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Biomedical subjects

J Diez Pardo

Publications and source records attributed to J Diez Pardo.

3 recordsLinked to original sources

The contribution of the adriamycin-induced rat model of the VATER association to our understanding of congenital abnormalities and their embryogenesis.

The adriamycin-induced rat model of the VATER association has provided a means of studying the morphogenesis of a variety of major congenital structural abnormalities similar to those seen in humans with the VATER association. Most interest has been centered on the foregut, where the model has clarified some aspects of the development of esophageal atresia (EA), tracheal agenesis, and other communicating bronchopulmonary foregut malformations. It has demonstrated aberrations in the nerve supply to the esophagus in EA and allowed the study of tracheomalacia. A relationship between an abnormal notochord, foregut abnormalities, and vertebral defects has been shown, and the model has reignited interest in the role of the notochord as a regional organizer of axial development. The normal temporospatial characteristics of apoptosis during fore- and hindgut development is disturbed in this model, resulting in abnormal morphology. The indications are that this model will continue to clarify the processes that lead to many of the structural congenital abnormalities that are seen in infants born with the VATER association.

Abnormalities, Drug-Induced↗

Lack of portal-venous hypertension after an arterioportal fistula in the rat.

The hepatic effects of an end-to-side arteriovenous fistula between the right renal artery and the portal vein were studied in rats. Fifty rats underwent surgery and were studied 3, 12, 24 weeks and 1 year later; Another 15 rats were used as controls. Rats did not have any portohepatic abnormality. Portal and caval pressure were measured, and the liver was evaluated histologically. No statistically significant differences were achieved between the control portal (10.37 +/- 0.29 cm H2O) and vena cava pressures (1.22 +/- 0.19 cm H2O) and those of the experimental groups. The overall liver architecture remained unchanged. A progressive enlargement of the intrahepatic portal and hepatic veins was noted. No hypertrophy of the fibrous tissue into the portal triads, hypertrophy of the muscularis of the portal vein radicals, or wall sclerotic thickening was seen. The forward overflow compensatory mechanisms are discussed.

Animals↗