Polglase Graeme R, Wallace Megan J, Morgan David L, Hooper Stuart B
Fetal and Neonatal Research Group, Department of Physiology, Monash University, Melbourne, Australia.
J Appl Physiol (1985). 2006 Jul;101(1):273-82. doi: 10.1152/japplphysiol.01544.2005. Epub 2006 Mar 30.
Prolonged increases in fetal lung expansion stimulate fetal lung growth and development, but the effects on pulmonary hemodynamics are unknown. Our aim was to determine the effect of increased fetal lung expansion, induced by tracheal obstruction (TO), on pulmonary blood flow (PBF) and vascular resistance (PVR). Chronically catheterized fetal sheep (n = 6) underwent TO from 120 to 127 days of gestational age (term approximately 147 days); tracheas were not obstructed in control fetuses (n = 6). PBF, PVR, and changes to the PBF waveform were determined. TO significantly increased lung wet weight compared with control (166.3 +/- 20.2 vs. 102.0 +/- 18.8 g; P < 0.05). Despite the increase in intraluminal pressure caused by TO (5.0 +/- 0.9 vs. 2.4 +/- 1.0 mmHg; P < 0.001), PBF and PVR were similar between groups after 7 days (TO 28.1 +/- 3.2 vs. control 34.1 +/- 10.0 ml.min(-1).100 g lung wt(-1)). However, TO markedly altered pulmonary hemodynamics associated with accentuated fetal breathing movements, causing a reduction rather than an increase in PBF at 7 days of TO. To account for the increase in intraluminal pressure, the pressure was equalized by draining the lungs of liquid on day 7 of TO. Pressure equalization increased PBF from 36.8 +/- 5.2 to 112.4 +/- 22.8 ml/min (P = 0.01) and markedly altered the PBF waveform. These studies provide further evidence to indicate that intraluminal pressure is an important determinant of PBF and PVR in the fetus. We suggest that the increase in PBF associated with pressure equalization following TO reflects an increase in growth of the pulmonary vascular bed, leading to an increase in its cross-sectional area.
胎儿肺扩张时间延长会刺激胎儿肺的生长和发育,但对肺血流动力学的影响尚不清楚。我们的目的是确定由气管阻塞(TO)引起的胎儿肺扩张增加对肺血流量(PBF)和血管阻力(PVR)的影响。对6只慢性插管的胎羊在妊娠120至127天(足月约147天)进行气管阻塞;对照组6只胎羊的气管未阻塞。测定了肺血流量、肺血管阻力以及肺血流量波形的变化。与对照组相比,气管阻塞显著增加了肺湿重(166.3±20.2克对102.0±18.8克;P<0.05)。尽管气管阻塞导致管腔内压力升高(5.0±0.9对2.4±1.0毫米汞柱;P<0.001),但7天后两组之间的肺血流量和肺血管阻力相似(气管阻塞组28.1±3.2对对照组34.1±10.0毫升·分钟-1·100克肺组织重量-1)。然而,气管阻塞显著改变了与胎儿呼吸运动加剧相关的肺血流动力学,在气管阻塞7天时导致肺血流量减少而非增加。为了解释管腔内压力的升高,在气管阻塞第7天通过排出肺内液体使压力平衡。压力平衡使肺血流量从36.8±5.2增加到112.4±22.8毫升/分钟(P=0.01),并显著改变了肺血流量波形。这些研究提供了进一步的证据表明管腔内压力是胎儿肺血流量和肺血管阻力的重要决定因素。我们认为,气管阻塞后压力平衡导致的肺血流量增加反映了肺血管床生长的增加,导致其横截面积增加。