ABSTRACT
De novo transcatheter fenestration of hemi-Fontan baffles has not been previously described. The purpose of this report is to present our experience in such de novo transcatheter fenestration in two consecutive patients with absent fenestration in whom the hemi-Fontan baffle was the only direct access to the pulmonary venous atrium.
Subject(s)
Catheterization , Fontan Procedure/adverse effects , Heart Atria/surgery , Stents , Cardiac Output, Low/physiopathology , Cardiac Output, Low/surgery , Child, Preschool , Fatal Outcome , Female , Fontan Procedure/methods , Hemodynamics , Humans , Infant , Male , Treatment OutcomeABSTRACT
UNLABELLED: Chronic injury to the healthy gastric mucosa with noxious agents such as aspirin or alcohol induces a progressive strengthening of the stomach wall against these insults. The present study examined the histologic response of the rat gastric mucosa to chronic destruction of the superficial mucosa for one month with hypertonic saline. The number, position and morphology of proliferating, parietal, G and D cells were followed during mucosal injury and one month of recovery. The results showed that chronic injury reduced parietal cell numbers by about 30 percent, particularly in the middle of the mucosal thickness where a clear zone was formed by hypertrophy of mucous neck-like cells. G cells were also reduced by about 50 percent, but there were no changes in D cells. Chronic injury induced a marked increase in the number of antral (+112 percent) and fundic (+250 percent) proliferating cells. CONCLUSION: The rat gastric mucosa responds to chronic superficial injury by down-regulation of acid secretory cells and gastrin secreting cells and an up-regulation of proliferating cells. The appearance of a prominent layer of mucous neck-like cells may indicate a new secretory function for these cells.
Subject(s)
Gastric Mucosa/drug effects , Gastric Mucosa/pathology , Animals , Cell Division , Disease Models, Animal , Epithelium/drug effects , Epithelium/pathology , Gastric Fundus/drug effects , Gastric Fundus/pathology , Gastric Mucosa/ultrastructure , Gastrins/immunology , Gastrins/metabolism , Immunohistochemistry , Male , Parietal Cells, Gastric/drug effects , Parietal Cells, Gastric/pathology , Pyloric Antrum/drug effects , Pyloric Antrum/pathology , Rats , Rats, Sprague-Dawley , Saline Solution, Hypertonic/pharmacology , Somatostatin/immunology , Somatostatin/metabolismABSTRACT
The effects of chronic superficial injury on the stomach were studied in rats dosed with a mild irritant (2 mol/L NaCl intragastrically) every 48 hours for 1 month followed by 1-month recovery. A single exposure to this mild irritant induced gross protection against 6 mol/L NaCl for 1 but not 2 days. Leukotriene C4 (LTC4) levels increased slightly. Prostaglandin E2 (PGE2) concentration was unchanged. After 2-week dosing, protection was concomitant with markedly elevated PGE2 concentration. LTC4 values remained unchanged. Superficial epithelial cells were more resistant to damage. After 4-week dosing, protection occurred at 1 but not 2 days after the dose with an inverse correlation of PGE2. LTC4 concentration increased significantly at both times. Chronic injury for 1 month did not alter rapid epithelial restitution or PGE2 and LTC4 released 15 minutes after challenge with 6 mol/L NaCl. The recovery period showed loss of protection. PGE2 values returned to control levels but LTC4 values remained slightly elevated. It is concluded that short- or long-term (4-week) "adaptive cytoprotection" is not mediated by endogenous PGE2. Only extremely high levels of LTC4 correlated with loss of protection. The role of the more resistant superficial epithelium remains unknown.
Subject(s)
Gastric Mucosa/drug effects , Irritants/toxicity , Animals , Dinoprostone/metabolism , Gastric Mucosa/metabolism , Gastric Mucosa/pathology , Gastrointestinal Hemorrhage/chemically induced , Indomethacin/toxicity , Male , Rats , Rats, Inbred Strains , SRS-A/metabolism , Sodium Chloride/toxicity , Time FactorsABSTRACT
A rapid immunohistochemical method using 5'-bromo-2'-deoxyuridine (BrdU), a thymidine analog, for labeling proliferating epithelial cells was modified and tested for accuracy against standard tritiated thymidine autoradiography (3H-TdR) in rat esophagus, stomach, duodenum, and colon. Either BrdU or 3H-thymidine or both compounds (simultaneously) were injected IP. Histological sections of these tissues were immunostained with monoclonal anti-BrdU antibody, linked to horseradish peroxidase by standard avidin-biotin techniques and stained with diaminobenzidine, or sections were dipped for autoradiography, or both techniques were applied to the same tissue section. Results showed that (a) BrdU labeled the same number of proliferating cells in all organs as 3H-TdR; (b) BrdU colabeled with 3H-thymidine; (c) immunostaining was complete in 3-4 days but standard 3H-TdR took 2 weeks; and (d) qualitative analysis took 50% less time with BrdU than with standard 3H-TdR.
