Parer J T, Dijkstra H R, Vredebregt P P, Harris J L, Krueger T R, Reuss M L
Eur J Obstet Gynecol Reprod Biol. 1980 Jul;10(6):393-9. doi: 10.1016/0028-2243(80)90025-8.
Fetal heart rate (FHR) and oxygen consumption were determined in 45 studies in 20 chronically instrumented, normoxic sheep. FHR variability was measured by a template device to determine amplitude range, and oscillatory frequency was manually counted over 5-min periods. During 26 min of isocapnic hypoxia, fetal O2 consumption decreased 39% and FHR decreased 18%, and FHR variability increased, the changes being maintained over the treatment period. It is suggested that the maintenance of FHR variability during this profound hypoxia denotes adequate cardiorespiratory compensatory mechanisms during the short period; prolongation of the hypoxia would probably result in fetal cerebral or myocardial decompensation, and disappearance of FHR variability. The increased variability may be due to increased alpha-adrenergic activity.
在20只长期植入仪器、处于常氧状态的绵羊身上进行了45项研究，测定了胎儿心率（FHR）和耗氧量。通过模板装置测量FHR变异性以确定振幅范围，并在5分钟时间段内人工计数振荡频率。在26分钟的等碳酸血症性缺氧期间，胎儿耗氧量下降39%，FHR下降18%，且FHR变异性增加，这些变化在治疗期间持续存在。提示在这种严重缺氧期间FHR变异性的维持表明短期内存在足够的心肺代偿机制；缺氧时间延长可能导致胎儿脑或心肌失代偿以及FHR变异性消失。变异性增加可能是由于α-肾上腺素能活性增加所致。
