CHRONIC ANEMIA IN PREGNANT EWES - MATERNAL AND FETAL EFFECTS
CHRONIC ANEMIA IN PREGNANT EWES - MATERNAL AND FETAL EFFECTS
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DOI：
10.1152/ajpregu.1991.261.5.r1075
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发表时间：
1991-11-01
影响因子：
--
通讯作者：
CLARK, KE
中科院分区：
文献类型：
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作者：
MOSTELLO, D;CHALK, C;CLARK, KE
为了检查在绵羊妊娠的第110-138天期间母体和胎儿对母体红细胞压积持续降低的反应，对22只母羊及其单胎胎儿进行了检测。通过重复交换输血，12只母羊的红细胞压积从28.1 +/- 0.8（基线，第110天）降至14.0 +/- 0.7%（第117天），并维持在该水平。与对照组动物相比，贫血母羊的心率从99 +/- 4次/分短暂增加至116 +/- 4次/分，心输出量从117 +/- 8次/分持续增加至153 +/- 11 ml.min-1.kg-1。对照组动物的子宫血流量从868 +/- 100（第110天）稳步增加至1，410 +/- 177 ml/min（第138天），但贫血母羊的子宫血流量未增加。随着贫血的产生，子宫氧输送从83 +/- 10降至39 +/- 4 ml/min，并在贫血母羊中保持较低水平。贫血母羊胎仔的动脉PO 2和氧含量短暂低于对照值（分别为19.9 +/- 0.8 vs. 23.4 +/- 1.0 mmHg和5.3 +/- 0.3 vs. 6.8 +/- 0.4 ml/dl），但未持续。贫血组妊娠138天的胎仔体重较低（2，596 +/- 329 vs. 4，313 +/- 132 g）。我们的结论是，慢性母体贫血导致子宫血流量减少以及子宫氧输送减少。胎儿的反应是生长减慢，但不会出现持续性缺氧或酸中毒。
To examine maternal and fetal responses to a sustained reduction in maternal hematocrit during days 110-138 of ovine gestation, 22 ewes and their singleton fetuses were instrumented. By repetitive exchange transfusions, the hematocrit in 12 ewes was decreased from 28.1 +/- 0.8 (baseline, day 110) to 14.0 +/- 0.7% (day 117) and maintained at that level. Anemic ewes demonstrated a transient increase in heart rate from 99 +/- 4 to 116 +/- 4 beats/min and a sustained increase in cardiac output from 117 +/- 8 to 153 +/- 11 ml.min-1.kg-1 compared with control animals. Uterine blood flow steadily increased in control animals from 868 +/- 100 (day 110) to 1,410 +/- 177 ml/min (day 138) but failed to increase in the anemic ewes. Uterine oxygen delivery fell from 83 +/- 10 to 39 +/- 4 ml/min with production of anemia and remained low in the anemic ewes. Arterial PO2 and oxygen content in the fetuses of anemic ewes fell transiently below control values (19.9 +/- 0.8 vs. 23.4 +/- 1.0 mmHg and 5.3 +/- 0.3 vs. 6.8 +/- 0.4 ml/dl, respectively) but did not persist. Fetal weights at 138 days gestation were lower in the anemic group (2,596 +/- 329 vs. 4,313 +/- 132 g). We conclude that chronic maternal anemia results in a decreased uterine blood flow as well as decreased uterine oxygen delivery. The fetus responds with decreased growth but does not develop sustained hypoxia or acidosis.