Sonn J, Acad B, Mayevsky A, Kedem J
Arch Int Physiol Biochim. 1981 Dec;89(5):445-55. doi: 10.3109/13813458109082641.
An attempt was made to differentiate between autoregulatory coronary vasodilation and changes in vasomotor tone produced by factors extrinsic to the heart. this was done by investigating the relation between local cardiac force and local coronary blood supply. Intracellular NADH redox levels were also measured in order to further elucidate the oxygen balance under various experimental conditions. In anaesthetized open-chest dogs, local blood supply was estimated with the aid of a thermistor probe, and the oxidation-reduction state of mitochondrial pyridine nucleotide was measured by a surface fluorometric technique. Local myocardial contractile force, as well as blood pressure and ECG were recorded simultaneously with the above parameters. The heart was paced at frequencies from 60/min to 300/min with an electronic stimulator, under both normoxic and hypopneic conditions. It was found that elevation of heart rate caused a progressive increase in local blood flow during both normal and hypopneic ventilation. The absolute flow values during hypopnea were approximately double those during normoxia. Heart rates above 120/min or 150/min resulted in a progressive increase in NADH fluorescence. This response to elevated heart rate was less prominent or absent during hypopnea. Contractile force during hypopnea was greater at elevated heart rates than during normal breathing. Data are brought which suggest that whereas vasodilation following increased heart rate is probably due to an autoregulatory mechanism, the marked vasodilatatory effect of hypopnea is related to elevated arterial CO2 levels. It is suggested that hypercapnia markedly stimulates extrinsic coronary vasodilation thereby supplying enough oxygen to maintain contractility even at very high heart rates. Moreover, intracellular O2 concentration (mitochondrial NADH level) is maintained at a normal level despite the greatly increased demand.
研究人员试图区分心脏自身调节性冠脉血管舒张与心脏外部因素引起的血管运动张力变化。这是通过研究局部心脏力量与局部冠脉血液供应之间的关系来实现的。还测量了细胞内NADH氧化还原水平，以进一步阐明各种实验条件下的氧平衡。在麻醉开胸犬中，借助热敏电阻探头估计局部血液供应，并通过表面荧光技术测量线粒体吡啶核苷酸的氧化还原状态。同时记录局部心肌收缩力、血压和心电图与上述参数。在常氧和低通气条件下，用电子刺激器将心脏起搏频率设定为60次/分钟至300次/分钟。结果发现，在正常通气和低通气期间，心率升高都会导致局部血流量逐渐增加。低通气时的绝对血流量值约为常氧时的两倍。心率高于120次/分钟或150次/分钟会导致NADH荧光逐渐增加。在低通气期间，这种对心率升高的反应不太明显或不存在。低通气时心率升高时的收缩力比正常呼吸时更大。数据表明，心率增加后的血管舒张可能是由于自身调节机制，而低通气的显著血管舒张作用与动脉血二氧化碳水平升高有关。有人认为，高碳酸血症明显刺激冠脉外血管舒张，从而即使在非常高的心率下也能提供足够的氧气以维持收缩力。此外，尽管需求大幅增加，但细胞内氧浓度（线粒体NADH水平）仍维持在正常水平。
