Krasney J A, Koehler R C
J Appl Physiol Respir Environ Exerc Physiol. 1977 Dec;43(6):1012-8. doi: 10.1152/jappl.1977.43.6.1012.
Arterial hypoxia was produced in 10 conscious, chronically instrumented, tracheostomized dogs by allowing them to breathe 7.5% O2 in N2 for 10 min. Hypoxia (Pao2 = 28 +/- 0.7 (SE) Torr) caused significant increases in coronary blood flow (+196%), left ventricular dP/dt max (+60%), aortic blood flow (+48%), heart rate (+50%), and left ventricular systolic (+12%) and aortic (+10%) pressures. Left ventricular end-diastolic pressure and stroke volume were unchanged, while systemic (-30%) and coronary diastolic (-66%) vascular resistances declined significantly. When equivalent levels of arterial hypoxia were produced in four of these dogs after chronic sinoaortic denervation, the coronary, cardiac, and systemic hemodynamic responses were not significantly different, with the exception that the small arterial pressure response was abolished. Thus the peripheral chemoreflexes are not essential for the normal coronary vasodilator and cardiac adjustments to occur during hypoxia in the conscious dog. The data support the hypothesis that a large part of the cardiac adjustments to hypoxia is initiated outside the sinoaortic reflexogenic zones, probably within the central nervous system.
对10只清醒、长期植入仪器并做了气管切开术的犬,通过让它们吸入含7.5%氧气的氮气10分钟来制造动脉性缺氧。缺氧状态(动脉血氧分压=28±0.7(标准误)托)导致冠状动脉血流量显著增加(+196%)、左心室dp/dt最大值显著增加(+60%)、主动脉血流量显著增加(+48%)、心率显著增加(+50%),以及左心室收缩压(+12%)和主动脉压(+10%)显著增加。左心室舒张末期压力和每搏输出量未发生变化,而全身血管阻力(-30%)和冠状动脉舒张期血管阻力(-66%)显著下降。在对其中4只犬进行慢性窦主动脉去神经支配后,当产生同等程度的动脉性缺氧时,冠状动脉、心脏和全身的血流动力学反应并无显著差异,只是小动脉压力反应消失。因此,在清醒犬缺氧期间,外周化学感受性反射对于正常的冠状动脉舒张及心脏调节并非必不可少。这些数据支持这样一种假说,即对缺氧的心脏调节很大一部分是在窦主动脉反射发生区之外启动的,可能是在中枢神经系统内启动的。