1. Intravenous injections of lobeline HCl into twenty‐six normal young male human volunteers produced sensations of choking, pressure or fumes in the throat and upper chest at a mean threshold dose of 12 micrograms kg‐1. 2. Reflex changes in breathing pattern usually appeared just before the sensations. Increasing the dose of lobeline increased the intensity of the sensations gradually until a dry cough appeared at a mean threshold dose of 24.3 micrograms kg‐1. At these doses there was a mean difference of 0.3s in the latencies for sensation and respiratory reflex; in four subjects there was no difference at all. 3. In cats anaesthetized with 35 mg kg‐1 sodium pentobarbitone, injecting 25‐67 micrograms kg‐1 lobeline into the right atrium sensitized thirteen out of seventeen rapidly adapting receptors (RARs). In three out of four cats lobeline had no excitatory effect on the RARs in the absence of normal activity (i.e. when it was injected while artificial respiration was suspended), but on restarting the respiration the activity increased greatly. After injecting lobeline, the activity increased during inflation or deflation or in both phases of the respiratory cycle. It also increased greatly during deflation produced by suction of air from the lungs after lobeline. Such presumed increased activity in the RARs of man produced by forced expiration to residual volume at the time lobeline‐induced sensations were expected did not enhance the sensations in any subject. 4. In all the subjects tested, forced expiration alone, which should stimulate RARs, never produced a dry cough or sensations similar to those produced by lobeline.(ABSTRACT TRUNCATED AT 250 WORDS)

The technique of ABR testing was applied to 25 infants with neonatal hyperbilirubinemia at levels exceeding that for exchange transfusion, in an attempt to study potential influence of bilirubin toxicity on the auditory brainstem pathway. The test was performed at a mean conceptional age of 40.4 +/- 0.6 weeks just after discharge. Twenty normal term neonates of comparable birth weights and conceptional ages, who had no hyperbilirubinemia, were also examined for comparison. Fifty six percent (n = 14) of the hyperbilirubinemic neonates had some abnormality in the ABR pattern, the major one being a transient increase in the threshold of wave V (7, fail-30; 5, fail-45). Wave V, however, was consistently present at 30 dBnHL click stimulus in all the normal neonates (pass-30; normal threshold). Further, mean ABR latencies (wave III, V) and 1-V interpeak latency (brainstem conduction time) were significantly prolonged in jaundiced neonates as compared with controls (P less than 0.01). ABR changes were strongly correlated with the serum bilirubin levels (P less than 0.001). On follow up retesting at 3 months, however, all infants were found to have normal ABR latencies and threshold. Neonatal jaundice was associated with significant transient aberrations of ABR, suggestive of a transient toxic brainstem encephalopathy.

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