Biomedical subjects
D Tibboel
Publications and source records attributed to D Tibboel.
The effects of temporary general hypoxia and local ischemia on the development of the intestines: an experimental study.
It is generally accepted that a circulatory disorder of the bowel during the embryonic stage of development plays an important part in the occurrence of atresias of the small bowel and colon, with the exception of the septal types of atresia. In most cases, the cause of this disorder is not known. An experimental study, making use of chick embryos, is presented and the results are discussed. Two sets of experiments were conducted. In the first set the bowel of the chick embryo was subjected to temporary ischemia. In the second one the chick embryo was subjected to a period of general hypoxia. Temporary ischemia of the bowel frequently resulted in stenosis or atresia. The duration of the vascular occlusion was significant factor. Temporary general hypoxia resulted in serious morphologic changes of the bowel and the liver. Stenosis or atresia did not occur in this case, but there was a strong resemblance to the histopathological picture of neonatal necrotizing enterocolitis.
Intestinal atresia and stenosis in animals: a report of 34 cases.
Intestinal atresia was found in 29 animals and stenosis in five. Atresia was found in the duodenum in one pup; in the jejunum in nine calves, two lambs and one piglet; in the ileum in one pup, one lamb and one piglet; and in the colon in one foal, seven calves, one lamb, one piglet and three kittens. Stenosis was found in the duodenum of a foal, in the jejunum in two calves and one pup, and in both the ileum and the colon of a kitten. One lamb showed ileal atresia as well as ileal stenosis. We classified the atresia as type 1, membrane atresia (four cases); type 2, cord atresia (six cases); and type 3, blind-end atresia (19 cases). In the literature and our own study, atresia was found only in the small intestine in puppies, but in foals and kittens it was found only in the colon. Atresia of the colon is more common in animals than in man, but multiple atresia, frequent in man, is rare in animals.
New perspectives in fetal surgery: the chicken embryo.
After a short literature a review a comparison is made between the development of the human digestive tract during the second trimester of gestation and that of the chick embryo (Gallus domesticus) during the last week of incubation. The surgical procedure for chick embryosis is discussed in connection with the the study of the pathogenesis of small bowel atresia and meconium peritonitis. The results corroborate that the chick embryo is a valuable laboratory animal in experimental fetal surgery.
Gastroschisis and omphalocele.
It has been widely acknowledged that exomphalos and gastroschisis are two different clinical entities. Their etiology and pathogenesis, however, remain controversial. Several techniques are available for making a prenatal diagnosis of these as well as many other malformations. Some prenatal treatment is possible, but operative management is the more usual course. In most cases, of omphalocele and gastroschisis, treated either conservatively or by any kind of surgery, intensive care is mandatory to support nutrition and often ventilation as well. Enteral nutrition at an early stage during the postoperative period might lead to bouts of necrotizing enterocolitis requiring aggressive medical treatment and sometimes even operative treatment.
"Changing concepts in the treatment of congenital diaphragmatic hernia".
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Alveolar epithelial composition and architecture of the late fetal pulmonary acinus: an immunocytochemical and morphometric study in a rat model of pulmonary hypoplasia and congenital diaphragmatic hernia.
The aim of the present study was to compare the architecture and alveolar epithelial cell composition of the pulmonary acinus in hypoplastic and normal fetal rat lungs. For this purpose, a rat model of pulmonary hypoplasia in association with congenital diaphragmatic hernia (CDH) induced by Nitrofen (100 mg on day 10 of pregnancy) was studied. Sections (5 microns) from lungs of control and Nitrofen-exposed fetal Sprague Dawley rats with or without CDH aged 18-22 days (vaginal plug on day 1, birth on day 23) were stained with hematoxylin and eosin. To identify developing alveolar epithelial cells, sections were incubated with anti-surfactant protein A (SP-A; rabbit anti-mouse) or preimmunization serum (indirect immunofluorescence). On days 18 and 19, control lungs and exposed lungs from fetuses with and without CDH looked similar (pseudoglandular stage of lung development). The prospective pulmonary acinus consisted of acinar tubules with small round lumens, lined by cuboid, fluorescent type II cells. Morphometric analysis on day 19 showed significantly smaller lung volumes and lung tissue volumes after Nitrofen exposure. On day 20 (canalicular stage), some tubules were slightly dilated and lined by cuboid and thinner fluorescent cells; these dilated tubules were less numerous in lungs from exposed fetuses with CDH. On days 21 and 22 (saccular stage), the saccular lining consisted of cuboid to thin fluorescent cells in exposed lungs from fetuses with and without CDH, and fluorescent (low) cuboid cells interspersed with dark zones (type I cell areas) in control lungs. In the exposed lungs from fetuses with CDH, the lumens of all airspaces were frequently slit-like, and the septa were thicker. These phenomena gave the lungs a primitive, compact aspect. Morphometric analysis on day 22 showed smaller lung volumes and lung tissue volumes, smaller airspace/tissue ratios, smaller epithelial surface areas, and more type II cells per surface area in Nitrofen-exposed lungs than in normal control lungs. The results suggest that Nitrofen-exposed, and thus hypoplastic, fetal rat lungs are retarded with respect to the differentiation of cuboid type II cells into squamous type I cells whether or not CDH is present, and with respect to the development of the future airspaces between days 20 and 22 if CDH is present.
Angiotensin-converting enzyme activity is increased in lungs of rats with pulmonary hypoplasia and congenital diaphragmatic hernia.
Lung hypoplasia (LH) and pulmonary hypertension are responsible for the high mortality rate in congenital diaphragmatic hernia (CDH) patients. Angiotensin-converting enzyme (ACE) plays a role in the regulation of pulmonary vascular resistance in the postnatal period and might be involved in the development of pulmonary hypertension of the newborn. A study was made of the development of ACE activity spectrophotometrically in a rat model of LH and CDH. It was previously shown that the lungs in this model are hypoplastic and the muscularization of the pulmonary vascular bed is increased. CDH was induced in fetal rats by oral administration of 115 mg/kg Nitrofen to the mother on day 10.5 of pregnancy. Fetuses were delivered by hysterotomy on days 19, 20, 21, and 22. Nitrofen-exposed rats showed significantly lower lung weights and not statistically significant lower total ACE activities than in controls. ACE activity expressed per milligram lung wet weight and per milligram protein was significantly increased compared to controls. ACE converts angiotensin I to the vasoconstrictor angiotensin II, and it inactivates the vasodilator bradykinin. Increased ACE activity may therefore contribute to pulmonary hypertension. Whether ACE and angiotensin II levels are increased in human newborns with a diaphragmatic defect and whether they contribute to the development of persistent pulmonary hypertension has not been studied up till now.