Cardiorespiratory failure is a major concern in the care of sick infants. Such failure may result from collapse of either respiratory or circulatory mechanisms, or from loss of proper coordination of these two systems which sustain metabolic gas transport. Our objective is to determine if altered function of neural mechanisms either near the ventral medullary surface (VMS) or in the carotid sinus area might predispose infants to cardiorespiratory failure by disrupting cardiorespiratory control mechanisms. Anesthetized neonatal kittens will be used as an animal model in the two sets of experiments. First we will assess the involvement of particular areas of the VMS in cardiorespiratory control at rest by locally blocking neuronal function using a temperature-controlled probe. We will test similarly the effects of carotid sinus nerve (CSN) section. Then we will determine the cardiorespiratory responses to two systemic stresses, hypercapnia and exercise, and ascertain the kind and degree of disruption of these responses caused by local cooling on the VMS and by CSN section. In the hypercapnia studies (paralyzed, ventilated animals) phrenic and hypoglossal nerve signals, heart rate, and blood pressure will be measured. In the exercise studies (spontaneously breathing animals; electrical stimulation of leg muscle) ventilation, cardiac output, heart rate and blood pressure will be measured. Both absolute responses and responses relative to phrenic nerve responses (to examine cardiorespiratory coordination) will be determined. These studies will locate VMS sites at which altered neuronal function may soon lead to cardiorespiratory failure because of their profound actions on cardiorespiratory control. They will also identify sites at which neuronal dysfunction may moderately alter cardiorespiratory control. The long-term implications of such alterations to the well-being of the animal might well be the subject of subsequent studies.