STUDY ON THE PATHOPHYSIOLOGY OF FETAL DISTRESS -ESPECIALLY ON THE MECHANISM OF REDISTRIBUTION OF FETAL CIRCULATION-

本研究旨在探讨胎儿循环再分配的机制。动物实验采用动静脉体外膜氧合体外培养系统对山羊胎儿进行体外培养。评估胎儿PaCO2变化对循环功能的影响。呼吸亢进是由体外循环系统膜氧合器的气体流量逐渐减少引起的。胎儿颈动脉血流量因呼吸亢进而明显增加。虽然在轻度呼吸亢进阶段心率略有增加，但在所有病例中，重度呼吸亢进都会引起心动过缓。我们发现，脑血流量增加是由于高呼吸对血管系统的直接影响，但外周化学感受器对高呼吸的反应似乎在慢性刺激下减弱。本文研究了胎胎盘循环变化对早产儿中枢神经系统的影响。采用5只山羊胚胎在体外培养系统中进行了引起中枢神经系统缺血再灌注的应激实验。5例胎儿中有3例可在脑深部白质中观察到凝血性坏死，对应于脑室周围白质软化的初始病变。我们还发现胎胎盘循环紊乱可能会对早产儿的中枢神经系统造成不良影响。

The aim of study was to study about the mechanisms of redistribution of fetal circulation. Animal experiments were performed with goat fetuses which were incubated using an extrauterine incubation system with arteriovenous extracorporeal membrane oxygenation. The effects of changes in fetal PaCO2 on circulatory functions were assessed. The hypercapnea was induced gradually by decreasing the flow of gas to the membrane oxygenator located on the extracorporeal circulation system. The fetal carotid arterial blood flow increased significantly due to the hypercapnea. Although a slight increase was observed in the heart rate at the mild hypercapnea stage, severe hypercapnea induced bradycardia in all cases. We found that cerebral blood flow increased due to hypercapnea's direct effect on the vascular system, but the response of the peripheral chemoreceptor to hypercapnea seemed to be attenuated in chronic stimulation.The effects of changes in fetoplacental circulation on the central nervous system (CNS) of premature fetuses were studies. Stress experiments to cause ischemia and reperfusion to the CNS were performed with 5 goat fetuses maintained in the extrauterine incubation system. Coagulation necrosis, which correspond to an initial lesion of periventricular leucomalacia could be observed in deep white matter of the brain in 3 out of 5 fetuses. We also found that disturbance of feto-placental circulation may cause an adverse effect in the CNS of premature fetuses.