Study On The Expression Of Heat Shock Protein After+Gz Exposure And Its Protective Effect On +Gz-induced Brain Injury

Modem aircraft with high performance is capable of producing acceleration in the +90z range and +6G/s increase rate lasting 45s, which may exceed a person's physiological tolerance. The increased rate of +Gz.-induced loss of consciousness(G-LOC) was so great that G-LOC had become the major factor threatening flying safety. Safety flying is a social question which has aroused general concern. The study of the mechanism of G-LOC aims at providing theory for its protect. +Gz exposure might produce ischema-reperfusion effect on rat brain and the function of repeated +Gz exposure was similar to that of ischemia prestirnulation. We presume that repeated low +Gz exposure would make rat brain endure high +Gz exposure. In fact, low G centrifuge training is of great value to the strengthening of a pilot's G tolerance. Investigation showed that VI the length of G-LOC time related to a pilot's centrifuge training and G-LOC experience. The pilot experiencing G-LOC many times was provided with the ability of performing an anti-G straining maneuver and had a better understanding of the physiological mechanism of G-stress and G-tolerance. Therefore, Gillingham (1987) suggested that G-LOC practice should be taken as one of the training contents in pilots?high G physiological training. However, some peopal lodge an objection against this because so little is known about the effects of G-LOC. Does repeated G-LOC cause the organic mental syndrome? Do repeated +Gz exposures produce any side effects? Unfortunately, we know little about the pathophysiological effects of +Gz exposure on the brain. So the effects of repeated +Gz exposure on the central nervous system and its mechanism remain a question to be answered through further research. The study delved the change rules of HSP7O protein and HSP7O mRNA expression after different +Gz exposure in rat brain and observed the change of histology variety by using animal centrifuge. It aimed at finding out the relativity of the expression changes of HSP7O protein and HSP7O mRNA with the brain injury after +Gz exposure. The aim of the present work was to expound if +Gz exposure could induce brain injury, if repeated low +Gz exposure could produce protective effect on rat brain before high +Gz exposure, and if this protective effect was relative to the HSP7O expression and its duration. The main findings of the study are as follows: 1. Different +Gz exposure could obviously induce HSP7O expression. The intensity, duration and extension of HSP7O expression were different with the degree of +Gz exposure. There was no or few HSP7O expression in normal rat brain. The HSP7O expression after different +Gz exposure was stronger than that in normal rat brain. The expression of HSP7O after +4Gz and +6Gz exposure was the strongest in all +Gz, and it took the second place after +2Gz exposure, and it was weakened after +lOGz exposure. The distribution of HSP7O expression after +2Gz, +4Gz and +6Gz exposure was same, but the intensity was different. After +lOGz exposure the intensity of 1-ISP7O expression was weak and the extension was localized. With the increased intensity of +Gz exposure, the expression of HSP7O in rat parietal cortex gradually became weak or disappear. Compared with CA2 and CA3 the expression of HSP7O in CAl was weak and its duration was sho...