Effects of positive acceleration (+Gz stress) on liver enzymes, energy metabolism, and liver histology in rats

Abstract

BACKGROUNDExposure to high sustained +Gz (head-to-foot inertial load) is known to have harmful effects on pilots’ body in flight. Although clinical data have shown that liver dysfunction occurs in pilots, the precise cause has not been well defined.AIMTo investigate rat liver function changes in response to repeated +Gz exposure.METHODSNinety male Wistar rats were randomly divided into a blank control group (BC group, n = 30), a +6 Gz/5 min stress group (6GS group, n = 30), and a +10 Gz/5min stress group (10GS group, n = 30). The 6GS and 10GS groups were exposed to +6 Gz and +10 Gz, respectively, in an animal centrifuge. The onset rate of +Gz was 0.5 G/s. The sustained time at peak +Gz was 5 min for each exposure (for 5 exposures, and 5-min intervals between exposures for a total exposure and non-exposure time of 50 min). We assessed liver injury by measuring the portal venous flow volume, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), liver tissue malondialdehyde (MDA), Na+-K+-ATPase, and changes in liver histology. These parameters were recorded at 0 h, 6 h, and 24 h after repeated +Gz exposures.RESULTSAfter repeated +Gz exposures in the 6GS and the 10GS groups, the velocity and flow signal in the portal vein (PV) were significantly decreased as compared to the BC group at 0 h after exposure. Meanwhile, we found that the PV diameter did not change significantly. However, rats in the 6GS group had a much higher portal venous flow volume than the 10GS group at 0 h after exposure. The 6GS group had significantly lower ALT, AST, and MDA values than the 10GS group 0 h and 6 h post exposure. The Na+-K+-ATPase activity in the 6GS group was significantly higher than that in the 10GS group 0 h and 6 h post exposure. Hepatocyte injury, determined pathologically, was significantly lower in the 6GS group than in the 10GS group.CONCLUSIONRepeated +Gz exposures transiently cause hepatocyte injury and affect liver metabolism and morphological structure.

Bombarderos en picado (1941): un modelo de estudio de la fisiología de la aviación

“…Todas estas alteraciones y estados de estrés, o una continua acumulación de estos factores, son ocasionados por el mal de altura (enfermedad aguda de altura), dando origen a edemas de altitud inducidas por hipoxia 1 , en concreto la aparición de edema pulmonar, el edema cerebral y/o el edema periférico. Gran parte de los pilotos que ascienden a elevada altitud presentaban cambios ventilatorios 22 , cardiovasculares en su presión arterial, frecuencia cardiaca, y en la señal eléctrica del corazón 20,24 , además de cambios funcionales hepáticos y otras alteraciones metabólicas 21 . Por un lado, parece tener relación la inducción de la hipoxia con la aparición de estos edemas por retención de sodio y agua 1 .…”

“…Aceleraciones mayores de +4 G a +6 G ocurridos en un rango de tiempo después de la ceguera y la inconciencia son peligrosas por incrementar el rango de letalidad. Otros datos clínicos que ocurren en pilotos, y cuya causa precisa sigue sin estar definida, es la presencia de cambios en la ondas eléctricas del corazón 20 y disfunción hepática con afección de su morfología y actividad metabólica 21 .…”