The area postrema of newborn swine is activated by hypercapnia: relevance to sudden infant death syndrome?

This study was performed to investigate a role of the neonatal area postrema (AP) in the chemoreceptor response to hypercapnia which is defective in sudden infant death syndrome (SIDS). AP responses to CO2 inhalation were monitored in 1 to 5 week old piglets by mapping neurons that were induced to express the c-fos gene product, Fos--a marker of functional activation. Interpretive confounds were minimized by controlling for hypoxia, the effects of surgical procedures and ambient environmental stressors on neuronal activity (c-fos expression). The AP demonstrated a powerful and reproducible response in neonatal swine breathing 10% CO2 for 1 h. Intensely immunolabeled nuclei were detected throughout the longitudinal extent of the circumventricular organ, and were especially heavily concentrated at rostral levels proximal to obex. Quantitative analysis verified statistically significant increases in numbers of cells that were induced to express Fos-like immunoreactivity (FLI) in the AP of CO2- stimulated piglets as compared to control groups. No detectable age-related differences were observed in AP response patterns. Conclusions. The AP responds to hypercapnic stress in the newborn piglet. A mature circumventricular organ response in the neonate may be crucial in defending against common environmental stressors, such as nicotine exposure--an emetic agent acting via the AP and a major risk factor in SIDS. Hence, a defect of the AP or its network may underlie a loss of state-dependent controls over cardiopulmonary reflex function in SIDS.

Development of a swine animal model for the study of sudden infant death syndrome.

An animal model with selective cardiac autonomic denervation was developed in neonatal swine for the purpose of future studies concerning the possible role of abnormal cardiac innervation in the etiology of sudden infant death syndrome. Twenty-six 4- to 8-day old piglets were randomly assigned to one of the following treatment groups: right stellate ganglionectomy (RSG), left stellate ganglionectomy (LSG), right cardiac vagotomy (RCV), and sham-operated control group. Piglets were anesthetized with Saffan and mechanically ventilated on room air. The thoracic wall was opened, and the sternum was divided, permitting exposure of pleura, heart, and lungs. After completion of one of these operative procedures, the thoracic wall was closed in layers. On successful recovery from anesthesia and extubation, piglets were returned to their sows. Postoperative administration of antibiotics was performed during the first week. Electrocardiograms were recorded once a week over an 8-week period. The sham-operated control group had a postnatal increase in QTc and decrease in heart rate. The RSG group had significantly longer QTc than the sham-operated control group QTc, whereas the RCV group had significantly shorter QTc interval than sham-operated controls. Surgical complications caused the death of two piglets (hemorrhage in one and aspiration in the other), infection caused the death of one piglet 2 weeks after surgery, and three died of unknown causes (one from the RSG group and two from the RCV group). The cause of death for these three animals could not be determined (necropsy was not revealing) because they were not monitored at the time of their demise.(ABSTRACT TRUNCATED AT 250 WORDS)