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Acute physiopathological and histopathological effects of fetal distress on the fetal stomach: an experimental study
A Aslan1, G Karagüzel, N Uysal
1Department of Pediatric Surgery, Akdeniz University School of Medicine, Antalya, Türkiye, Turkey.
Insights
Fetal distress significantly increases stomach acid and reduces protective factors in rabbit fetuses, leading to gastric injury. This highlights a potential complication in distressed newborns.
Area of Science:
- Perinatal Physiology
- Gastroenterology
- Fetal Medicine
Background:
- Limited understanding of fetal distress (FD) impact on fetal stomach.
- Extensive research exists on stress effects in children and adults, but not in fetuses.
Purpose of the Study:
- To investigate the effects of fetal distress on fetal gastric physiology and histology.
- To elucidate the mechanisms behind potential gastric injury in distressed fetuses.
Main Methods:
- Created a fetal distress model in pregnant rabbits via intermittent maternal aortic occlusion.
- Analyzed fetal gastric acid secretion and prostaglandin E2 (PGE2) levels.
- Performed histopathological examination of fetal stomachs.
Main Results:
- Significantly increased fetal gastric acid secretion in the distress group (18.08 muEq/h) compared to controls (4.24 muEq/h).
- Significantly decreased fetal gastric PGE2 levels in the distress group (9.86 mg/g) versus controls (16.59 mg/g).
- Histopathology revealed mild hemorrhagic and erosive changes in distressed fetuses, absent in controls.
Conclusions:
- Fetal distress adversely affects fetal gastric physiology in rabbits.
- Mechanisms include increased gastric acid secretion and decreased gastric protection.
- Gastric injury is a potential complication of fetal distress and hypoxia.
Abstract:
Although effects of stress on the stomach have been extensively investigated in children and adults, our knowledge about effects of fetal distress (FD) on the fetal stomach is quite limited. Therefore, an experimental study was planned to evaluate the effects of FD on fetal gastric physiology and histology. In this study, a model of FD was created by way of intermittent maternal aortic occlusion in pregnant rabbits. In total, 21 fetuses of 6 pregnant rabbits were available for surgical and laboratory procedures. Laboratory examinations showed that (1) fetal gastric acid secretion was 4.24 +/- 2.68 muEq/h in the control group and 18.08 +/- 6.34 muEq/h in the distress group (p < 0.01) and (2) fetal gastric PGE2 level was 16.59 +/- 6.15 mg/g wet weight in the control group and 9.86 +/- 3.46 mg/g wet weight in the distress group (p < 0.05). Histopathologically, there were mild hemorrhagic and errosive changes in the distressed fetuses, but not in control fetuses. These findings support that FD adversely affects fetal gastric physiology through two mechanisms consisting of increased gastric acid secretion and decreased fetal gastric protection in rabbits. Consequently, gastric injury should be noted as a potential problem among hypoxia-associated abnormalities encountered in the distressed fetus.
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