K+ATP channels and adenosine are not necessary for coronary autoregulation.
K+ATP channels and adenosine are not necessary for coronary autoregulation.
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K ATP 通道和腺苷对于冠状动脉自动调节不是必需的。
DOI：
10.1152/ajpheart.1997.273.3.h1299
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Feigl,EO
中科院分区：
文献类型：
--
作者：
Stepp,DW;Kroll,K;Feigl,EO
自动调节被定义为器官在面对变化的灌注压时保持恒定流量的内在能力。本研究评价了几种潜在的冠状动脉自动调节介质的作用：间质腺苷，ATP敏感性K+（K+ATP）通道，心肌氧和二氧化碳的张力，反映了冠状动脉静脉氧和二氧化碳的张力。左冠状动脉主干插管，并在控制压力下灌注血液在闭胸犬。利用先前描述的数学模型从动脉和静脉腺苷浓度估计间质腺苷浓度。在100和60 mmHg之间观察到冠状动脉血流量的自动调节。格列本脲是一种K+ATP通道抑制剂，在每个灌注压下使冠状动脉血流量减少19%，但保留了自身调节。在冠状动脉压力逐步降低至>或= 70 mmHg后，腺苷浓度未增加至高于基础水平。腺苷浓度在60 mmHg时升高，表明腺苷在冠状动脉自动调节极限时的作用。不需要腺苷，因为腺苷介导的血管舒张抑制剂格列本脲不会降低自身调节或增加腺苷浓度。冠状静脉氧和二氧化碳的张力变化不大，在自动调节之前，抑制K+ATP通道和腺苷血管舒张与格列本脲。然而，格列本脲后冠状静脉二氧化碳张力随着冠状动脉压力的降低而逐渐升高。二氧化碳的增加间接表明二氧化碳介导的血管舒张补偿了K+ ATP通道功能的丧失。总之，K+ATP通道和腺苷都不是维持冠状动脉血流在100至60 mmHg的冠状动脉压力自动调节范围内所必需的。
Autoregulation is defined as the intrinsic ability of an organ to maintain constant flow in the face of changing perfusion pressure. The present study evaluated the role of several potential mediators of coronary autoregulation: interstitial adenosine, ATP-sensitive K+ (K+ATP) channels, and myocardial oxygen and carbon dioxide tensions as reflected by coronary venous oxygen and carbon dioxide tensions. The left main coronary artery was cannulated, and blood was perfused at controlled pressures in closed-chest dogs. Interstitial adenosine concentration was estimated from arterial and venous adenosine concentrations with a previously described mathematical model. Autoregulation of coronary blood flow was observed between 100 and 60 mmHg. Glibenclamide, an inhibitor of K+ATP channels, reduced coronary blood flow by 19% at each perfusion pressure, but autoregulation was preserved. After stepwise reductions in coronary pressure to values > or = 70 mmHg, adenosine concentrations did not increase above basal levels. Adenosine concentration was elevated at 60 mmHg, suggesting a role for adenosine at the limit of coronary autoregulation. Adenosine is not required because glibenclamide, an inhibitor of adenosine-mediated vasodilation, did not reduce autoregulation or increase adenosine concentration. Coronary venous oxygen and carbon dioxide tensions were little changed during autoregulation before the inhibition of K+ATP channels and adenosine vasodilation with glibenclamide. However, coronary venous carbon dioxide tension rose progressively with decreasing coronary pressure after glibenclamide. The increase in carbon dioxide indirectly suggests that carbon dioxide-mediated vasodilation compensated for the loss of K+ATP-channel function. In summary, neither K+ATP channels nor adenosine is necessary to maintain coronary flow in the autoregulatory range of coronary arterial pressure from 100 to 60 mmHg.