Peters J, Kindred M K, Robotham J L
Department of Anesthesiology and Critical Care Medicine, Francis Scott Key Medical Center, Johns Hopkins University Medical Institutions, Baltimore, Maryland 21205.
J Appl Physiol (1985). 1988 Apr;64(4):1506-17. doi: 10.1152/jappl.1988.64.4.1506.
The etiology of the fall in left ventricular stroke volume (LVSV) with negative intrathoracic pressure (NITP) during inspiration has been ascribed to a reduction in LV preload. This study evaluated the effects of NITP with and without airway obstruction confined to early (ED), mid- (MD), or late diastole (LD) on the subsequent LVSV, anteroposterior (AP), and right-to-left (RL) aortic diameters (DAO) (series I, n = 6) as well as on phasic arterial blood flow out of the thorax (series II, n = 6) in anesthetized dogs. Transient NITP was obtained by electrocardiogram-triggered phrenic nerve stimulation. In series I, NITP applied for 60% of diastole with the airway obstructed caused decreases of LVSV during ED [-7.7 +/- 3.2% (SE) NS], MD (-11.7 +/- 3.9%, P less than 0.05), and LD (-14.6 +/- 1.5%, P less than 0.01) associated with significant increases of left ventricular end-diastolic pressures relative to both atmospheric and esophageal pressures during MD and LD. NITP increased DAO(AP) and DAO(RL), resulting in increases in diastolic aortic cross-sectional area by an average of 6.1-8.3% (P less than 0.01). Similar changes were seen with the airway unobstructed during NITP. In series II, NITP caused diminished diastolic antegrade carotid artery and/or descending aortic flow run off in all dogs. Transient retrograde arterial flows with NITP were observed in more than half of the animals consistent with increases in aortic diameters. We conclude that a decrease of intrathoracic pressure confined to diastole can 1) diminish the ensuing LVSV, presumptively reducing preload by ventricular interdependence; 2) distend the intrathoracic aorta; 3) diminish antegrade flow out of the thorax independent of effects on cardiac performance; and 4) cause transient retrograde carotid and aortic blood flow. The intrathoracic aorta and, presumably, the arterial intrathoracic vascular compartment can be viewed as an elastic container driven by changes in intrathoracic pressure.
吸气时左心室每搏输出量（LVSV）随胸内负压（NITP）降低的病因被归因于左心室前负荷的减少。本研究评估了在麻醉犬中，气道阻塞与否的情况下，分别在舒张早期（ED）、中期（MD）或晚期（LD）施加NITP对随后的LVSV、前后径（AP）和左右径（RL）主动脉直径（DAO）（系列I，n = 6）以及胸腔外向相性动脉血流（系列II，n = 6）的影响。通过心电图触发膈神经刺激获得短暂的NITP。在系列I中，气道阻塞时，在舒张期60%的时间内施加NITP，导致ED期间LVSV降低[-7.7 +/- 3.2%（标准误），无统计学意义]，MD期间降低（-11.7 +/- 3.9%，P < 0.05），LD期间降低（-14.6 +/- 1.5%，P < 0.01），且与MD和LD期间相对于大气压力和食管压力的左心室舒张末期压力显著升高相关。NITP增加了DAO(AP)和DAO(RL)，导致舒张期主动脉横截面积平均增加6.1 - 8.3%（P < 0.01）。在NITP期间气道通畅时也观察到类似变化。在系列II中，NITP导致所有犬的舒张期颈动脉和/或降主动脉顺行血流减少。超过一半的动物观察到NITP引起的短暂逆行动脉血流，这与主动脉直径增加一致。我们得出结论，局限于舒张期的胸内压降低可：1）减少随后的LVSV，推测通过心室相互依赖减少前负荷；2）扩张胸内主动脉；3）减少胸腔外向相性血流，与对心脏功能的影响无关；4）引起短暂的颈动脉和主动脉逆行血流。胸内主动脉以及推测的胸内动脉血管腔可被视为由胸内压变化驱动的弹性容器。
