Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart.
Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart.
复制标题
导致跳动犬心脏冠状循环反应性充血的微血管部位和机制。
DOI：
10.1161/01.res.71.4.912
复制
发表时间：
1992
影响因子：
20.1
通讯作者：
T. Takishima
中科院分区：
文献类型：
--
作者：
H. Kanatsuka;N. Sekiguchi;Kouichi Sato;K. Akai;Yan Wang;T. Komaru;K. Ashikawa;T. Takishima
我们的目的是阐明反应性充血在冠状动脉循环中的位置和机制。在离体犬心脏跳动中，用浮动物镜显微镜观察冠状动脉左前降支（LAD）的微血管。用抽吸式多普勒探头测量左前降支流速。将LAD闭塞20或30秒，然后释放，并且在8-苯基茶碱（7.5mg/kg i. v.）或格列本脲（200 μ g/kg注入LAD）输注。在闭塞过程中，只有直径小于100微米的动脉微血管扩张。这些血管的扩张被8-苯基茶碱部分减弱，被格列本脲完全消除。在反应性充血的早期阶段，所有动脉微血管扩张，并且与大于100微米的血管相比，小于100微米的血管的峰值扩张幅度更大。反应性充血期间的血管舒张在小于100微米的血管中在60秒内停止，但在大于100微米的血管中持续超过120秒。8-苯茶碱不改变动脉微血管的峰值扩张，但降低峰值后的扩张。在反应性充血的整个阶段，格列本脲显著减弱了所有动脉微血管的扩张。这些结果表明，所有的动脉微血管负责反应性充血后，冠状动脉闭塞20-30秒，但有更大的参与血管小于100微米的反应性充血的早期阶段。大于100微米的血管扩张在后期阶段中起重要作用。ATP敏感性K+通道介导短暂缺血和反应性充血时动脉微血管的扩张。
Our aim was to elucidate the site and mechanism responsible for reactive hyperemia in coronary circulation. In in vivo beating canine hearts, microvessels of the left anterior descending coronary artery (LAD) were observed through a microscope equipped with a floating objective. Flow velocity of the LAD was measured with a suction-type Doppler probe. The LAD was occluded for 20 or 30 seconds and then released, and reactive hyperemia was observed before and after 8-phenyltheophylline (7.5 mg/kg i.v.) or glibenclamide (200 micrograms/kg into the LAD) infusion. During the occlusion, only arterial microvessels smaller than 100 microns in diameter dilated. Dilation of those vessels was partially attenuated by 8-phenyltheophylline and completely abolished with glibenclamide. In the early phase of reactive hyperemia, all arterial microvessels dilated, and the magnitude of peak dilation was greater in vessels smaller than 100 microns compared with those larger than 100 microns. Vasodilation during reactive hyperemia ceased within 60 seconds in vessels smaller than 100 microns but was sustained for more than 120 seconds in those larger than 100 microns. 8-Phenyltheophylline did not change peak dilation of arterial microvessels but reduced dilation after the peak. Glibenclamide remarkably attenuated dilation of all arterial microvessels in the whole phase of reactive hyperemia. These results indicate that all arterial microvessels are responsible for reactive hyperemia after coronary artery occlusions of 20-30 seconds, but there is greater participation of vessels smaller than 100 microns in the early phase of reactive hyperemia. Dilation of vessels larger than 100 microns assumes an important role in the later phase. ATP-sensitive K+ channels mediate dilation of arterial microvessels both in brief ischemia and reactive hyperemia.
影响因子：
37.8
作者：
VITA, JA;TREASURE, CB;GANZ, P
通讯作者：
GANZ, P
反应性充血中的心肌高能磷酸盐。
DOI：
10.1152/ajpheart.1990.259.4.h1190
发表时间：
1990
期刊：
The American journal of physiology
影响因子：
--
作者：
Schwartz,GG;Schaefer,S;Gober,J;Meyerhoff,DJ;Smekal,A;Massie,B;Weiner,MW
通讯作者：
Weiner,MW
影响因子：
56.9
作者：
J. Weiss;S. Lamp
通讯作者：
J. Weiss;S. Lamp