Olsen C O, Tyson G S, Maier G W, Davis J W, Rankin J S
Circulation. 1985 Sep;72(3):668-79. doi: 10.1161/01.cir.72.3.668.
In 12 conscious dogs, a three-dimensional array of pulse-transit ultrasonic transducers was used to measure left ventricular anterior-posterior minor, septal-free wall minor, and basal-apical major diameters. Matched micromanometers measured left ventricular, right ventricular, and intrapleural pressures. Electromagnetic ascending aortic blood flow and right ventricular transverse diameter were measured in five of the dogs. A major cause of the inspiratory decline in stroke volume in this preparation appeared to be reflex tachycardia and autonomic changes associated with inspiration. However, when heart rate was controlled by atrial pacing or pharmacologic autonomic attenuation (propranolol and atropine), stroke volume still decreased around 10%, with an inspiratory decrease in pleural pressure of 10 mm Hg. Based on the measurements of ventricular dimension, venous return to the right ventricle appeared to be augmented significantly during inspiration and the transient increase in right ventricular volume was associated with leftward interventricular septal shifting and altered diastolic left ventricular geometry. However, left ventricular end-diastolic volume was changed minimally, implying that alterations in preload were not important. Moreover, transmural left ventricular ejection pressure, calculated as intracavitary minus pleural pressure, was not significantly changed, and it seemed that neither pressure nor geometric components of afterload were altered significantly by inspiration. The inspiratory fall in left ventricular stroke volume correlated best with the decline in intracavitary left ventricular ejection pressure referenced to atmospheric pressure. It is hypothesized that during ejection, left ventricular pressure referenced to atmospheric pressure is the hydraulic force effecting stroke volume and that the decline in this effective left ventricular ejection pressure is responsible for the inspiratory fall in stroke volume through a reverse thoracic pump mechanism.
在12只清醒犬中，使用三维脉冲传输超声换能器阵列测量左心室前后径、室间隔-游离壁径和基底-心尖径。匹配的微压计测量左心室、右心室和胸腔内压力。在其中5只犬中测量电磁升主动脉血流量和右心室横径。在此准备过程中，每搏量吸气时下降的一个主要原因似乎是与吸气相关的反射性心动过速和自主神经变化。然而，当通过心房起搏或药物性自主神经抑制（普萘洛尔和阿托品）控制心率时，每搏量仍下降约10%，同时胸膜压力吸气时下降10 mmHg。根据心室尺寸测量，吸气期间右心室的静脉回流似乎显著增加，右心室容积的短暂增加与室间隔向左移位以及舒张期左心室几何形状改变有关。然而，左心室舒张末期容积变化很小，这意味着前负荷的改变并不重要。此外，以心腔内压力减去胸膜压力计算的跨壁左心室射血压力没有显著变化，似乎吸气并未使后负荷的压力或几何成分发生显著改变。左心室每搏量的吸气性下降与以大气压为参考的心腔内左心室射血压力的下降最相关。据推测，在射血期间，以大气压为参考的左心室压力是影响每搏量的水力，并且这种有效的左心室射血压力的下降通过反向胸泵机制导致每搏量的吸气性下降。
