Naltrexone therapy of apnea in children with elevated cerebrospinal fluid β‐endorphin

Myer, Edwin C.; Morris, Dale L.; Brase, David A.; Dewey, William L.; Zimmerman, Andrew W.

doi:10.1002/ana.410270112

Cited by 41 publications

(18 citation statements)

References 27 publications

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“…Children with apnoea and increased levels of BENDI in CSF have been successfully treated with the opioid antagonist, naltrexone [29]. Furthermore, certain types of apnoea can be triggered by emotional stimuli such as fear, anger and pain [39].…”

Section: Introductionmentioning

confidence: 99%

Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death

Storm

Rognum²,

Reichelt

1994

Eur J Pediatr

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In nucleus tractus solitarius (NTS) beta-endorphin (BEND) induces bradycardia and respiratory depression which have been reported to precede death in sudden infant death (SID). Of SID victims, 50% have elevated levels of beta-endorphin immunoreactivity (BENDI) in the cerebrospinal fluid (CSF), and 50% had undetectable levels. We therefore investigated the relationship of BENDI in the CSF to BENDI levels in the NTS area. This study included SID victims (CSF from n = 47, brain stem from n = 16), borderline SID victims (CSF and brain stem from n = 2), sudden death in childhood (CSF and brain stem from n = 1), and controls (CSF from n = 32, brain stem from n = 11). BEND in CSF and NTS area, after extraction, was measured by radioimmunoassay. High performance liquid chromatography was used for closer identification of BENDI. We found that the SID victims divided into two subpopulations, one having a relatively high BENDI level in CSF and one having no detectable level (P < 0.01). Furthermore, an inverse relationship was found between BENDI level in CSF and BENDI level in NTS area in the SID victims (P < 0.05). We conclude that increased BENDI level in CSF is associated with low BENDI level in the NTS area in 50% of SID victims. The low BENDI level in the NTS area may be due to increased release of BEND.

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Section: Introductionmentioning

confidence: 99%

Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death

Storm

Rognum²,

Reichelt

1994

Eur J Pediatr

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“…Children suffering from apnoeas, siblings of SID victims, and 50% of SID victims have increased levels of beta-endorphin immunoreactivity (BENDI) in CSF [12,26]. Children with apnoeas and an increased level of BENDI in CSF have been successfully treated with the opioid antagonist, naltrexone [13].…”

Section: Introductionmentioning

confidence: 99%

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Storm

Rognum²,

Saugstad

et al. 1993

Eur J Pediatr

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Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n = 19) and controls (n = 18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P < 0.01); one with undetectable levels (< 4.3 fmol/ml) (n = 10) and one with high levels (160-400 fmol/ml) (n = 9). In the SID subpopulation with high levels of BENDI in CSF, we found a correlation between BENDI in CSF and HX in VH (r = 0.92). Control infants who died a stressful death, such as during heart operations (n = 2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n = 11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…This lack of additive effects, and the similarity in response to nicotine and endotoxin might indicate the involvement of a final common pathway: Investigators at our institute have earlier demonstrated that CSF ß-endorphin prolongs apneas by laryngeal chemoreflex in piglets [28,29]. Infants with severe apnea, ALTE, and siblings of SIDS victims have higher levels of CSF ß-endorphin [30][31][32][33], although not in the newborn [34]. Increased CSF ß-endorphin is also found post-mortem in some SIDS victims [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Prolonged Apneas and Hypoxia Mediated by Nicotine and Endotoxin in Piglets

et al. 2002

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Objective: Infections and maternal smoking are risk factors for SIDS, and toxins from common bacteria have been proposed as a causative link between infections and SIDS. Nicotine can be transferred in significant amounts postnatally to the infant through environmental tobacco smoke or maternal smoking before nursing. We investigated the acute effects of nicotine and endotoxin on repeated apnea by laryngeal reflex stimulation and the following autoresuscitation. Design: Thirty-four 1-week-old (± 1 day) piglets were sedated and randomized to 1 of 4 pretreatment groups: (1) 1 µg endotoxin i.v./kg; (2) 5 µg nicotine i.v./kg; (3) 1 µg endotoxin i.v./kg and 5 µg nicotine i.v./kg, and (4) placebo. Apnea was induced by insufflation of 0.1 ml of acidified saline (pH 2) in the subglottic space of the trachea three times with intervals of 2 min. Results: Pretreatment with endotoxin caused a significant increase in plasma TNF-α in the endotoxin groups (mean value ± SEM 953 ± 246 and 980 ± 226 pg/ml, respectively) but no significant change in plasma IL-1β. Blood pressure, respiratory rate or S_aO₂ was not significantly affected before induced apnea. Both pretreatment with nicotine and endotoxin caused prolonged apneas by 35–45%, a complete loss of normal hyperventilation during autoresuscitation, and prolonged hypoxia after apnea. Conclusions: Nicotine and endotoxin interferes with autoresuscitation after apnea. This experimental model on piglets may shed light over important mechanisms involved in the causation of SIDS.

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Naltrexone therapy of apnea in children with elevated cerebrospinal fluid β‐endorphin

Cited by 41 publications

References 27 publications

Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death

Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Prolonged Apneas and Hypoxia Mediated by Nicotine and Endotoxin in Piglets

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