1% of control, which was significantly (P less than 0.01) improved relative to the unblocked condition. In another experiment (n = 4), a less severe stenosis was imposed upon the left circumflex vessel. During pacing, muscle shortening decreased to 94 +/- 8.5% of control. Infusion of phenylephrine, an alpha-agonist, for ten minutes (0.1 mg/min) resulted in a 56.7 +/- 5.9% decrease in shortening during pacing; this was significantly greater (P less than 0.01) than the previous decrease. These data indicate that coronary alpha-adrenergic tone can significantly compromise regional myocardial function even in ischemic muscle whose coronary blood flow reserve has been exhausted.
在清醒的杂种犬身上研究了神经源性冠状动脉血管舒缩张力对缺血心肌收缩的影响。这些动物长期在左旋冠状动脉周围安装液压闭塞器；还在血管内植入一根小导管。超声晶体对置于左旋动脉灌注的心肌中闭塞器远端。起搏电极缝在右心室圆锥上。在实验过程中（n = 6），使闭塞器充气以狭窄血管；在此狭窄基础上施加心脏起搏（210次/分钟），通过超声晶体评估发现，闭塞器远端心肌收缩减弱：节段缩短降至非起搏对照的45.4±5.4%。然后将α拮抗剂酚妥拉明以0.1毫克/分钟的速度注入左旋导管10分钟，并重复实验。α受体阻断后，冠状动脉狭窄与心率起搏相结合使节段缩短仅降至对照的84.6±10.1%，相对于未阻断状态有显著改善（P<0.01）。在另一项实验中（n = 4），对左旋血管施加较轻程度的狭窄。起搏期间，肌肉缩短降至对照的94±8.5%。注入α激动剂去氧肾上腺素10分钟（0.1毫克/分钟），导致起搏期间缩短减少56.7±5.9%；这比之前的减少幅度显著更大（P<0.01）。这些数据表明，即使在冠状动脉血流储备已耗尽的缺血心肌中，冠状动脉α肾上腺素能张力也会显著损害局部心肌功能。
