Published online Feb 15, 2000. doi: 10.3748/wjg.v6.i1.84
Revised: November 22, 1999
Accepted: October 9, 1999
Published online: February 15, 2000
AIM: To investigate the changes of gastric acid production and its mechanism in shock period of severe burn in rats.
METHODS: A rat model with 30% TBSA full-thickness burn injury w as employed and the gastric acid production, together with gastric mucosal blood flow (GMBF) and energy charge (EC) were measured serially within 48 h postburn.
RESULTS: The gastric acid production in the acute shock period was markedly inhibited after severe burn injury. At the 3rd h postburn, the gas tricjuice volume, total acidity and acid output were already significantly decreased (P < 0.01), and reached the lowest point, 0.63 mL/L ± 0.20 mL/L, 10.81 mmol/L ± 2.58 mmol/L and 2.23 mmol/h ± 0.73 mmol/h respectively, at the 12th h postburn. Although restored to some degree 24 h after thermal injury, the variables above were still statistically lower, compared with those of control animals at the 48th h postburn. The GMBF and EC were also significantly reduced after severe burns, co nsistent with the trend of gastric acid production changes.
CONCLUSION: Gastric acid production, as well as GMBF and EC was predominantly decreased in the early postburn stage, suggesting that gastric mucosal ischemia and hypoxia with resultant disturbance in energy metabolism, but not gastric acid proper, might be the decisive factor in the pathogenesis of AGML after thermal injury, and that the preventive use of anti-acid drugs during burn shock period was unreasonable in some respects. Therefore, taking effective measures to improve gastric mucosal blood perfusion as early as possible postburn might be more preferable for the AGML prevention and treatment.