Development of the neonatal rat as a model for sudden infant death syndrome: Cardiorespiratory effects of ethanol

The current pathogenesis of Sudden Infant Death Syndrome (SIDS) is unknown. Elevated endogenous ethanol production by gastrointestinal yeast has been proposed as a possible mechanism for SIDS. To investigate the role of ethanol in SIDS, three studies were undertaken. In the first study, transcutaneous blood gas technology was evaluated for repeated monitoring of arterial blood gases. The second study identified the cardiorespiratory responses to inhaled CO₂ challenge in juvenile rats, to determine the age corresponding to the age range of peak incidence of SIDS in human infants. Finally, utilizing the optimized juvenile rat model, the cardiorespiratory responses to ethanol and CO₂ challenge were examined. The following observations were made: (1) A transcutaneous probe temperature of 44.5°C provided the best correlation with arterial blood gas levels, though extended skin contact caused thermal burns. (2) The transcutaneous probe could be maintained in place for 3 hours utilizing probe temperatures of 44°C (adults) and 42°C (juveniles) without producing thermal burns, while providing modest correlation between arterial and transcutaneous CO₂. (3) On post embryonic (PE) days 30 & 31, pups exhibited higher heart rates and responded more slowly to and recovered slower from CO₂ challenge versus older ages tested. (4) On PE days 30 and 31, pup respiratory rate was unchanged in response to 10% inhaled CO₂ challenge, whereas older animals decreased respiratory rate approximately 38%. (5) Simultaneous challenge with ethanol and CO₂ inconsistently elevated transcutaneous CO₂ to levels over those observed for CO₂ challenge alone. (6) Respiratory responses to modest levels of CO₂ and ethanol were ineffective in lowering transcutaneous CO₂ levels. (7) Ethanol alone elevated transcutaneous CO₂ levels without a concurrent depression of respiration.; In summary, transcutaneous blood gas methodology provides an effective means of serially monitoring changes in arterial CO₂ concentrations in small rodents. Juvenile rats of PE age 29–31 days (≈post natal days 8–10) provide a useful rodent model for future investigations into the pathogenesis of SIDS. Finally, low blood ethanol concentrations may exacerbate the effects of inhaled CO₂ and should be further investigated as a mechanism for the pathogenesis of SIDS.