James E Fewell and Chunfen Zhang
Failure to auto resuscitate from hypoxic-induced apnea by gasping has been suggested to play a role in sudden infant death. Little is known, however, about factors that influence gasping and its ability to sustain life during acute hypoxia in the newborn. Given that cardiac dysfunction and circulatory failure likely play a role in mediating auto resuscitation failure, the present experiments were carried out on 206 rat pups to investigate the influence of heart glycogen -- a metabolic substrate that supports cardiac function during acute hypoxia -- on the time to last gasp (TLG) during a single period of unrelenting hypoxia, and on the ability to auto resuscitate (AR) from primary apnea during repeated hypoxic challenge. On days 1-2, 5-6, and 10-11 postpartum, each pup was placed into a temperature controlled chamber regulated to 37 ± 1° C and exposed either to a single period of unrelenting hypoxia produced by breathing an anoxic gas mixture (97% N2 and 3% CO2) and the TLG determined, or repeatedly exposed to hypoxia and the ability to AR from primary apnea determined. Pups were studied with normal heart glycogen concentrations and with decreased heart glycogen concentrations effected by prior isoproterenol-induced transient tachycardia. A decrease in heart glycogen concentration did not significantly alter the TLG upon exposure to a single period of unrelenting hypoxia. It did, however, significantly decrease the number of successful AR from primary apnea during repeated hypoxic exposures in 1-2, 5-6, and 10-11 day-old pups. Thus, heart glycogen concentration influences the ability of rat pups to AR from hypoxic-induced primary apnea during early postnatal life.
