Berning R A, Klautz R J, Teitel D F
Cardiovascular Research Institute, University of California, San Francisco 94143, USA.
Pediatr Res. 1997 Jan;41(1):57-64. doi: 10.1203/00006450-199701000-00009.
Left ventricular (LV) output nearly triples at birth, in association with increases in serum catecholamines. Similar increases in catecholamines in utero, however, do not increase output. We hypothesized that catecholamines increase contractility in utero, but that output cannot increase until LV loading conditions are changed by oxygen ventilation. To address this hypothesis, we studied nine fetal sheep acutely placed in a warm water bath (40 degrees C). Conductance and manometric catheters were placed in the LV to generate pressure-volume loops during caval occlusion in the nonventilated and oxygen-ventilated states, each under control, dobutamine, and propranolol conditions. Contractility was estimated by the end-systolic pressure-volume relationship, preload by end-diastolic volume, and afterload by arterial elastance. Oxygen ventilation increased LV output 1.4-fold, despite a decrease in contractility to about three-fourths of the nonventilated value. Heart rate remained constant, whereas preload increased and afterload decreased significantly. During oxygen ventilation, dobutamine increased output to 2.3 times the control, nonventilated value, associated with increases in contractility and heart rate and no change in preload and afterload. Although dobutamine increased contractility and heart rate similarly in the nonventilated and oxygen ventilated states, output increased significantly more during ventilation. Similarly, propranolol decreased contractility and heart rate equally in both states, but output decreased far more during ventilation. Thus, oxygen ventilation is associated with advantageous changes in LV load such that the positive inotropic and chronotropic effects of dobutamine are translated into greater increases in LV output.
出生时左心室（LV）输出量几乎增加两倍，这与血清儿茶酚胺水平升高有关。然而，子宫内儿茶酚胺水平的类似升高并不会增加输出量。我们推测，儿茶酚胺在子宫内会增加心肌收缩力，但在通过氧气通气改变左心室负荷条件之前，输出量无法增加。为了验证这一假设，我们对九只急性置于温水浴（40摄氏度）中的胎羊进行了研究。将电导和测压导管置入左心室，以便在非通气和氧气通气状态下的腔静脉闭塞期间生成压力-容积环，每种状态均在对照、多巴酚丁胺和普萘洛尔条件下进行。通过收缩末期压力-容积关系估算心肌收缩力，通过舒张末期容积估算前负荷，通过动脉弹性估算后负荷。尽管心肌收缩力降至非通气值的约四分之三，但氧气通气使左心室输出量增加了1.4倍。心率保持恒定，而前负荷增加，后负荷显著降低。在氧气通气期间，多巴酚丁胺使输出量增加至对照非通气值的2.3倍，这与心肌收缩力和心率增加以及前负荷和后负荷无变化有关。尽管多巴酚丁胺在非通气和氧气通气状态下对心肌收缩力和心率的增加作用相似，但通气期间输出量的增加更为显著。同样，普萘洛尔在两种状态下均使心肌收缩力和心率同等程度降低，但通气期间输出量的降低幅度要大得多。因此，氧气通气与左心室负荷的有利变化相关，使得多巴酚丁胺的正性肌力和变时作用转化为左心室输出量的更大增加。
