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Maternal smoking increases the risk of the sudden infant death syndrome (SIDS) 2-4-fold. The mechanism is unknown but may be related to hypoxia responses. Recovery from hypoxic apnea by young mammals depends on gasping and bradycardia. We asked whether prenatal nicotine exposure, reported to reduce hypoxic survival in 2 day old rat pups, acted by impairing gasping or bradycardia. Pregnant rats were infused throughout gestation and 1 week postnatally with nicotine tartrate (NIC) 12 mg/kg per day or saline (CON). Maternal plasma nicotine was 134.4 +/- 42 ng/ml, significantly reducing pup body weight. Pups at 3-28 days were exposed to anoxia (97% N2/3% CO2) until gasping ceased, while breathing and heart rate were recorded. NIC and CON groups were not significantly different at any age, in baseline heart rate, respiratory rate, the time course for bradycardia, time to gasp onset, duration of gasping, or number of gasps, although most of these variables declined significantly with age. We conclude that responses to anoxia are not affected by prenatal high-dose nicotine.

In experiments to assess its value in the study of fetal arterial chemoreceptor reflexes, doxapram (0.5 - 2 mg i.a.) given to unanaesthetized fetal lambs in utero in low voltage electrocortical activity stimulated fetal breathing in 73% of trials. The response began within a few seconds and lasted up to 5 min. This response to doxapram was present in intact or mid-collicular brainstem transected fetuses and after bilateral section of the carotid sinus nerves and cervical vagosympathetic trunks (denervation). In intact and brainstem transected fetuses, doxapram injections were followed by a modest rise in arterial pressure and a small fall in heart rate. After denervation the rise in arterial pressure was fourfold and the heart rate increased. Electrocortical activity and limb movements were not affected in any group of lambs, and fetal breathing was not induced during isocapnic hypoxia. It is concluded that doxapram stimulates fetal breathing by a central action below the pons, and that it can therefore not be used to study peripheral arterial chemoreceptor function in utero.

Oxygen consumption (VO2), heart rate, body temperature, and stride frequency were measured in Marabou storks walking on a treadmill at a range of speeds and gradients. VO2 was linearly related to speed at gradients up to 11 degrees and speeds up to 1.4 m . s-1, and the slope of the VO2/speed regression increased with the treadmill angle up to 9 degrees. At 11 degrees there was a fall in the slope. Analysis indicates the cost of horizontal movement of about 1.1 ml O2 . m-1 (mean wt 4.5 kg). The cost of vertical movement is 7.13 ml O2 . m-1 and the efficiency about 30%. Maximum recorded VO2 was about five times resting, and there was no indication of an oxygen debt at any value for VO2. Heart rate was directly proportional to vO2 over the range studied, and at high heart rates successive cardiac cycles overlapped. Body temperature did not change significantly during exercise. Stride frequency was linearly related to walking speed but with a nonzero intercept so that stride length changed with speed, but there was no observed change in gait with speed. These data are discussed in comparison with published scaling equations and with data from mammals.