胆胃关系探析

脏腑相关论治是中医学基本理论框架的重要内容之一。胆胃同为六腑,二者关系十分密切,生理上相互影响,病理上互为因果。明确其生理、病理关系对于理论研究和指导临床具有重大的意义。胆胃同病,多以口苦或呕苦、咽干为主要临床表现,胆胃同治就是要利胆和胃,佐以清热消导。

厚朴对兔离体胃肠平滑肌运动的影响

目的：研究厚朴对兔离体胃肠平滑肌运动的作用.方法：采用Magnus实验装置,用BL-410生物信号记录系统同步记录胃、肠平滑肌的活动变化曲线,待活动稳定后记录5min作为对照,然后观察药物对其作用30～35 min曲线变化并与对照组比较.结果：给厚朴煎剂后,十二指肠平滑肌收缩的幅度、频率和张力均降低,与对照组比较差异显著（P＜0.05或P＜0.01）;但对胃底条平滑肌的张力明显升高,与对照组比较差异显著（P＜0.05或P＜0.01）.结论：厚朴对十二指肠平滑肌有松弛作用,而对胃底平滑肌的运动具有增强作用,促进胃蠕动,有利胃排空.厚朴并对乙酰胆碱所致的十二指肠平滑肌加强有明显拮抗作用.厚朴增加胃底平滑肌张力作用可被阿托品阻断.厚朴对胃肠平滑肌运动的此作用可能部分是由M受体所介导.

Expression of vascular endothelial growth factor and its prognostic significance in gastric carcinoma

AIMS To investigate the clinical significance of vas- cular endothelial growth factor (VEGF) expression in gastric carcinoma. METHODS The expression of VEGF in 128 gastric carcinomas was investigated by immunohistochemical staining with a polyclonal antibody against VEGF. Cor- relations between the expression of VEGF and various clinicopathologic factors and prognosis were studied. RESULTS The VEGF-rich expression rate was 64.1% in gastric carcinoma. VEGF-rich expression rate of patients with stage Ⅲ and stage Ⅳ disease was greater than that of patients with stage f disease (P <0.05). Significant differences of expression rate ex- isted with respect to growth pattern,serosal invasion and lymph node metastasis. The VEGF-rich rate was much higher in tumors with expanding growth pattern (71.8%) or serosal invasion (73.5%) than in those with infiltrative growth pattern (52.0%) or non-serosal invasion (53.3%) (P<0.025,respectively),and it was also significantly higher in patients with lymph node metastases (75.0%) than in those without such metastases (50.0%) (P<0.05). In addition,postop- erative survey of 86 patients who had been followed up for at least 5 years demonstrated that the 5-year sur- vival rate of patients with VEGF-rich tumors was signifi- cantly lower than that of patients with VEGF-poor tu- mors (P<0.05). CONCLUSIONS The expression of VEGF may be as- sociated with the invasion and metastasis and may also be a useful prognostic indicator of gastric carcinoma.

Experimental human pain models in gastro-esophageal reflux disease and unexplained chest pain

Methods related to experimental human pain research aim at activating different nociceptors, evoke pain from different organs and activate specific pathways and mechanisms. The different possibilities for using mechanical, electrical, thermal and chemical methods in visceral pain research are discussed with emphasis of combinations (e.g., the multimodal approach). The methods have been used widely in assessment of pain mechanisms in the esophagus and have contributed to our understanding of the symptoms reported in these patients. Hence abnormal activation and plastic changes of central pain pathways seem to play a major role in the symptoms in some patients with gastro-esophageal reflux disease and in patients with functional chest pain of esophageal origin. These findings may lead to an alternative approach for treatment in patients that does not respond to conventional medical or surgical therapy.

Novel mechanisms in functional dyspepsia

Functional dyspepsia （FD） is a highly prevalent but heterogeneous disorder in which multiple pathogenetic mechanisms are involved. Although there are many studies that have investigated various pathophysiologic mechanisms, the underlying casual pathways associated with FD remain obscure. The currently proposed pathophysiologic mechanisms associated with FD include genetic susceptibility, delayed as well as accelerated gastric emptying, visceral hypersensitivity to acid or mechanical distention, impaired gastric accommodation, abnormal fundic phasic contractions, abnormal antroduodenal motility, acute and chronic infections, and psychosocial comorbidity. A greater understanding of the abnormalities underlying FD may lead to improved management. The aim of this editorial is to provide a critical overview of current pathophysiologic concepts in functional dyspepsia.

