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Beta-endorphin immunoreactivity levels in CSF after laryngeal chemoreflex activation correlate with apnoea duration
H Storm1, L Stoltenberg, O D Saugstad
1Department of Paediatric Research, National Hospital, Oslo, Norway.
Insights
The laryngeal chemoreflex may cause apnoea, potentially mediated by beta-endorphin. Naloxone, a beta-endorphin antagonist, shortened apnoea duration in piglets, suggesting a role for beta-endorphin in this reflex.
Area of Science:
- Neuroscience
- Respiratory Physiology
- Neonatal Medicine
Background:
- The laryngeal chemoreflex is implicated in apnoea, apparent life-threatening events, and Sudden Infant Death Syndrome (SIDS).
- Elevated beta-endorphin levels in cerebrospinal fluid (CSF) have been observed in infants with apnoea.
- Naloxone, a beta-endorphin antagonist, has shown success in treating such infants, suggesting beta-endorphin's role in respiratory depression.
Purpose of the Study:
- To investigate the role of beta-endorphin in laryngeal chemoreflex-induced apnoea.
- To measure beta-endorphin levels in CSF before and after apnoea triggered by the laryngeal chemoreflex.
- To assess the effect of naloxone on apnoea duration and beta-endorphin levels.
Main Methods:
- A study involving 13 piglets aged 5-10 days.
- Administration of naloxone or placebo to piglets.
- Monitoring of respiration, blood pressure, and heart rate.
- CSF sampling before and after induced apnoea.
- Measurement of beta-endorphin immunoreactivity in CSF.
Main Results:
- Piglets treated with naloxone experienced a significantly shorter duration of apnoea compared to controls (p = 0.02).
- Beta-endorphin immunoreactivity levels in CSF increased after apnoea.
- Increased beta-endorphin levels correlated positively with apnoea duration in non-naloxone treated piglets (r = 0.94, p = 0.02).
- This correlation was not observed in naloxone-pretreated piglets (r = 0.1, p = 0.8).
Conclusions:
- Laryngeal chemoreflex-induced apnoea may be partly mediated by beta-endorphin.
- Naloxone administration can reduce the duration of apnoea, supporting the involvement of beta-endorphin.
- These findings suggest a potential therapeutic target for conditions involving apnoea and respiratory depression.
Unlabelled:
The activation of the laryngeal chemoreflex may be a pathogenic mechanism in apnoea, apparent life threatening events, and SIDS. Infants with apnoea and increased levels of beta-endorphin immunoreactivity in CSF have been successfully treated with naloxone. Beta-endorphin may induce respiratory depression, and naloxone is a beta-endorphin antagonist. We therefore wanted to measure beta-endorphin levels in CSF before and after the chemoreflex induced apnoea. This study includes 13 piglets, 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 levels in CSF increased after apnoea, and the increased levels correlated positively with the duration of the apnoea in the piglets which had not received naloxone (r = 0.94, p = 0.02), but not in those pretreated with naloxone (r = 0.1, p = 0.8). The median amount of beta-endorphin immunoreactivity in CSF after apnoea in the naloxone-treated piglets 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 before the apnoea were less than 4.3 fmol/ml CSF.
Conclusion:
The laryngeal chemoreflex induced apnoea may possible be partly mediated by beta-endorphin.