Acute Physiopathological and Histopathological Effects of Fetal Distress on the Fetal Stomach: An Experimental Study

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 (xEq/h in the control group and 18.08 ± 6.34 (xEq/h in the distress group (p < 0.01) and (2) fetal gastric PGE 2 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.Although precise definition of the term "fetal distress" (FD) is not sufficiently clear, it is frequently used in perinatology to express fetal hypoxia. It is believed that fetal hypoxia shows close relation with increased perinatal morbidity and mortality. 1 Therefore, awareness in the context of hypoxia-induced problems has a critical importance in clinical practice.Because FD represents a generalized disorder in fetal oxygenation, it may compromise any tissue or organ. Acute respiratory distress syndrome is the best known entity related with FD. 2 Additionally, some studies on the subject suggest that FD causes neurological damage, neonatal sepsis, necrotizing enterocolitis, or acute renal failure. 34 Recently, it has been reported that a number of the newborns with esophagogastritis had the history of FD. 5 However, the effects of the FD on fetal gastric physiology and histology have not been investigated previously. In this study, we designed an FD model in maternal origin and investigated its effects on gastric acid secretion, PGE 2 levels, and histopathology of the fetal stomach.

Prophylactic Ranitidine in Experimental Fetal Distress: Acute Phase Effects on the Fetal Stomach

“…14 Our previous study showed that gastric acid secretion was significantly increased and gastric damage occurred in the fetuses subjected to distress. 5 This observation led us to search for a preventive approach regarding the use of ranitidine. Although improving effects of the ranitidine on the stress-induced gastric damage is well known in children and adults, the present study showed that ranitidine failed in the prevention of fetal gastric damage.…”

“…In our previous experimental study, we found that acute FD affects fetal stomach adversely through increased fetal gastric acid secretion and decreased fetal gastric PGE 2 , which results in gastric damage. 5 In this study, we condensed our efforts to prevent the harmful gastric effects that occur in the early period following FD. Accordingly, we aimed to determine whether prophylactic administration of ranitidine in acute FD prevents unfavorable physiopathological and histopathological effects seen in fetal stomach during early poststress period.…”