Physiological Changes of Penaeus vannamei in Response to Combined Stress of Acute Cold Exposure and Waterless Duration

To elucidate the physiological regulation mechanism of Penaeus vannamei in response to combined stress of acute cold exposure and waterless duration, and provide a solid foundation for waterless live transport management and improvement in the survival rate, the effects of acute cold exposure combined with waterless duration on the metabolic homeostasis and hepatopancreas histopathology of Penaeus vannamei were explored under conditions simulating waterless live transport. The results showed that the level of lactic acid (LD) in the hemolymph and the activity of lactate dehydrogenase (LDH) in the hepatopancreas and muscle increased, the activities of LDH, hexokinase (HK), succinate dehydrogenase (SDH), phosphofructokinase (PFK) and Na⁺/K⁺-ATPase in the hemolymph increased initially and then decreased with increasing waterless duration, while the contents of adenosine triphosphate (ATP) and glycogen decreased. After resuscitation, the concentrations of glucose (Glu) and LD in the hemolymph were (23.92 ± 0.59) and (6.27 ± 0.32) mmol/L, respectively, and were still significantly higher than those in the normal control group (P < 0.05); the contents of ATP and glycogen in muscle tissues were (4.88 ± 0.31) μmol/g and (1.74 ± 0.10) mg/g, respectively, and were significantly lower than those in the normal control group (P < 0.05). The other indices tested returned to the normal levels. The glycolysis reaction of Penaeus vannamei accelerated with increasing waterless duration from 0 to 3 h, and aerobic respiration was the major respiration pattern. After 3 h, the gluconeogenesis reaction was strengthened, and the anaerobic metabolism was dominant. A waterless duration of 9 h resulted in metabolic disorder, but it could be restored after resuscitation. These findings show that the combined stress of acute cold exposure and waterless duration results in compensatory adjustments in Penaeus vannamei and causes damage to the structure of hepatopancreas, which will provide a theoretical basis for targeted control of metabolism imbalance.