BETA-ENDORPHIN IMMUNOREACTIVITY LEVELS IN CSF AFTER LARYNGEAL CHEMOREFLEX ACTIVATION CORRELATE WITH APNEA DURATION IN PIGLETS

The activation of the laryngeal chemoreflex may be a pathogenic mechan ism in apnoea, apparent life threatening events, and SIDS. Infants wit h apnoea and increased levels of beta-endorphin immunoreactivity in CS F have been successfully treated with naloxone. Beta-endorphin may ind uce respiratory depression, and naloxone is a beta-endorphin antagonis t. We therefore wanted to measure beta-endorphin levels in CSF before and after the chemoreflex induced apnoea. This study includes 13 pigle ts, 5-10 days of age, treated with and without naloxone. Respiration, blood pressure, and heart rate were monitored. CSF was sampled before and after the laryngeal chemoreflex induced apnoea. We found a shorter duration of apnoea in the piglets which had received naloxone than in those which did not (p = 0.02). The beta-endorphin immunoreactivity l evels in CSF increased after apnoea, and the increased levels correlat ed positively with the duration of the apnoea in the piglets which had not received naloxone (r = 0.94, p = 0.02), bur nor in those pretreat ed with naloxone (r = 0.1, p = 0.8). The median amount of beta-endorph in immunoreactivity in CSF after apnoea in the naloxone-treated piglet s was not significantly different from that in the non-treated piglets : 615 +/- 589 (n = 7) fmol/ml CSF and 984 +/- 851 (n = 6) fmol/ml CSF, respectively. The beta-endorphin immunoreactivity levels measured bef ore the apnoea were less than 4.3 fmol/ml CSF. Conclusion: The larynge al chemoreflex induced apnoea may possible be partly mediated by beta- endorphin.