Wead W B, Norton J F
J Appl Physiol Respir Environ Exerc Physiol. 1981 May;50(5):1027-35. doi: 10.1152/jappl.1981.50.5.1027.
Left ventricular diameter, pressure, and dP/dt, as well as aortic and intrapleural pressures, were recorded simultaneously from 10 acute anethetized mongrel dogs. Normal inspiration produced a significant decrease in end-diastolic diameter (46.9 +/- 1.2 to 43.1 +/- 1.0 mm) and end-systolic diameter (35.5 +/- 1.4 to 34.2 +/- 1.7 mm), reducing stroke diameter 2.5 mm. Airway occlusion (greater than or equal to 60%) produced a reduction in the decrease of end-diastolic diameter seen with normal inspiration and, to a lesser degree, in end-systolic diameter. Because only acute airway occlusion greater than or equal to 80% produced a significant increase in left ventricular afterload, the authors conclude that normal spontaneous inspiration results in a decrease in left ventricular preload due to pooling of blood in the pulmonary vasculature. The data suggest that this decrease in left ventricular preload is the predominant mechanism responsible for the inspiratory decrease in left ventricular stroke volume.
从10只急性麻醉的杂种犬身上同时记录左心室直径、压力、压力变化率(dP/dt)以及主动脉和胸膜腔内压力。正常吸气会使舒张末期直径显著减小(从46.9±1.2毫米降至43.1±1.0毫米)和收缩末期直径减小(从35.5±1.4毫米降至34.2±1.7毫米),使搏出径减少2.5毫米。气道阻塞(大于或等于60%)会使正常吸气时舒张末期直径的减小幅度降低,对收缩末期直径的影响程度较小。由于只有大于或等于80%的急性气道阻塞会使左心室后负荷显著增加,作者得出结论,正常的自主吸气会导致左心室前负荷降低,原因是血液在肺血管系统中淤积。数据表明,左心室前负荷的这种降低是导致左心室搏出量吸气期减少的主要机制。