Abstract：
OBJECTIVE: We evaluated fetal cardiovascular physiology and mode of cardiac failure in premature miniature piglets on a pumped artificial placenta (AP) circuit.
METHODS: Fetal pigs were cannulated via the umbilical vessels and transitioned to an AP circuit composed of a centrifugal pump and neonatal oxygenator and maintained in a fluid-filled biobag. Echocardiographic studies were conducted to measure ventricular function, umbilical blood flow, and fluid status. In utero scans were used as control data.
RESULTS: AP fetuses (n = 13; 102±4d gestational age [term 115d]; 616 ± 139 g [g]; survival 46.4 ± 46.8 h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24 h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24 h.
CONCLUSIONS: Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.
METHODS: Fetal pigs were cannulated via the umbilical vessels and transitioned to an AP circuit composed of a centrifugal pump and neonatal oxygenator and maintained in a fluid-filled biobag. Echocardiographic studies were conducted to measure ventricular function, umbilical blood flow, and fluid status. In utero scans were used as control data.
RESULTS: AP fetuses (n = 13; 102±4d gestational age [term 115d]; 616 ± 139 g [g]; survival 46.4 ± 46.8 h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24 h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24 h.
CONCLUSIONS: Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.
摘要：
目的：我们评估了人工胎盘（AP）回路中早产小型仔猪的胎儿心血管生理和心力衰竭模式。
方法：胎猪通过脐带血管插管，过渡到由离心泵和新生儿充氧器组成的AP回路，并保持在充满液体的生物袋中。进行超声心动图研究以测量心室功能，脐血流,和液体状态。子宫内扫描用作对照数据。
结果：AP胎儿（n=13；胎龄102±4d[足月115d]；616±139g[g]；存活46.4±46.8h）为心动过速和高血压，最初为生理上回路血流。观察到心肌壁厚度增加。所有仔猪均存在胎儿水肿的迹象。过渡到回路后，左心室（LV）的整体纵向应变（GLS）测量值增加。与子宫内测量相比，右心室（RV）和LV应变率在AP支持期间早期降低，但在实验结束时恢复。支持>24小时的胎儿与子宫内对照具有相似的RVGLS，并且与仅存活24小时的仔猪相比，GLS显着更高。
结论：泵支持的AP电路上的胎儿后负荷增加，以及AP和全身循环之间的血流重新分布，与舒张末期充盈压升高有关。这导致心力衰竭和水肿。这些早产胎儿不能容忍与连接到当前AP电路相关的血液动力学变化。为了更好地模拟天然胎盘的生理，并保持正常的胎儿心血管生理，需要进一步优化电路。
方法：胎猪通过脐带血管插管，过渡到由离心泵和新生儿充氧器组成的AP回路，并保持在充满液体的生物袋中。进行超声心动图研究以测量心室功能，脐血流,和液体状态。子宫内扫描用作对照数据。
结果：AP胎儿（n=13；胎龄102±4d[足月115d]；616±139g[g]；存活46.4±46.8h）为心动过速和高血压，最初为生理上回路血流。观察到心肌壁厚度增加。所有仔猪均存在胎儿水肿的迹象。过渡到回路后，左心室（LV）的整体纵向应变（GLS）测量值增加。与子宫内测量相比，右心室（RV）和LV应变率在AP支持期间早期降低，但在实验结束时恢复。支持>24小时的胎儿与子宫内对照具有相似的RVGLS，并且与仅存活24小时的仔猪相比，GLS显着更高。
结论：泵支持的AP电路上的胎儿后负荷增加，以及AP和全身循环之间的血流重新分布，与舒张末期充盈压升高有关。这导致心力衰竭和水肿。这些早产胎儿不能容忍与连接到当前AP电路相关的血液动力学变化。为了更好地模拟天然胎盘的生理，并保持正常的胎儿心血管生理，需要进一步优化电路。
