红霉素收缩金黄地鼠胆囊的研究

通过离体试验观察红霉素对金黄地鼠胆囊运动的影响，结果发现红霉素可以使正常组和致石组胆囊产生剂量依赖性收缩，而且发现在胆囊结石形成前后红霉素的作用同样存在，红霉素收缩金黄地鼠胆囊的作用可能是通过激活胃动素受体介导的，这一发现有助于胆囊运动能障碍的治疗。     

Experimental study on tissue engineering of the small intestine by mesenchymal stem cell seeding.

BACKGROUND: We have succeeded in regenerating the small intestine by the use of tissue engineering techniques. However, the regenerated intestine proved to lack the muscle layer, which is essential for functional peristalsis. To induce regeneration of the muscle layer, we focused on autologous mesenchymal stem cells (MSC) as a source of muscle tissue. The aim of this study was to investigate the effect of MSC seeding onto the collagen scaffold on induction of the muscle layer. MATERIALS AND METHODS: We used six female beagle dogs. The small intestine was resected over a length of 5 cm and reconstructed by a collagen sponge graft in the same way as in our previous study. Autologous MSC derived from bone marrow (10(7) cells) were seeded onto the collagen sponge just before implantation. Animals were sacrificed at 2, 4, and 16 weeks after surgery, and specimens were examined histologically. RESULTS: All six dogs survived until the scheduled time of sacrifice. At 4 weeks, regeneration of the intestine was observed at the reconstructed site. Cells positive for alpha-smooth muscle actin appeared on the scaffold in the MSC-seeded group. However, they disappeared by 16 weeks and only a thin muscle layer regenerated beneath the mucosal layer, although the regenerated mucosal layer covered the luminal surface of the regenerated intestine. CONCLUSIONS: MSC seeding induced a transient distribution of cells positive for alpha-smooth muscle actin on the scaffold, but did not induce regeneration of the muscle layer. Further investigation is necessary to achieve this aim.     

Novel effect of leptin on small intestine adaptation

BACKGROUND: Leptin is a 16-kDa peptide produced by adipocytes that plays an important role in the regulation of body fat and satiety. We have previously shown that leptin is a growth factor for normal rat small intestine. This study was designed to examine the effect of systemic leptin administration on small bowel absorptive function after massive small bowel resection (MSBR). MATERIALS and METHODS: Twenty-one adult male Sprague-Dawley rats underwent an 80% small bowel resection and end-to-end jejunoileal anastomosis. Seven days following resection, all rats had placement of a jugular venous catheter connected to a subcutaneously placed osmotic minipump and were divided into three groups based on the content of each minipump: Group 1 (n = 7) 0.1% bovine serum albumin; Group 2 (n = 7) leptin 2 microg/kg/day; and Group 3 (n = 7) leptin 4 microg/kg/day. Following a 14-day infusion period, [(14)C]galactose absorption was measured using a closed-recirculation technique. Mucosal DNA content was determined for all groups using a standard DNA purification kit. Mucosal RNA was extracted and RT-PCR was performed using the following primers: sodium/glucose cotransporter (SGLT-1), fructose transporter (GLUT-5), and glyceraldehyde-3-phosphate dehydrogenase, an internal standard. PCR products were separated on a 4% agarose gel and relative band intensities were measured. Statistical analysis was performed using ANOVA and expressed as means +/- SEM. RESULTS: Group 2 showed a 44% increase in galactose absorption (P < 0.01) and a 14% increase in GLUT-5 band intensity (P < 0.05), but no change in DNA content or SGLT band intensity. CONCLUSIONS: This study demonstrates for the first time that leptin enhances small intestine carbohydrate absorption beyond the normal adaptive response following MSBR. Leptin may be clinically useful in patients with inadequate intestinal function.     

Surgical manipulation of the small intestine and its effect on the lung

BACKGROUND: Surgical manipulation of the intestine results in generation of oxygen free radicals leading to mucosal damage as evidenced by ultrastructural and biochemical changes. It is likely that the gut-derived mediators can bring about damage to distant organs such as the lung. METHODS: Surgical manipulation of the gut was performed by opening the abdominal wall and handling the intestine. Lung damage was assessed by histology, markers of oxidative stress, and protein content in bronchoalveolar lavage fluid. Protection offered by pretreatment with various compounds such as allopurinol, L-arginine, quinacrine, and indomethacin was also studied. RESULTS: Gut manipulation resulted in neutrophil infiltration, oxidative stress, and permeability changes in the lung and these changes were maximum 30 and 60 min following surgical manipulation, which recovered with time and reversed to normal by 24 h. Prior treatment with inhibitors of xanthine oxidase, phospholipase A(2), or cyclooxygenase showed a protective effect against lung damage. CONCLUSION: This study has shown that laparotomy and intestinal handling result in distant organ (lung) damage which is probably brought about by neutrophil infiltration and oxidative stress on the lung. This is likely mediated by compounds generated in the intestine and transported into the systemic circulation since inhibition of generation of chemical mediators in the intestine offers protection against lung damage.     

Studies of paralytic ileus. Effects of intraperitoneal injury on motility of the canine small intestine.

This study is significant in demonstrating that the small intestine of the dog is extremely resistant to paralytic ileus. The various types of intra-abdominal irritation studied were quite severe. After a transient period of inhibition, however, in most instances motility of the small intestine returned and continued until near the time of death. Various types of intra-abdominal irritation were used to study paralytic ileus in dogs, including intraperitoneal injection of gastric juice, gastroperitoneal fistula, appendiceal ligation, intraperitoneal injection of Lugol's iodine solution, retroperitoneal injection of blood, and mechanical and thermal irritation of the intestine and peritoneum. The electrical and mechanical activity of the small intestine was observed by means of a Thomas cannula implanted in the jejunum. The presence or absence of fluid accumulation within the intestinal lumen or peritoneal cavity was noted at autopsy. Intra-abdominal chemical irritation caused a transient inhibition of intestinal motility, which was reversed when the irritation was stopped. Repeated irritation did not appear to cause progressive, irreversible inhibition of intestinal motility. When intestinal motility was depressed, spike potentials were absent in the recordings of electrical activity of the intestine. The "slow" electrical waves were distinguishable at all times. With the exception of the gastroperitoneal fistulas, the procedures were tolerated with only transient inhibition of intestinal motility. Accumulation of intraperitoneal fluid occurred in dogs subjected to gastroperitoneal fistulas. A small amount of intraluminal fluid accumulated in dogs subjected to repeated thermal and mechanical irritation of the intestines and peritoneum. In the other groups of dogs no significant increase in intestinal or intraperitoneal fluid was observed.