beta-endorphin and Reperfusion-Injury

To explore the main pathogenic factors in the development of neuronal death during normothermic reperfusion in rabbits.. Ninety-six New Zealand rabbits were randomly allocated into two groups: group I served as non-ischemic controls; group II served as postischemic normothermic reperfusion models. Complete cerebral ischemia was induced by the four-vessel model for 30 minutes. After ischemia, rabbits in group II were further divided into three subgroups according to the duration of reperfusion: subgroup A, 30 minutes; subgroup B, 180 minutes and subgroup C, 360 minutes. Twenty-eight biochemical parameters in the brain were measured, and neuronal changes were observed by histomorphological assessment. Neurons of 12 regions were differentiated into four types: type A (normal), type B (mildly damaged), type C (severely damaged) and type D (necrotic). Bivariate correlate analysis between the levels of biochemical parameters and the percentages of each type of neurons was carried out.. The main parameters involved in the progressive decrement of type A neurons were VIP, beta-EP, PGI2, T3, T4 and Na+, K(+)-ATPase; in the increment of type B were beta-EP and TXB2; in the increment of type C were GLU and TXB2/PGI2 respectively; in the stepwise increment of percentages of type D neurons were T4, Na+, K(+)-ATPase, GLU, T3 and VIP (P < 0.05).. The main factors involved in the development of neuronal death during postischemic normothermic reperfusion in rabbits include hypermetabolism, deactivation of Na+, K(+)-ATPase, release of excitatory amino acids and disorder of neuropeptides.

Topics: Animals; beta-Endorphin; Brain Ischemia; Cell Death; Female; Male; Neurons; Rabbits; Random Allocation; Reperfusion Injury; Sodium-Potassium-Exchanging ATPase; Thromboxane B2; Vasoactive Intestinal Peptide