Beta-endorphin immunoreactivity in spinal fluid and hypoxanthine in vitreous humour related to brain stem gliosis in sudden infant death victims.

Beta-endorphin may induce respiratory depression and bradycardia. Elevated levels of hypoxanthine (HX) in vitreous humour (VH) may possibly indicate hypoxia before death. Furthermore, gliosis in the brain stem may reflect a previous hypoxic/ischaemic injury in the brain. In the present study we relate beta-endorphin immunoreactivity (BENDI) in the CSF to the presence or absence of reactive astrocytosis in the nucleus olivae inferior (NOI). The relationship between the HX concentration in VH and the number of reactive astrocytes in sudden infant death (SID) cases (n = 17) and controls (n = 23) was also studied. The number of reactive astrocytes was examined in the NOI by immunohistochemical demonstration of glial fibrillary acidic protein (GFAP). The BENDI in CSF and the number of reactive astrocytes in the NOI divided the SID victims into two subpopulations (P < 0.01). One had a median of < 4 fmol/ml BENDI in CSF (range < 4) and 2 reactive astrocytes (range 0-15), and was similar to the controls that died from infections. The other subpopulation had a median of 260 fmol/ml BENDI in CSF (range 160-400) and 13 reactive astrocytes (range 7-33), similar to the control infants with previous hypoxia. In this latter SID subpopulation the number of reactive astrocytes correlated positively with BENDI in CSF (r = 0.7, P < 0.05). All the SID victims had elevated levels of HX in VH. In the SID subpopulation with high level of BENDI in CSF and increased number of activated astrocytes, the correlation factor between HX in VH and activated astrocytes was r = 0.7 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)