CONGENITAL DUODENAL
ATRESIA IN RAT MODEL INDUCED BY ADRIAMYCIN
Chen Yichen, Li Long,
Diao Mei, Zhang Jinzhe
Beijing Children’s
Hospital, Beijing, China
Objective: To describe the
relationships among the developments of duodenal, liver and pancreas in a
fetal model of congenital duodenal atresia induced by Adriamycin.
Methods: Ten time-mated pregnant
Wistar rats were given 1.75mg/kg of Adriamycin intraperitoneally on days 6
through 9 of gestation, the embryos were harvested carefully by cesarean
section on day 20. The fetuses
were dissected microscopically and studied histologically to detect the
internal malformation. The
findings were compared with those of age-matched saline embryos.
Results: 35 fetus were harvested from the
control group and 67 embryos from the Adriamycin group. All saline fetus were normal,
whereas 52.2% (35/67) of Adriamycin fetus had duodenal atresia. The
intraluminal atresia was found in 2.9% (1/35)of duodenal atresia fetus, gapped
atresia with pancreatic tissue filling in the gap in 77.1% (27/35) and
gapped atresia in 20.2% (7/35).
A double duodenal atresia was found in one fetus. The malformation
was anatomically identical to that of human neonates.
22 (32.8%) fetus in
Adriamycin group had some degree of hepatic agenesis and 21 fetus among
them had duodenal atresia too.
Absence of caudate lobe was found in 63.6% (13/22) of hepatic
agenesis fetus, absence of caudate and mastoid lobes in 22.7% (5/22), and
absence of caudate, mastoid and right lobes in 13.6% (3/22). At the same time, the dysplastic
hepatic lobules were noticed by microscopy.
Interestingly, all
except one duodenal atresia fetus were associated with pancreatic agenesis,
on the other hand, pancreatic agenesis occurred without duodenal atresia,
53.7% (36/67) fetus in Adriamycin group had pancreatic agenesis. Among them, 63.9% (23/36) had
absence of the pancreatic neck, body and tail and 36.1% (13/36) had absence
of the body and tail.
Microscopically, dysplastic acinus of pancreas were found too.
Conclusion: Adriamycin is a
dependable way to induce congenital duodenal malformation. This easily
reproducible experimental model permits new research into the embryogenesis
of the duodenal atresia.