BETA-ENDORPHIN IMMUNOREACTIVITY IN SPINAL-FLUID AND HYPOXANTHINE IN VITREOUS-HUMOR RELATED TO BRAIN-STEM GLIOSIS IN SUDDEN INFANT DEATH VICTIMS

Beta-endorphin may induce respiratory depression and bradycardia. Elev ated 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 p resent 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 (SI D) cases (n = 17) and controls (n = 23) was also studied. The number o f reactive astrocytes was examined in the NOI by immunohistochemical d emonstration of glial fibrillary acidic protein (GFAP). The BENDI in C SF and the number of reactive astrocytes in the NOI divided the SID vi ctims 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), a nd was similar to the controls that died from infections. The other su bpopulation had a median of 260 fmol/ml BENDI in CSF (range 160-400) a nd 13 reactive astrocytes (range 7-33), similar to the control infants with previous hypoxia. In this latter SID subpopu lation the number o f 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 t he SID subpopulation with high level of BENDI in CSF and increased num ber of activated astrocytes, the correlation factor between HX in VH a nd activated astrocytes was r = 0.7 (P < 0.05).