ABSTRACT
Physiology teaches us the wisdom of creating harmony and balance not only at the level of cells, tissues, and organs, but also in ourselves, and in relation to the world and environment where we live. Even in the fascinating world of intrauterine life, many fetal organ systems function in order to develop and maintain homeostasis. Only recently have we come to understand just how significantly our life outside the uterus is determined by our 40 or so weeks within it. There is a growing pool of evidence that many severe neurologic disorders, as well as the minimal cerebral dysfunctions, originate from the intrauterine rather than the perinatal or postnatal period. 1,2 Although developmental processes are genetically determined, only in the optimal intrauterine environment can the fetus reach its full genetic potential. Therefore, one should not be surprised by the diversity of the fetal mechanisms that have evolved to protect and defend the interior milieu. For example, the physiologic control mechanisms that are activated in the fetal organism in response to hypoxia include the cardiovascular, endocrine, and metabolic systems. As is well known, fetal cardiovascular adaptation to hypoxia is manifested by the redistribution of blood flow primarily toward the fetal brain. However, our latest investigations have shown that severe brain damage can develop despite the fetal blood flow redistribution and increased brain perfusion3–5 (and personal unpublished data). These results indicate that the border between physiologic adaptation and pathophysiologic processes is extremely fragile and needs to be determined precisely in order to prevent brain damage, as well as lesions in other organ systems. Fortunately, our preliminary results indicate that in the case of chronic fetal hypoxia, this border can be determined by the use of a new vascular score, the hypoxia index. It is our belief that this new vascular score could represent a significant advance in the prevention of hypoxic brain damage, which is one of the most frequent causes of perinatal morbidity and mortality 6 (and personal unpublished data).
