Wright C, Drinkhill M J, Hainsworth R
The Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK.
J Physiol. 2000 Oct 15;528 Pt 2(Pt 2):349-58. doi: 10.1111/j.1469-7793.2000.00349.x.
Previous studies which have indicated that the stimulation of ventricular mechanoreceptors induces significant reflex responses can be criticised because of the likelihood of concomitant stimulation of coronary arterial baroreceptors. We therefore undertook this investigation to examine the coronary and ventricular mechanoreflexes in a preparation in which the pressure stimuli to each region were effectively separated. Dogs were anaesthetised, artificially ventilated and placed on cardiopulmonary bypass. A balloon at the ventricular outflow separated pressure in the left ventricle from that perfusing the coronary arteries. Ventricular pressures were changed by varying inflow and outflow of blood entering and leaving the ventricle through an apical cannula, and coronary pressure by changing pressure in a reservoir connected to a cannula tied in the aortic root. Pressures distending carotid and aortic baroreceptors were controlled. Changes in descending aortic perfusion pressure (flow constant) were used to assess systemic vascular responses. Large changes in carotid sinus and coronary pressures decreased vascular resistance by 35+/-1.9 and 40+/-2.5%, respectively. Intracoronary injections of veratridine (30-60 microg) decreased vascular resistance by 31+/-2.5%. However, large increases in ventricular pressure decreased resistance by only 9+/-2.2%. Significant changes in vascular resistance were obtained with increases in coronary arterial pressure from 60 to 90 mmHg. However, ventricular pressures had to increase to 152/18 mmHg (systolic/end-diastolic) before there was a significant response. These results show that coronary mechanoreceptors are likely to play an important role in cardiovascular control. If ventricular receptors have any function at all, it is as a protective mechanism during gross distension, possibly associated with myocardial ischaemia.
先前的研究表明，刺激心室机械感受器会引发显著的反射反应，但这些研究可能受到批评，因为有可能同时刺激冠状动脉压力感受器。因此，我们进行了这项研究，以在一种能有效分离对每个区域的压力刺激的制备方法中检查冠状动脉和心室机械反射。对狗进行麻醉、人工通气并置于体外循环。心室流出道处的一个球囊将左心室内的压力与灌注冠状动脉的压力分隔开。通过改变经心尖插管进出心室的血液流入和流出量来改变心室压力，通过改变与系于主动脉根部的插管相连的储液器中的压力来改变冠状动脉压力。控制扩张颈动脉和主动脉压力感受器的压力。使用降主动脉灌注压力（流量恒定）的变化来评估全身血管反应。颈动脉窦和冠状动脉压力的大幅变化分别使血管阻力降低了35±1.9%和40±2.5%。冠状动脉内注射藜芦碱（30 - 60微克）使血管阻力降低了31±2.5%。然而，心室压力的大幅升高仅使阻力降低了9±2.2%。冠状动脉压力从60毫米汞柱升高到90毫米汞柱时，血管阻力有显著变化。然而，心室压力必须升高到152/18毫米汞柱（收缩压/舒张压）才会有显著反应。这些结果表明，冠状动脉机械感受器可能在心血管控制中起重要作用。如果心室感受器确实有任何功能的话，那也是在严重扩张期间作为一种保护机制，可能与心肌缺血有关。
