Diamine oxidase (DAO) is an intestinal mucosal enzyme which serves as a marker of cellular maturity and integrity in ontogeny and after mucosal injury in the gastrointestinal tract. Since total parenteral nutrition is known to result in intestinal hypoplasia, this study was done to determine the effect of enteral and parenteral delivery of nutrients on gut structure and DAO levels. Central venous catheters were placed in 27 Sprague-Dawley rats (180-260 g), which received nutrients for 12 days via parenteral nutrition (GpI n = 10), oral intake of the parenteral solution (GpII n = 8), or standard rat chow (GpIII n = 9). Gross and microscopic measurements were made at sacrifice. Mucosal DAO levels were determined by metabolism of [3H] putrescine. Group III animals had a greater caloric intake than groups I and II, and were the only group with a significant increase in body weight. Gut weight, mucosal weight, and villous height were significantly less in group I vs groups II and III; group II values were less than group III (p less than 0.05). Both DAO specific activity and total gut DAO were significantly less in group I and group II. Mucosal DAO content correlated with total gut and mucosal weight. DAO mucosal levels decrease with parenteral nutrition, reflecting the intestinal hypoplasia that occurs. Mucosal DAO content may be dependent on both caloric intake and diet composition. Since serum DAO levels are known to correlate with mucosal DAO content, DAO activity may prove useful as a circulating marker of the effect of nutritional therapy on the intestinal mucosa.
The effects of portal hypertension on gastric motor function were investigated using the rat staged portal vein ligation model. Gastric emptying of liquids and solids was studied separately following meals labeled with 51Cr or 99Tc by whole stomach scintillation counting. Portal hypertension was consistently established in experimental rats (splenic pulp pressure: mean +/- SEM, portal hypertension versus control, 16.8 +/- 0.7 vs 11.8 +/- 0.7 mm Hg, P less than 0.0001). Although liquids were emptied in an exponential manner and solids in a linear fashion, gastric emptying of both meals was more rapid in the experimental rats. Ten minutes after the liquid meal, more than 50% of the meal had emptied from the stomachs of portal hypertensive rats while only one third of the meal had cleared in the control group (P less than 0.02). Gastric emptying of the solid meal was significantly accelerated in experimental rats at 60 and 120 min (percent meal remaining: portal hypertension versus control, 41.9 +/- 4.0 vs 55.4 +/- 3.5 and 21.5 +/- 4.9 vs 32.6 +/- 4.3, P less than 0.05). Stomachs of portal hypertensive animals were heavier (P less than 0.009) and histologic examination revealed submucosal edema. Thus, a possible mechanism of the disrupted gastric motor function in portal hypertension is decreased gastric wall compliance secondary to edema.
Acute and chronic effects of Se as sodium selenite given as a supplement in the drinking water of Sprague-Dawley rats for 35 d, 1 yr, and 2 yr are compared. For the 35-d study the experimental groups were untreated controls and rats supplemented with 1, 4, 8, 16, and 64 ppm Se. Survival was 100% in the control and 1 and 4 ppm groups, decreased in the 8 and 16 ppm groups, and was zero in the 64 ppm group. Body weights increased and were equivalent in the control and 1 and 4 ppm groups and substantially decreased in the 16 and 64 ppm groups., Serum alkaline phosphatase and glutamic-oxaloacetic transaminase (SGOT) increased with 16 ppm Se and higher supplements. Se toxicity was apparent in microscopic pathology showing liver congestion, fatty degeneration of parenchymal cells, and necrosis. In the chronic studies untreated controls are compared with rate receiving 4 ppm Se in the drinking water. In general, the weight gains throughout were equivalent for both groups. The 1-yr survival in each was above 90% and the 2-yr survival above 50%. With increased age there was a slight reduction in hemoglobin and white blood cells. The latter effect was greater in Se-treated then in control rats. Several serum components were equivalent in both groups, including alkaline and acid phosphatase, SGOT, protein, glucose, and sialic acid. Liver glutathione peroxidase was half and Se levels in the Se-treated rats were twice those in the controls. Data are presented for male rats in the chronic study with occasional reference to data on females. The parameters measured in the chronic study are highly dependent on the age of the rat when Se-supplemented drinking water is initiated.
Se as sodium selenite was administered by gavage (three consecutive times) and as drinking water supplements for 46 d to male and female Swiss mice. With respect to survival in 7-wk-old mice, Se was less toxic in males than in females when gavaged. Drinking water supplements of 1-64 ppm Se resulted in 1 male and 1 female death in mice first given Se at 7 wk of age. Se supplements to the drinking water of adult (18-wk-old) mice was less toxic in females. All young (7-wk-old) and adult (18-wk-old) mice provided 1-16 ppm Se in the drinking water survived the 46-d treatment, but in adult mice 64 ppm Se significantly reduced survival. Only 64 ppm Se supplements caused a sharp reduction in body weight in young and adult mice of both sexes. Supplements of 1-8 ppm Se in all mice elicited growth responses similar to those of untreated controls. Occasional liver and kidney congestion, liver necrosis, parenchymal cell degeneration, and bile duct proliferation were observed in control and treatment groups. Serum alkaline phosphatase and glutamic-oxaloacetic transaminase (SGOT) increased with 32 ppm Se and higher supplements. Survival, growth, serum enzymes, and pathology were normal in untreated controls and in mice of growth ages and sexes give 1, 4, and 8 ppm Se supplements. A chronic toxicity study was conducted in female Swiss mice given 1, 4, and 8 ppm Se supplements for 50 wk. The survival of Se-treated groups was more than 90% and that of controls was only 72% after 50 wk. All mice gained weight, but the group treated with 8 ppm Se gained half as much as other groups. Both liver Se and glutathione peroxidase activity increased in Se-treated mice compared to controls at 25 and 50 wk. A reduced white blood cell count and increased alkaline phosphatase and SGOT suggested a mild toxic effect of the 8 ppm Se supplement in the chronic study.
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