The comparative evaluation of cellular localization of viral antigens with microscopic changes in the ileum of cattle infected with bovine viral diarrhea

The correlation between microscopic changes with cellular localization of viral antigens was studied in the ileum of 16 cases infected with bovine viral diarrhea virus (BVDV). Microscopic lesions in the ileum included multifocal erosive and ulcerative ileitis, severe congestion and hemorrhage, crypt dilation and mucus engorgement, epithelial debris and leukocytes, lymphoid depletion of Peyer’s patches, herniation of mucosal epithelium into depleted Peyer’s patches, and fibrinoid vasculitis of submucosal vessels. BVDV antigen was detected by immunohistochemistry in macrophages, dendritic cells, smooth muscle cells, endothelial cells, epithelial cells of crypts, and mucosal epithelium, together with other mononuclear cells including lymphocytes, plasma cells, fibroblasts, and intramural ganglial cells. No consistent correlation between the presence of BVDV antigen and vascular lesions in the ileum was identified. The intensity and distribution of the immunoperoxidase stain in the ileum was graded as highly positive (18.7%), moderately positive (56.3%), and mildly positive (25%). In conclusion, the pattern and density of distribution and localization of BVDV antigen in the ileum was not consistently correlated with the severity of microscopic lesions.     

Opioid inhibition of cholinergic transmission in the guinea-pig ileum is independent of intracellular cyclic AMP

This study examined whether the inhibitory actions of opioids in the guinea-pig ileum were influenced by agents which mimic or elevate intracellular cyclic adenosine 3′,5′-monophospate (cyclic AMP) levels. In longitudinal muscle-myenteric plexus preparations, the mu agonist, [D-Ala², NMePhe⁴,Gly-ol⁵]enkephalin (DAGO) and the kappa agonist, dynorphin A-(1–13) depressed contractions of the longitudinal muscle evoked by electrical stimulation of myenteric neurons. Mean IC₅₀ values were 19 and 2.8 nM for DAGO and dynorphin, respectively. Neither forskolin, cholera toxin nor dibutyryl cyclic AMP affected significantlythe IC₅₀s for the opioid agonists. The experiments suggest that μ and agonists inhibit excitatory cholinergic transmission to the longitudinal muscle by intracellular effector mechanisms that do not involve cyclic AMP.     

腹腔镜辅助下截取带血管蒂回肠段转移阴道成形术

目的 探索在腹腔镜辅助下截取带血管蒂回肠段转移再造阴道的可能性，为临床提供阴道成形术的新方法。方法 应用腹腔镜引导下，配合使用超声刀，通过小切口完成肠系膜分离、回肠段截取、肠端吻合、回肠段下拉转移形成阴道。结果 2002年2月至2006年7月，共为38例需再造阴道患者成功地施行腹腔镜辅助下截取带血管蒂回肠段转移阴道成形术。随访1个月～4年，其中36例移植回肠段成活良好，再造阴道符合生理要求。结论 由于避免了剖腹和以往术式的供区瘢痕，较好地缓解了此类患者巨大的心理压力，腹腔镜下回肠段代阴道是目前较为理想的阴道成形术新方法。     

Optimization of uretero-intestinal anastomosis in urinary diversion: an experimental study in dogs

Summary A new antireflux uretero-ileal reimplantation technique suitable for use with bladder substitutes is presented. This procedure entails creation of a serouslined extramural tunnel. Following detubularization of the bowel segment, the adjacent flaps are approximated by continuous 4/0 non-absorbable sutures 1.5 cm from the cut edges. The ureters are laid in the trough thus fashioned. Button-holes are created in the bowel flaps and a mucosa-to-mucosa uretero-ileal anastomosis is carried out. The mucosal edges of the flaps are then approximated by one layer of continuous 4/0 (PGA) suture resulting in closure of this artificial tunnel. The feasibility and functional outcome of this technique were experimentally investigated in 8 dogs. Follow-up was carried out up to 30 weeks. Assessment by intravenous urography and ascending studies showed that the procedure is an efficient method of providing an unobstructed unidirectional flow of urine.     

Effects of probenecid and brilliant blue G on rat enteric glial cells following intestinal ischemia and reperfusion

The P2X7 receptor participates in several intracellular events and acts with the pannexin-1 channel. This study examined the effects of probenecid (PB) and brilliant blue G (BBG), which are antagonists of the pannexin-1 channel and P2X7 receptor, respectively, on rat ileum enteric glial cells after on ischemia and reperfusion. The ileal vessels were occluded for 45 min with nontraumatic vascular tweezers, and reperfusion was performed for periods of 24 h and 14 and 28 days. After ischemia (IR groups), the animals were treated with BBG (BG group) or PB (PB group). The double-labeling results demonstrated the following: the P2X7 receptor was present in enteric glial cells (S100β) and enteric neurons positive for HuC/D; enteric glial cells exhibited different phenotypes; some enteric glial cells were immunoreactive to only S100β or GFAP; and the pannexin-1 channel was present in enteric glial cells (GFAP). Density (in cells/cm²) analyses showed that the IR group exhibited a decrease in the number of cells immunoreactive for the P2X7 receptor, pannexin-1, and HuC/D and that treatment with BBG or PB resulted in the recovery of the numbers of these cells. The number of glial cells (S100β and GFAP) was higher in the IR group, and the treatments decreased the number of these cells to the normal value. However, the PB group did not exhibit recovery of S100β-positive glia. The cell profile area (μm²) of S100β-positive enteric glial cells decreased to the normal value after BBG treatment, whereas no recovery was observed in the PB group. The ileum contractile activity was decreased in the IR group and returned to baseline in the BG and PB groups. BBG and PB can effectively induce the recovery of neurons and glia cells and are thus potential therapeutic agents in the treatment of gastrointestinal tract diseases.     

