Abstract：
UNASSIGNED: Baroreflex is a regulatory mechanism that slows the fetal heart rate. This study aimed to investigate the effects of lipopolysaccharide (LPS)-induced endotoxemia on fetal baroreceptor sensitivity in preterm fetal sheep.
UNASSIGNED: The changes in fetal baroreceptor sensitivity were measured in seven chronically instrumented preterm fetal sheep. Fetal baroreceptor sensitivity was measured in three phases: (A) control phase, defined as the 24 h before the first injection of LPS; (B) acute phase, defined as the 24 h between the first and second injections of LPS; and (C) fetal acidosis phase, defined as the time from the second LPS injection until intrauterine fetal death. Histological examinations of the fetal membrane and umbilical cord were also conducted.
UNASSIGNED: Each fetus developed metabolic acidosis after the second injection of LPS. The fetuses died 24.7 (SD = 6.1) hours after the second injection of LPS. Both the umbilical cord and fetal membranes showed histological evidence of severe inflammation. In total, 163 fetal baroreceptor measurements were performed in this experiment (A, n = 77 times; B, n = 60 times; C, n = 26 times). Fetal baroreceptor sensitivity showed significant differences in all three phases (A: 2.7 [SD = 0.2]; B: 2.5 [SD = 0.2]; and C: 1.5 [SD = 0.2]). Post hoc tests showed that baroreceptor sensitivity in the acidosis phase had decreased significantly compared to that in the control and acute phases (p<.001 and p=.002, respectively).
UNASSIGNED: Fetal baroreceptor sensitivity decreased during fetal acidosis induced by LPSs.
UNASSIGNED: The changes in fetal baroreceptor sensitivity were measured in seven chronically instrumented preterm fetal sheep. Fetal baroreceptor sensitivity was measured in three phases: (A) control phase, defined as the 24 h before the first injection of LPS; (B) acute phase, defined as the 24 h between the first and second injections of LPS; and (C) fetal acidosis phase, defined as the time from the second LPS injection until intrauterine fetal death. Histological examinations of the fetal membrane and umbilical cord were also conducted.
UNASSIGNED: Each fetus developed metabolic acidosis after the second injection of LPS. The fetuses died 24.7 (SD = 6.1) hours after the second injection of LPS. Both the umbilical cord and fetal membranes showed histological evidence of severe inflammation. In total, 163 fetal baroreceptor measurements were performed in this experiment (A, n = 77 times; B, n = 60 times; C, n = 26 times). Fetal baroreceptor sensitivity showed significant differences in all three phases (A: 2.7 [SD = 0.2]; B: 2.5 [SD = 0.2]; and C: 1.5 [SD = 0.2]). Post hoc tests showed that baroreceptor sensitivity in the acidosis phase had decreased significantly compared to that in the control and acute phases (p<.001 and p=.002, respectively).
UNASSIGNED: Fetal baroreceptor sensitivity decreased during fetal acidosis induced by LPSs.
摘要：
未经证实：Baroreflex是一种减缓胎儿心率的调节机制。本研究旨在探讨脂多糖(LPS)诱导的内毒素血症对早产胎羊胎儿压力感受器敏感性的影响。
UNASSIGNED：在7只长期使用仪器的早产羊中测量了胎儿压力感受器敏感性的变化。在三个阶段测量胎儿压力感受器敏感性：（A）对照阶段，定义为第一次注射LPS前24小时；(B)急性期，定义为第一次和第二次注射LPS之间的24小时；和（C）胎儿酸中毒期，定义为从第二次LPS注射到胎儿宫内死亡的时间。还进行了胎膜和脐带的组织学检查。
未经证实：每个胎儿在第二次注射LPS后出现代谢性酸中毒。胎儿在第二次注射LPS后24.7小时死亡(SD=6.1)。脐带和胎膜均显示出严重炎症的组织学证据。总的来说,在本实验中进行了163次胎儿压力感受器测量(A，n=77倍；B，n=60倍；C，n=26倍)。胎儿压力感受器敏感性在所有三个阶段均显示出显着差异（A：2.7[SD=0.2]；B：2.5[SD=0.2]；C：1.5[SD=0.2]）。事后测试表明，与对照组和急性期相比，酸中毒期的压力感受器敏感性显着下降（分别为p<.001和p=.002）。
UnASSIGNED：LPS诱发的胎儿酸中毒期间胎儿压力感受器敏感性降低。
UNASSIGNED：在7只长期使用仪器的早产羊中测量了胎儿压力感受器敏感性的变化。在三个阶段测量胎儿压力感受器敏感性：（A）对照阶段，定义为第一次注射LPS前24小时；(B)急性期，定义为第一次和第二次注射LPS之间的24小时；和（C）胎儿酸中毒期，定义为从第二次LPS注射到胎儿宫内死亡的时间。还进行了胎膜和脐带的组织学检查。
未经证实：每个胎儿在第二次注射LPS后出现代谢性酸中毒。胎儿在第二次注射LPS后24.7小时死亡(SD=6.1)。脐带和胎膜均显示出严重炎症的组织学证据。总的来说,在本实验中进行了163次胎儿压力感受器测量(A，n=77倍；B，n=60倍；C，n=26倍)。胎儿压力感受器敏感性在所有三个阶段均显示出显着差异（A：2.7[SD=0.2]；B：2.5[SD=0.2]；C：1.5[SD=0.2]）。事后测试表明，与对照组和急性期相比，酸中毒期的压力感受器敏感性显着下降（分别为p<.001和p=.002）。
UnASSIGNED：LPS诱发的胎儿酸中毒期间胎儿压力感受器敏感性降低。
