ABSTRACT
Fetal distress (FD) adversely affects fetal gastric physiology and histology, increasing
gastric acid secretion and disturbing gastric protective mechanism. Considering these
findings, an experimental study was planned to test whether ranitidine prevents FD-related
gastric physiological and histological changes during late gestational period. In
this study, a rabbit model of FD was created by way of intermittent maternal aortic
occlusion. In group 1 (SC), saline treated animals underwent control operation. In
group 2 (SD), FD was created in saline treated animals. In group 3 (RC), ranitidine
treated animals underwent control operation. In group 4 (RD), FD was created in ranitidine
treated animals. Blood lactic acid levels of the fetuses were 2.3 ± 1.0 mg/L in SC
group and 4.7 ± 1.8 mg/L in group SD (p < 0.01); 2.5 ± 0.9 mg/L in group RC and 6.7 ± 2.5 mg/L in group RD (p < 0.01). Fetal gastric acid secretion was 5.94 ± 2.13 μEq/h in group SC and 8.26
± 2.24 μEq/h in group SD (p < 0.05); 6.63 ± 2.3 μEq/h in group RC and 6.04 ± 2.43 μEq/h in group RD (p < 0.05). Fetal gastric PGE2 level was 16.4 ± 2.65 μg/g-wet weight in group SC and 7.62 ± 1.86 μg/g-wet weight
in group SD (p < 0.01); 15.6 ± 2.61 μg/g-wet weight in group RC and 8.44 ± 1.44 μg/g-wet weight
in group RD (p < 0.01). In addition, histopathological examination showed normal gastric structure
in groups SC and RC, but there were mild erosive and hemorrhagic changes in groups
SD and RD. Because prophylactic ranitidine significantly decreased gastric acid secretion,
but did not prevent harmful histopathologic effects in FD, it is suggested that gastric
damage cannot be avoided by decreasing gastric acid secretion alone. However PGE2
analogs with or without H2 receptor blockers may have a potential role to prevent
FD-related gastric damage.
Keywords
Ranitidine - fetal distress - gastritis