Interaction of class III antiarrhythmic drugs with muscarinic M2 and M3 receptors: radioligand binding and functional studies

We have recently reported that class III antiarrhythmic drugs inhibit the muscarinic acetylcholine (ACh) receptor-operated K⁺ current (I _K, ACh) in guinea-pig atrial cells by different molecular mechanisms. The data obtained from the patch-clamp study suggest that d,l-sotalol inhibits I _{K, ACh} by blocking the muscarinic receptors, whereas MS-551 inhibits the K⁺ current by blocking the muscarinic receptors and depressing the function of the K⁺ channel itself and/or the guanine nucleotide-binding protein (G protein). This study was undertaken to determine whether the class III antiarrhythmic drugs d,l-sotalol and MS-551 interact with the muscarinic receptors of cardiac and peripheral tissues. Both drugs inhibited concentration dependently the specific [³H]N-methylscopolamine ([³H]-NMS) binding to membrane preparations obtained from guinea-pig atria and submandibular glands. The competition curves of these drugs for [³H]-NMS binding to glandular membranes were monophasic, suggesting competition with [³H]-NMS at a single site. Although the competition curve of d,l-sotalol for [³H]-NMS binding to atrial membranes was monophasic, that of MS-551 was biphasic and showed high- and low-affinity states of binding. d,l-Sotalol showed slightly, but significantly, higher affinity for cardiac-type muscarinic receptors (M₂) than for glandular-type muscarinic receptors (M₃). The inhibition constant (K _i) for MS-551 in glandular membranes was also slightly greater than the high-affinity K _i value for the drug in atrial membranes. In guinea-pig left atria and ilea, d,l-sotalol shifted the concentration-response curves for the negative inotropic effect and the contracting effect of carbachol in a parallel manner. The slopes of Schild plot were not significantly different from unity, suggesting competitive antagonism, and the pA₂ for d,l-sotalol in left atria was slightly greater than that in ilea. MS-551 also shifted the concentration response curve for the negative inotropic effect of carbachol in atrial preparations to a greater extent than that for the contracting effect in ileal preparations, although MS-551 failed to show a pure competitive antagonism. These results suggest that both d,l-sotalol and MS-551 interact with cardiac M₂ and peripheral M₃ receptors, and that at high concentrations they exert anticholinergic activity in cardiac and peripheral tissues.     

Congenital leiomyoma of the distal ileum associated with ileal atresia and malrotation

A leiomyoma of the small bowel in a neonate was found causing luminal occlusion and was associated with malrotation. This association and the lack of intestinal mucosa at the level of the tumor suggest that the growth originated at or near the solid core stage of intestinal development.     

黄龙汤对动物肠运动的影响

目的：探讨黄龙汤对实验动物肠运动的作用。方法：采用肠管运动在体实验法测定排便时间及频度和肠推进运动．肠管运动的离体实验法测定动物不同肠段运动情况。结果：黄龙汤能使动物排便时间增快，次数增加，便稀且不成形。能明显促进动物在体肠推进运动。能增加动物离体回肠蠕动作用，对离体十二指肠及结肠则显示明显的抑制作用．且这种作用能被Ach短暂拮抗。结论：黄龙汤对实验动物有明显的泻下作用。可能是由于黄龙汤有促进动物肠肌运动的结果。对十二指肠及结肠显示的这种抑制作用表明本方在致泻的同时，可能有解痉止痛作用。     

Program

The main objective of this study was to investigate the role and the underlying mechanism of Na-H exchanger-3 (NHE-3) expression in spontaneously hypertensive rat (SHR) intestine. Expression of colonic and ileal NHE-3 isoform, its regulatory factor-1 (NHERF-1) and cyclic GMP kinase II (cGKII) were examined using western blot analysis. Since NHE-3 activity is regulated by its abundance on the plasma membrane, its levels were also examined in lipid rafts-enriched membrane fractions. The lipid rafts fractions were characterized by examining the concentration of flotillin-1 and caveolin-1, total protein, and cholesterol. Twelve-weeks-old SHR used in this study developed significant hypertension, proteinuria, and renal and cardiac hypertrophy. These changes were significantly reversed by captopril treatment. There was a significant decrease in the levels of NHE-3 and NHERF-1 proteins, and sodium pump activity, but an increase in the cGKII levels in both tissues from SHR. Reduction in NHERF-1 levels was reversed by captopril but not of the other proteins. Cholesterol profile was significantly different in SHR colon as compared to normo-tensive Wistar Kyoto rats. These findings suggest that suppression of NHE-3 in intestine is a counteracting mechanism of hypertension and is regulated by NHERF-1 through cGKII activation in SHR. NHE-3 suppression together with decrease in the sodium pump activity would accumulate intracellular Na⁺ and may contribute to the reported hypertension-induced tissue damage in the GI-tract.