Role of calcium and other trace elements in the gastrointestinal physiology

Calcium is an essential ion in both marine and terrestrial organisms, where it plays a crucial role in processes ranging from the formation and maintenance of the skeleton to the regulation of neuronal function. The Ca^2＋ balance is maintained by three organ systems, including the gastrointestinal tract, bone and kidney. Since first being cloned in 1993 the Ca^2＋-sensing receptor has been expressed along the entire gastrointestinal tract, until now the exact function is only partly elucidated. As of this date it still remains to be determined if the Ca^2＋-sensing receptor is involved in calcium handling by the gastrointestinal tract. However, there are few studies showing physiological effects of the Ca^2＋-sensing receptor on gastric acid secretion and fluid transport in the colon. In addition, polyamines and amino acids have been shown to activate the Ca^2＋-sensing receptor and also act as allosteric modifiers to signal nutrient availability to intestinal epithelial cells. Activation of the colonic Ca^2＋-sensing receptor can abrogate cyclic nucleotide-mediated fluid secretion suggesting a role of the receptor in modifying secretory diarrheas like cholera. For many cell types changes in extracellular Ca^2＋ concentration can switch the cellular behavior from proliferation to terminal differentiation or quiescence. As cancer remains predominantly a disease of disordered balance between proliferation, termination and apoptosis, disruption in the function of the Ca^2＋-sensing receptor may contribute to the progression of neoplastic disease. Loss of the growth suppressing effects of elevated extracellular Ca^2＋ have been demonstrated in colon carcinoma, and have been correlated with changes in the level of CaSR expression.

Serum-free culture of H pylori intensifies cytotoxicity

AIM： To perform a long culture passage of H pylori without serum, taking into account its cytotoxicity and the presence of the probable new cytotoxic factor. METHODS： One sample of H pylon 60190 （ATCC 49503） was grown on Brain Heart Infusion （BHI） agar containing 0.5% 2,6-di-O-methyl-β-cyclodextrin without any serum, being passaged 70-100 times every 3-4 d for approximately 2 h, while another sample of H pylori contained 70 mL/L fetal calf serum without 2,6-di-O- methyl-β-cyclodextrin. Their supernatant and extract after 16 h in culture were evaluated for changes in cell morphology and for cell viability using HeLa cells. Furthermore, the characteristics of the probable cytotoxic factor in the extract were examined on partial purification studies and its oytotoxicity was evaluated in various human cells. RESULTS： The supernatant and the extract of the bacterium grown on serum-free medium had strong cytotoxicity compared with those grown on serumcontaining medium. They irreversibly damaged HeLa cells without vacuolation that was altogether different from that of the bacterium when grown with serum. Their cytotoxicity was easily measured by cell viability assay. The probable cytotoxic factor partially purified and detected by chromatography had characteristics difference from that of vacuolating toxin and a broad cytotoxicity toward various cell lines. CONCLUSION： Serum-free long culture method of H pylorl makes its supernatant and its extract cytotoxic enough to be easily measured by cell viability assay. The probable cytotoxic factor has a unique characteristic and might be a new cytotoxin.

Multimodal pain stimulation of the gastrointestinal tract

Understanding and characterization of pain and other sensory symptoms are among the most important issues in the diagnosis and assessment of patient with gastrointestinal disorders. Methods to evoke and assess experimental pain have recently developed into a new area with the possibility for multimodal stimulation （e.g., electrical, mechanical, thermal and chemical stimulation） of different nerves and pain pathways in the human gut. Such methods mimic to a high degree the pain experienced in the clinic. Multimodal pain methods have increased our basic understanding of different peripheral receptors in the gut in health and disease. Together with advanced muscle analysis, the methods have increased our understanding of receptors sensitive to mechanical, chemical and temperature stimuli in diseases, such as systemic sclerosis and diabetes. The methods can also be used to unravel central pain mechanisms, such as those involved in allodynia, hyperalgesia and referred pain. Abnormalities in central pain mechanisms are often seen in patients with chronic gut pain and hence methods relying on multimodal pain stimulation may help to understand the symptoms in these patients. Sex differences have been observed in several diseases of the gut, and differences in central pain processing between males and females have been hypothesized using multimodal pain stimulations. Finally, multimodal methods have recently been used to gain more insight into the effect of drugs against pain in the GI tract. Hence, the multimodal methods undoubtedly represents a major step forward in the future characterization and treatment of patients with various diseases of the gut.

