Fetal chemoreception: a developing story.

Abstract

The central and peripheral chemoreceptors are critical to the efficient uptake and delivery of oxygen and the removal of carbon dioxide after birth. However, the importance and activity of fetal chemoreception has been questioned, since oxygen uptake and carbon dioxide removal are not regulated in the lungs in the fetus. Early studies suggested that chemotransduction-the conversion of a chemical stimulus to cardiovascular and ventilatory responses via the integration of chemoreceptor stimulation, neural afferent activity and neurohormonal effector mechanisms-was immature in its individual components or their interaction. However, it now appears that the chemoreceptor cascade is structurally and functionally intact in the late-term fetus, and responds actively to normal and other chemical stimuli. The differences between fetal and postnatal chemotransduction appear to be primarily dependent on the central inhibition of the ventilatory response, the inhibitory area being localized to the lateral pons. It appears to be mediated in part by a placental factor which is removed at birth, allowing for the expression of the ventilatory response. The suppression of this response is also responsible for the difference in the heart rate response: the postnatal tachycardia is caused by the lung inflation reflex; when abolished, bradycardia is seen, just as in the fetus. Despite the suppression of the ventilatory component of chemoreception, the fetal carotid chemoreceptor is more important than the aortic, even though it has been considered to be more important to ventilatory than to cardiovascular stability. This review discusses current knowledge of the various components of the mature chemoreceptor cascade, and presents the fetal story within that framework.