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M C Fina

Publications and source records attributed to M C Fina.

2 recordsLinked to original sources

A canine model of gastroesophageal reflux disease (GERD).

BACKGROUND: Although a variety of antireflux procedures and medications are used to treat gastroesophageal reflux disease (GERD), reliable large-animal models of GERD that can be used to objectively compare the efficacy of these treatments are lacking. METHODS: Esophageal manometry and 24-h gastroesophageal pH monitoring with event data were performed in 18 mongrel dogs with a cervical esophagopexy. We then calculated a modified DeMeester score: The Duke Canine reflux score (DCR). Thereafter, the animals underwent a 4-cm anterior distal esophageal myotomy, incision of the left diaphragmatic crus, and intrathoracic gastric cardiopexy. Postoperative 24-h pH and manometry were obtained 2 weeks later. RESULTS: The postoperative 24-h pH results showed a significant increase in the mean DCR score (5.9 +/- 4.5 vs 84.9 +/- 56.1, p < 0.0002), and manometry indicated a significant decrease in mean lower esophageal sphincter (LES) pressure (7.1 +/- 2.9 vs 3.2 +/- 2.5 mmHg, p < 0.0001). CONCLUSION: This technique reliably creates a canine model of GERD.

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Intraperitoneal immunity and pneumoperitoneum.

BACKGROUND: Carbon dioxide (CO(2)) pneumoperitoneum has been implicated as a possible factor in depressed intraperitoneal immunity. Using in vitro functional assays, CO(2) has been shown to decrease the function of peritoneal macrophages harvested from insufflated mice. However, an effective in vivo assessment is lacking. Listeria monocytogenes (LM), an intracellular pathogen, has served as a well-established in vivo model to study cell-mediated immune responses in mice. This study examines the immune competence of mice based on their ability to clear intraperitoneally administered LM following CO(2) vs helium (He) insufflation. METHODS: Eighty-five mice (C57Bl/6, males, 4-6 weeks old) were divided between the following four treatment groups: CO(2) insufflation, He insufflation, abdominal laparotomy (Lap), and control (anesthesia only). Immediately postoperatively, each group was inoculated percutaneously and intraperitoneally with a sublethal dose (.015 x 10(6) org) of virulent LM (EGD strain). Half of the animals were killed on postoperative day 3 and half on day 5. Spleens and livers (sites of bacterial predilection) were harvested, homogenized, and plated on TSB agar. The amount of bacteria (1 x 10(6) LM/spleen and liver) from each group was then compared. Statistical significance was set at p </= 0.05. RESULTS: Control animals had nominal bacteria on day 3 (0.016 x 10(6) LM/spleen and liver), and the bacterial burden remained low at day 5 (0.038 x 10(6) LM/spleen and liver) postchallenge. On day 3, the bacterial burden was significantly higher in the CO(2) group (5.46 x 10(6) LM/spleen and liver) as compared to He (0.093 x 10(6) LM/spleen and liver) and controls. The Lap group (3.44 x 10(6) LM/spleen and liver) had significantly more bacteria than the controls. There were no significant differences between any of the groups on day 5. CONCLUSIONS: In this animal model, CO(2) pneumoperitoneum impaired cell-mediated intraperitoneal immunity significantly more than He pneumoperitoneum and controls on day 3. Also on day 3, laparotomy caused impairment of intraperitoneal immunity when compared to controls. Finally, intraperitoneal immunosuppression resolved by day 5.

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