Sensory testing of the human gastrointestinal tract

The objective of this appraisal is to shed light on the various approaches to screen sensory information in the human gut. Understanding and characterization of sensory symptoms in gastrointestinal disorders is poor. Experimental methods allowing the investigator to control stimulus intensity and modality, as well as using validated methods for assessing sensory response have contributed to the understanding of pain mechanisms. Mechanical stimulation based on impedance planimetry allows direct recordings of luminal cross-sectional areas, and combined with ultrasound and magnetic resonance imaging, the contribution of different gut layers can be estimated. Electrical stimulation depolarizes free nerve endings non-selectively. Consequently, the stimulation paradigm （single, train, tetanic） influences the involved sensory nerves. Visual controlled electrical stimulation combines the probes with an endoscopic approach, which allows the investigator to inspect and obtain small biopsies from the stimulation site. Thermal stimulation （cold or warm） activates selectively mucosal receptors, and chemical substances such as acid and capsaicin （either alone or in combination） are used to evoke pain and sensitization. The possibility of multimodal （e.g. mechanical, electrical, thermal and chemical） stimulation in different gut segments has developed visceral pain research. The major advantage is involvement of distinctive receptors, various sensory nerves and different pain pathways mimicking clinical pain that favors investigation of central pain mechanisms involved in allodynia, hyperalgesia and referred pain. As impairment of descending control mechanisms partly underlies the pathogenesis in chronic pain, a cold pressor test that indirectly stimulates such control mechanisms can be added. Hence, the methods undoubtedly represent a major step forward in the future characterization and treatment of patients with various diseases of the gut, which provides knowledge to dinicians about the underlying symptoms and treatment of these patients.

Do probiotics have a therapeutic role in gastroenterology?

Several hundred species of bacteria inhabit the gut, and affect its cell biology, morphology and homeostasis. Many bacteria are however potential pathogens, especially if the integrity of the epithelial barrier is physically or functionally breached. Conversely, the interaction between host and commensal microbes can confer important health benefits. This has led to commercial and public interest in ＇probiotics＇, live microbes principally taken as food supplements. Might probiotics also be used in disease therapy？ Experimental evidence that probiotics modulate gut physiology, particularly barrier integrity and immunological function, underpins exciting new gastroenterological research. We discuss below the scientific basis for probiotic effects and present a critical perspective for their use in relation to gastrointestinal disease.

Lactobacillus plantarum B7 inhibits Helicobacter pylori growth and attenuates gastric inflammation

AIM:To determine the anti-Helicobacter property of Lactobacillus plantarum B7(L.plantarum)B7 supernatants in vitro and the protective effects of L.plantarum B7 on serum tumor necrosis factor-alpha(TNF-?),gastric malondialdehyde(MDA)level,apoptosis,and histopathology in Helicobacter pylori(H.pylori)-induced gastric inflammation in rats. METHODS:In vitro,the inhibition of H.pylori growth was examined using L.plantarum B7 supernatants at pH 4 and pH 7 and at the concentration of 1×,5×and 10×on plates inoculated with H.pylori.The inhibitory effect of H.pylori was interpreted by the size of the inhibition zone.In vitro,male Sprague-Dawley rats were randomly divided into four groups including group 1(control group),group 2(H.pylori infected group), group 3(H.pylori infected with L.plantarum B7 106 CFUs/mL treated group)and group 4(H.pylori infected with L.plantarum B7 1010 CFUs/mL treated group).One week after H.pylori inoculation,L.plantarum B7 106 CFUs/mL or 10 10 CFUs/mL were fed once daily to group 3 and group 4,respectively,for one week.Blood and gastric samples were collected at the end of the study. RESULTS:In vitro,at intact pH 4,mean inhibitory zone diameters of 8.5 mm and 13 mm were noted at concentrations of 5×and 10×of L.plantarum B7 supernatant disks,respectively.At adjusted pH 7, L.plantarum B7 supernatants at concentrations of 5 ×and 10×yielded mean inhibitory zone diameters of 6.5 mm and 11 mm,respectively.In the in vitro study, in group 2,stomach histopathology revealed mild to moderate H.pylori colonization and inflammation.The level of gastric MDA and epithelial cell apoptosis were significantly increased compared with group 1.The serum TNF-??level was significant decreased in group 3 compared with group 2(P<0.05).In addition,L.plantarum B7 treatments resulted in a significant improvement in stomach pathology,and decreased gastric MDA level and apoptotic epithelial cells. CONCLUSION:L.plantarum B7 supernatant inhibits H.pylori growth.This inhibition was dose-dependent and greater at pH 4.Moreover,L.plantarum B7 attenuated H.pylori-induced gastric inflammation.