Yada T, Hiramatsu O, Kimura A, Tachibana H, Chiba Y, Lu S, Goto M, Ogasawara Y, Tsujioka K, Kajiya F
Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Japan.
Circ Res. 1995 Sep;77(3):622-31. doi: 10.1161/01.res.77.3.622.
To study the vasodilatory capacity of subendocardial (ENDO) arterioles, we evaluated the reactive hyperemic responses of ENDO as well as subepicardial (EPI) arterioles in 40 dogs by our needle-probe intravital microscope. We also examined the individual and combined effects of an ATP-sensitive K+ channel blocker (glibenclamide, 200 micrograms/kg), an inhibitor of nitric oxide synthase (NG-monomethyl-L-arginine [L-NMMA], 2 mumol/min, 20 minutes), and an adenosine-receptor antagonist (8-phenyltheophylline [8PT], 0.75 mumol/min, 15 minutes). The percent increase in end-diastolic diameter of ENDO arterioles was larger (P < .01) than that of EPI arterioles during reactive hyperemia, especially for the arterioles larger than 120 microns (P < .01). The diastolic-to-systolic vascular pulsation amplitude at the peak flow was greater in ENDO than EPI arterioles (25% versus 6%, P < .05). Compared with control conditions, the presence of both glibenclamide and L-NMMA suppressed the vasodilation responses of ENDO arterioles (P < .01 for both) and EPI arterioles (P < .05 for both). The effect of L-NMMA was greater in ENDO arterioles (P < .01), but that of glibenclamide was not different between ENDO and EPI arterioles. 8PT influenced the hyperemic response, although statistical significance was found only in the flow response. The effect of combined infusion of L-NMMA and glibenclamide with or without 8PT was greater than that of individual infusions in both ENDO and EPI arterioles. Conclusions are as follows: (1) The vasodilatory response of ENDO arterioles was even larger than that of EPI arterioles. Thus, the smaller flow reserve of ENDO arterioles may be caused by other factors, including the greater effects of myocardial compression and nitric oxide on the ENDO arterioles. (2) The vascular responses of ENDO and EPI arterioles were modulated by both endothelium-independent and -dependent vasodilative factors, and the effect of each factor including adenosine was associated with the effects of others.
为研究心内膜下(ENDO)小动脉的血管舒张能力,我们通过针式探头活体显微镜评估了40只犬的心内膜下小动脉以及心外膜下(EPI)小动脉的反应性充血反应。我们还研究了ATP敏感性钾通道阻滞剂(格列本脲,200微克/千克)、一氧化氮合酶抑制剂(NG-单甲基-L-精氨酸[L-NMMA],2微摩尔/分钟,持续20分钟)和腺苷受体拮抗剂(8-苯基茶碱[8PT],0.75微摩尔/分钟,持续15分钟)单独及联合应用的效果。在反应性充血期间,ENDO小动脉舒张末期直径的增加百分比大于EPI小动脉(P <.01),尤其是对于直径大于120微米的小动脉(P <.01)。ENDO小动脉在峰值血流时的舒张期与收缩期血管搏动幅度大于EPI小动脉(25%对6%,P <.05)。与对照条件相比,格列本脲和L-NMMA同时存在时抑制了ENDO小动脉(两者均P <.01)和EPI小动脉(两者均P <.05)的血管舒张反应。L-NMMA对ENDO小动脉的作用更大(P <.01),但格列本脲对ENDO和EPI小动脉的作用无差异。8PT影响充血反应,尽管仅在血流反应中发现统计学意义。L-NMMA和格列本脲联合输注(加或不加8PT)的效果在ENDO和EPI小动脉中均大于单独输注。结论如下:(1)ENDO小动脉的血管舒张反应甚至大于EPI小动脉。因此,ENDO小动脉较小的血流储备可能由其他因素引起,包括心肌压迫和一氧化氮对ENDO小动脉的更大影响。(2)ENDO和EPI小动脉的血管反应受内皮依赖性和非依赖性血管舒张因子调节,并且包括腺苷在内的每种因子的作用都与其他因子的作用相关。