Factors involved in the neuronal death during postischemic reperfusion: experimental study in rabbits

Citation
Ml. Duan et al., Factors involved in the neuronal death during postischemic reperfusion: experimental study in rabbits, CHIN MED J, 112(2), 1999, pp. 153-156
Citations number
18
Categorie Soggetti
General & Internal Medicine
Journal title
CHINESE MEDICAL JOURNAL
ISSN journal
03666999 → ACNP
Volume
112
Issue
2
Year of publication
1999
Pages
153 - 156
Database
ISI
SICI code
0366-6999(199902)112:2<153:FIITND>2.0.ZU;2-S
Abstract
Objective To explore the main pathogenic factors in the development of neur onal death during normothermic reperfusion in rabbits. Methods Ninety-six New Zealand rabbits were randomly allocated into two gro ups: group I sewed as non-ischemic controls; group II served as postischemi c normothermic reperfusion models. Complete cerebral ischemia was induced b y the four-vessel model for 30 minutes. After ischemia, rabbits in group II were further divided into three subgroups according to the duration of rep erfusion: subgroup A, 30 minutes; subgroup B, 180 minutes and subgroup C, 3 60 minutes. Twenty-eight biochemical parameters in the brain were measured, and neuronal changes were observed by histomorphological assessment. Neuro ns of 12 regions were differentiated into four types: type A (normal), type B (mildly damaged), type C (severely damaged) and type D (necrotic). Bivar iate correlate analysis between the levels of biochemical parameters and th e percentages of each type of neurons was carried out. Results The main parameters involved in the progressive decrement of type A neurons were VIP, beta-EP, PGI(2), T-3, T-4 and N-a(+), K+-ATPase; in thf increment of type B were beta-EP and TXB2; in the increment of type C were GLU and TXB2/PGI(2) respectively; in the stepwise increment of percentages of type D neurons were T-4, N-a(+),K+-ATPase, GLU, T-3 and VIP (P<0.05). Conclusion The main factors involved in the development of neuronal death d uring postischemic normothermic reperfusion in rabbits include hypermetabol ism, deactivation of N-a(+), K+-ATPase, release of excitatory amino acids a nd disorder of neuropeptides.