Published online Jan 21, 2019. doi: 10.3748/wjg.v25.i3.346
Peer-review started: October 30, 2018
First decision: November 14, 2018
Revised: December 12, 2018
Accepted: December 21, 2018
Article in press: December 21, 2018
Published online: January 21, 2019
Processing time: 83 Days and 20.5 Hours
Some clinical data show that liver dysfunction was observed in pilots. However, there are many reasons for this: hepatitis virus, drug abuse, excessive drinking and so on. The objective of this study was to probe into whether positive acceleration affects rat liver function.
Exposure to high sustained +Gz (head-to-foot inertial load) is conclusively known to have harmful effects on the human body during aviation activities. High-acceleration force exposures, particularly when occurring repeatedly, may result in accumulative adverse stress responses in the body, and safe flying is a social problem that has attracted broad attention. An important question to address is whether changes in the blood flow direction after +Gz exposure impair liver function in rats. Moreover, the manner in which the portal venous hemodynamics changes after repeated +Gz exposures, and whether oxidative stress parameters increase the duration of these changes are additional questions awaiting answers. To clarify these questions, further studies on liver damage and the mechanisms of liver damage induced by high +Gz exposures are needed, and this will provide evidence to take effective preventive measures.
In this article, an animal centrifuge model was used to study whether positive acceleration impairs liver function. This research may help find more potential adverse effects of high +Gz stress on the human liver, and help develop practical, effective protective measures. In the future, we will further expand our study to explore the effects of +Gz exposures of longer duration on the liver function, to illuminate the pathophysiological mechanisms that are involved.
Completely random grouping design and exploratory experimental research were performed based on the experimental animals. We adopted the method of acceleration exposure in rats. The difference of experimental data was detected by analysis of variance using SPSS version 13.0 statistical software (SPSS, Chicago, IL, United States). Experimental results are expressed as the mean ± standard deviation.
The main findings of the study showed that repeated +Gz exposures not only transiently impair liver function but also affect liver metabolism and morphological structure. Although there are some gaps between experimental animal model and real flight environment, this research may help find more potential adverse effects of high +Gz stress on the human liver, and help develop practical effective protective measures.
While fighter pilots are frequently exposed to high Gz acceleration with the vector in the foot-head direction, the blood and fluid of the body will be redistributed and flow along the direction of inertia force to the lower body. Many studies have demonstrated the harmful effects of repeated +Gz stress on the cardiac ultrastructure, metabolism, and function. It was, however, of scarcity that to investigate the effect of high +Gz exposure on the hepatobiliary system. Therefore, we propose some doubts: Do high +Gz exposures impair liver function of rats? How does the portal venous hemodynamics change after repeated +Gz exposures? Do oxidative stress parameters increase? Well then, should the changes of blood flow direction after +Gz exposure cause hepatic ischemia, so as to affect the liver function? We hypothesized that repeated +Gz exposures could transiently impair the liver function in rats.
The main findings of the study can be summarized as follows: First, short-term repeated exposures to either +6 Gz or +10 Gz reduced the portal venous flow. Blood redistribution between the liver and body surface or other organs is similar to liver ischemia reperfusion. Repeat +Gz exposures may result in liver ischemia-reperfusion injury. Second, alanine aminotransferase and aspartate aminotransferase levels were only slightly increased and could soon revert back to normal. With an increase in the G force, additional damage also occurred in the liver function of the rats. The results showed that this damage should be functional and reversible. Third, oxidative damage might be engaged in the pathophysiologic process during liver ischemia. After repeated +Gz exposures, the blood and nutrient substance supplied to the liver were reduced. The exposed group had oxidative stress injury, as reflected in the higher malondialdehyde (MDA) levels. In addition, the MDA levels increased as the G value increased. Fourth, repeated +Gz exposures had something to do with a temporary reduction of the liver metabolism, as indicated by a decrease in the Na+-K+-ATPase activity. The main role of the Na+-K+-ATPase is to maintain the structure and function of mitochondria. When the activities of the Na+-K+-ATPase decline, the structure of mitochondria is likely to change. Morphologically mitochondria became swelling and matrix density decreased.
Although trained pilots may not use the same way as the rats under similar conditions of exposure due to species difference, the research method in rats may help in investigating the pathophysiological mechanism of high +Gz stress in humans. In addition, this research may aid discovery of more potentially harmful effects of high +Gz stress on the human liver, and subsequently, help to prevent liver injury. Flight crews will be the research subject of the project in the future. Prospective study will be the best research method.