Tousoulis D, Tentolouris C, Crake T, Toutouzas P, Davies G
Cardiology Unit, Hippokration Hospital, Athens University Medical School, Greece.
J Am Coll Cardiol. 1997 May;29(6):1256-62. doi: 10.1016/s0735-1097(97)00046-6.
This study assessed the effects of inhibition of nitric oxide synthesis on epicardial human coronary arteries and on coronary flow velocity during baseline conditions and during atrial pacing.
Epicardial coronary artery dilation occurs in response to an increase in heart rate. It is not known whether the dilation of both angiographically normal and diseased epicardial coronary arteries during atrial pacing is nitric oxide dependent in humans.
The effects of an intracoronary infusion (4 mumol/min for 8 min) of NG-monomethyl-L-arginine (LNMMA), an inhibitor of nitric oxide synthesis, was studied in 16 patients with coronary artery disease and in 6 patients with normal coronary arteriograms. In all patients atrial pacing was performed during normal saline and during LNMMA infusion. the lumen diameter of epicardial coronary arteries was assessed by quantitative angiography, and changes in blood flow velocity were measured with a Doppler catheter.
During saline infusion a significant increase in the lumen diameter of the proximal (p < 0.05) and distal (p < 0.01) segments of both normal and diseased arteries occurred during atrial pacing. No significant lumen diameter changes occurred in either group when atrial pacing was performed during LNMMA infusion. Stenosis diameter decreased during LNMMA infusion but did not change with atrial pacing either during saline infusion or during LNMMA infusion. The mean percent change in coronary blood flow with atrial pacing was less (p < 0.05) during LNMMA infusion than during saline infusion in both groups.
These findings confirm that epicardial coronary artery dilation induced by pacing is nitric oxide dependent. Nitric oxide production contributes to the vasomotor tone of coronary resistance vessels. Nitric oxide is produced at the site of atheromatous stenosis but is unaffected by pacing.
本研究评估了一氧化氮合成抑制对心外膜人类冠状动脉以及基础状态和心房起搏期间冠状动脉血流速度的影响。
心外膜冠状动脉扩张是对心率增加的反应。尚不清楚心房起搏期间血管造影正常和病变的心外膜冠状动脉扩张在人类中是否依赖一氧化氮。
在16例冠状动脉疾病患者和6例冠状动脉造影正常的患者中，研究了冠状动脉内输注一氧化氮合成抑制剂NG-单甲基-L-精氨酸（LNMMA，4 μmol/分钟，持续8分钟）的效果。在所有患者中，在输注生理盐水和LNMMA期间进行心房起搏。通过定量血管造影评估心外膜冠状动脉的管腔直径，并用多普勒导管测量血流速度的变化。
在输注生理盐水期间，正常和病变动脉的近端（p < 0.05）和远端（p < 0.01）节段的管腔直径在心房起搏期间显著增加。当在输注LNMMA期间进行心房起搏时，两组均未出现显著的管腔直径变化。在输注LNMMA期间狭窄直径减小，但在输注生理盐水或LNMMA期间心房起搏时均未改变。两组在输注LNMMA期间心房起搏时冠状动脉血流的平均变化百分比均低于输注生理盐水期间（p < 0.05）。
这些发现证实起搏诱导的心外膜冠状动脉扩张依赖一氧化氮。一氧化氮的产生有助于冠状动脉阻力血管的血管舒缩张力。一氧化氮在动脉粥样硬化狭窄部位产生，但不受起搏影响。
