McCrabb G J, Harding R
Department of Physiology, Monash University, Melbourne, Vic., Australia.
Biol Neonate. 1997;71(6):385-94. doi: 10.1159/000244440.
Our aim was to determine the effects of 12 h of hypoxaemia on cerebral blood flow (CBF) and cerebral O2 delivery in ovine fetuses at 0.6 gestation. During fetal hypoxaemia, induced by reduced uterine blood flow, fetal SaO2 and PaO2 were reduced (p < 0.01) from control values of 77.0 +/- 1.6% and 27.3 +/- 1.0 mm Hg, respectively, to 28.4 +/- 3.4% and 15.6 +/- 0.6 mm Hg; fetal pHa decreased from control values of 7.37 +/- 0.01 to 7.20 +/- 0.02 at 3 h, but returned to control values before 12 h. CBF (ml/min/100 g) was 2.0- to 2.6-fold higher (p < 0.01) than control values during hypoxaemia, but only 1.7-fold higher (p < 0.01) at 3 h when pHa was lowest. Cerebral O2 delivery (ml/min/100 g) was lower (p < 0.01) than control values of 3.15 +/- 0.29 at 1.5h (2.09 +/- 0.36) and 3h (1.84 +/- 0.22) of hypoxaemia and higher 1 h after hypoxaemia had ceased (3.81 +/- 0.22, p < 0.01). We conclude that the ovine fetus at 0.6 gestation is unable to sustain increased CBF and hence maintain cerebral O2 delivery during the first 6 h of hypoxaemia, a time which coincides with acidaemia; in contrast, at 6 and 12 h of hypoxaemia, when pHa was normal, cerebral O2 delivery was similar to control values. Reduced cerebral O2 delivery during the early, acidaemic, stages of hypoxaemia may lead to impaired neural development.
我们的目的是确定妊娠0.6期绵羊胎儿低氧血症持续12小时对脑血流量（CBF）和脑氧输送的影响。在通过减少子宫血流量诱导的胎儿低氧血症期间，胎儿动脉血氧饱和度（SaO2）和动脉血氧分压（PaO2）分别从对照值77.0±1.6%和27.3±1.0毫米汞柱降至28.4±3.4%和15.6±0.6毫米汞柱（p<0.01）；胎儿动脉血pH值（pHa）在3小时时从对照值7.37±0.01降至7.20±0.02，但在12小时前恢复到对照值。低氧血症期间，CBF（毫升/分钟/100克）比对照值高2.0至2.6倍（p<0.01），但在pHa最低的3小时时仅高1.7倍（p<0.01）。脑氧输送（毫升/分钟/100克）在低氧血症1.5小时（2.09±0.36）和3小时（1.84±0.22）时低于对照值3.15±0.29（p<0.01），在低氧血症停止1小时后升高（3.81±0.22，p<0.01）。我们得出结论，妊娠0.6期的绵羊胎儿在低氧血症的前6小时内无法维持CBF增加，因此无法维持脑氧输送，这段时间与酸血症同时发生；相反，在低氧血症6小时和12小时时，当pHa正常时，脑氧输送与对照值相似。低氧血症早期酸血症阶段脑氧输送减少可能导致神经发育受损。
