Toyota E, Goto M, Nakamoto H, Ebata J, Tachibana H, Hiramatsu O, Ogasawara Y, Kajiya F
Department of Systems Cardiology and Medical Engineering, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Ann Thorac Surg. 1999 May;67(5):1254-61. doi: 10.1016/s0003-4975(99)00156-3.
High shear rate with pulsation is one of the major stimuli for the release of endothelium-derived nitric oxide leading to coronary arteriolar dilation. Intraaortic balloon pumping mechanically enhances shear rate and diastolic-to-systolic flow oscillation. We aimed to evaluate whether or not coronary blood flow augmentation during intraaortic balloon pumping is mediated by coronary arteriolar dilation through endothelium-derived nitric oxide release.
Using a charge-coupled device intravital videomicroscope, we observed epicardial coronary arterioles (40 to 220 microm in diameter) in anesthetized open-chest dogs (n = 10) during 2:1 mode of intraaortic balloon pumping. Endothelium-derived nitric oxide-mediated vasodilatory effects of intraaortic balloon pumping were evaluated by comparing end-diastolic arteriolar diameters between the coupled beats of on and off intraaortic balloon pumping before and after intracoronary endothelium-derived nitric oxide synthesis inhibition with Nomega-nitro-L-arginine (L-NNA, 2 micromol/min) administration.
Intraaortic balloon pumping increased coronary arteriolar diameters and coronary blood flow by 11.4%+/-1.8% (p < 0.0001) and 33.4%+/-4.1% (p < 0.001), respectively. Vasodilation was greater in small arterioles (<110 microm; 15.4%+/-2.2%) than in large arterioles (> or =110 microm; 4.2%+/-1.2%, p < 0.0001). L-NNA attenuated the intraaortic balloon pumping-induced vasodilation and augmentation of coronary blood flow to 4.6%+/-1.0% (p < 0.001) and to 20.8%+/-2.1%, (p < 0.05), respectively. Attenuation of vasodilatory effect by L-NNA was observed mainly in small arterioles (from 15.4%+/-2.2% to 5.9%+/-1.2%).
Intraaortic balloon pumping augmented coronary blood flow by dilating coronary arterioles in diastole, more significantly in small arterioles than in large arterioles. Endothelium-derived nitric oxide inhibition markedly attenuated these effects. We conclude that, in a canine model, endothelium-derived nitric oxide contributes to mechanical enhancement of the coronary blood flow with diastolic arteriolar vasodilation during intraaortic balloon pumping.
伴有搏动的高剪切速率是导致冠状动脉小动脉扩张的内皮源性一氧化氮释放的主要刺激因素之一。主动脉内球囊反搏可机械性增强剪切速率以及舒张期与收缩期血流振荡。我们旨在评估主动脉内球囊反搏期间冠状动脉血流增加是否通过内皮源性一氧化氮释放引起冠状动脉小动脉扩张来介导。
使用电荷耦合器件活体显微镜，我们在10只麻醉开胸犬身上观察了2:1模式主动脉内球囊反搏期间的心外膜冠状动脉小动脉（直径40至220微米）。通过比较在冠状动脉内给予Nω-硝基-L-精氨酸（L-NNA，2微摩尔/分钟）抑制内皮源性一氧化氮合成前后，主动脉内球囊反搏开启和关闭的耦合搏动之间的舒张末期小动脉直径，评估主动脉内球囊反搏的内皮源性一氧化氮介导的血管舒张作用。
主动脉内球囊反搏使冠状动脉小动脉直径和冠状动脉血流分别增加11.4%±1.8%（p<0.0001）和33.4%±4.1%（p<0.001）。小动脉（<110微米；15.4%±2.2%）的血管舒张程度大于大动脉（≥110微米；4.2%±1.2%，p<0.0001）。L-NNA将主动脉内球囊反搏诱导的血管舒张和冠状动脉血流增加分别减弱至4.6%±1.0%（p<0.001）和20.8%±2.1%（p<0.05）。L-NNA对血管舒张作用的减弱主要在小动脉中观察到（从15.4%±2.2%降至5.9%±1.2%）。
主动脉内球囊反搏通过在舒张期扩张冠状动脉小动脉来增加冠状动脉血流，小动脉比大动脉更显著。内皮源性一氧化氮抑制明显减弱了这些作用。我们得出结论，在犬模型中，内皮源性一氧化氮在主动脉内球囊反搏期间通过舒张期小动脉血管舒张有助于冠状动脉血流的机械性增强。
