The St. Paul Infant Apnea Program. An approach to the evaluation and treatment of infantile apnea.
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Apnea↗
Biomedical subjects
C Reardon
Publications and source records attributed to C Reardon.
Hypercarbic ventilatory responses of infants at risk for SIDS.
We examined the hypercarbic ventilatory responses (HVR) of 143 infants at risk for sudden infant death syndrome (SIDS) and 34 normal control infants. Sixty-five of the at-risk infants had experienced apparent life-threatening events (ALTE), and 78 were siblings of SIDS victims. Twenty-three (35%) of the ALTE infants experienced subsequent apnea; one died of SIDS. Seven (9%) of the SIDS siblings experienced subsequent apnea; two ultimately died of SIDS. In the HVR studies, we measured tidal volume (VT), minute ventilation (VE), frequency of breathing (f), and end-tidal PCO2 (PETCO2) at rest and while breathing 2% and 4% CO2. Mean HVR vales for the ALTE, sibling, and control groups were all similar. The mean HVR values for those at-risk infants who experienced subsequent apnea were not different from those who did not experience subsequent apnea. However, those infants experiencing subsequent apnea had higher mean VT/kg values (P less than 0.01) and lower mean PETCO2 values (P less than 0.001) than those who did not. The SIDS siblings had significantly lower resting VT/kg values than either the near-miss infants or normal controls (P less than 0.01). We did not find depressed HVR values in infants at risk for SIDS. On the contrary, those infants who experienced subsequent apnea had evidence suggesting relative hyperventilation. SIDS siblings had evidence suggesting relative hypoventilation. These findings are interesting and thought-provoking. However, HVR studies do not appear to be sensitive, specific, or appropriate for the general screening of infants at risk for SIDS.
Apnea↗
Differential transmural distribution of gene expression for collagen types I and III proximal to aortic coarctation in the rabbit.
To assess the effects on the biosynthesis of collagen types I and III associated with an acute increase in blood pressure, we established a mid-thoracic aortic coarctation in the rabbit and studied gene expression and protein accumulation of these collagen types proximal to the stenosis 1, 3 and 7 days and 2, 4 and 8 weeks after coarctation. The mRNA level of type I collagen pro-alpha2(I) was maximal at 3 days and returned to normal at 4 weeks. mRNA of pro-alpha2(I) was localized mainly in the outer media, adventitia and intima. Accumulation of type I collagen and its precursors was increased by 3 days, peaked at 4 weeks, and decreased toward normal by 8 weeks, corresponding to the distribution of pro-alpha2(I) mRNA. Gene expression for pro-alpha1(III) was similar to that of pro-alpha2(I) but was distributed throughout the media. We conclude that the mechanical stresses associated with an acutely induced alteration in pressure initiate rapid gene expression for collagen types I and III in the aortic wall. The response for collagen type I, predominantly in the outer media and adventitia, suggests that these regions play an immediate role in the resistance to excessive dilatation of the aorta. The diffuse response for collagen type III in the media suggests participation in a more extensive remodeling response associated with the reinforcement and reorganization of the musculo-elastic fascicles.
Animals↗