Brief Reports Open Access
Copyright ©The Author(s) 2001. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 15, 2001; 7(3): 399-402
Published online Jun 15, 2001. doi: 10.3748/wjg.v7.i3.399
Gastrin, somatostatin, and experimental disturbance of the gastrointestinal tract in rats
Yong-Li Yao, Wan-Dai Zhang, Yu-Gang Song, Institute of Gastrointestinal Diseases, Nanfang Hospital, First Military Medical University, Guangzhou 510515, Guangdong Province, China
Bo Xu, Department of Orthopedics Nanfang Hospital, First Military Medical University, Guangzhou 510515, Guangdong Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Military Science Foundation of China, No. 96M060
Correspondence to: Yong-Li Yao, Institute of Gastrointestinal Diseases, Nanfang Hospital, First Military Medical University, Guangzhou 510515, Guangdong Province, China. xbyyl@fimmu.edu.cn
Telephone: +86-20-85141544
Received: November 15, 2000
Revised: November 24, 2000
Accepted: November 30, 2000
Published online: June 15, 2001

Abstract
Key Words: stomach neoplasms/etiology, stomach neoplasms/surgery, gastrectomy, duodenogastric reflux, intestinal secretions, carcinogens



INTRODUCTION

The field of gastrointestinal hormones has expanded at a dizzying rate[1-4]. Gastrointestinal hormones as regulatory peptides that appear to be major components of bodily integration and have important regulatory actions on physiological function of the gastrointestinal tract. The successful isolation of some gastrointestinal hormones and the development of sensitive methods for their detection have led to the unexpected finding that they also exist in the brain. Recent studies[5-8] have indicated that some disorders of gastrointestinal tract are related to gastrointestinal hormones. We explored this relationship by measuring concentrations of gastrin, somatostatin, G cell and D cell.

MATERIALS AND METHODS

We used healthy adult male Sprague Dawley rats weighing 220 g ± 30 g. The rats were housed in individual cages in a temperature-controlled room (23 °C ± 2 °C) with a 12 h light-dark cycle. The rats were fed standard rat chow (provided by Experimental Animal Center, First Military Medical University) and water ad labium. Rats were acclimatized to the environment for 7 days prior to the experiments.

Reserpine was obtained from the Hongqi Pharmaceutical Factory (lot No. 960313). Si Junzi Tang, composed of ginseng, bighead, Fuling and Zhi Gancao, was prepared by routine method.

Fifty rats were randomly divided into five groups of ten rats each. Group A, the negative control group was injected with physiological saline, 0.5 mL·kg-1·d-1, ip and distilled water, 2 mL, twice daily, ig, for 14 days. Group B was injected with reserpine, 0.5 mL·kg-1·d-1, ip and distilled water, 2 mL, twice daily, ig, for 14 days. Group C was reserpine (0.5 mL·kg-1·d-1, ip) and Si Junzi Tang (2 mL, twice daily, ig), for 14 days. Group D was first injected with reserpine and distilled water for 14 days (similar to Group B). Group D was then injected with distilled water (2 mL twice daily, ig) for 6 days. Group E was first injected with reserpine and water for 14 days (similar to Group B). Group E was then injected with Si Junzi Tang (2 mL, twice daily, ig) for 6 days.

We collected samples of body fluids (intestinal juice[9], gastric juice[10], plasma) and tissues (gastric antrum, jejunum, hypothalamus[11]) after treatment was finished for each group. All samples were stored at -70 °C until analysis. All gastroduodenal sections collected were fixed with neutral-buffered 10% formalin and embedded in paraffin.

Gastrin levels in samples were measured with radioimmunoassay kits from the Chinese Atomic Energy Research Institute of Immunotechnology. Somatostatin levels were measured with radioimmunoassay kits from Dong-Ya Research Institute of Immunotechnology. G cells and D cells of gastroduodenal mucosa were analyzed with immunohistochemical technique (using polyclonal antibody to gastrin and somatostatin) and the Quantimet 500 image analysis system (Leica, USA). Staining was performed using a streptavidin/peroxidase kit (SPTM, ZYMED, USA). Immunostaining by replacing primary antibody with PBS was also conducted as a negative control. G cells and D cells of gastroduodenal mucosa were stained in continuous sections. Under magnification × 400, five randomly-selected cyclograms of each section were entered into the main computer of Quantimet 500 image analysis system from the photograph system. The main computer system analyzed graphs with corresponding software and obtained data of cell number, even square and even grey. The ratio of the cell number to square of G/D cells was calculated in continuous sections of G cells and D cells stained as follows: ratio of number of G/D cells = G cells number/D cells number; ratio of square on G/D cells = G cells square/D cells square.

Statistical analysis

Data were expressed as mean ± standard error of the mean. Experimental results were analyzed by analysis of variance and t tests for multiple comparisons. Statistical significance was determined at P < 0.05.

RESULTS
Levels of gastrin and somatostatin in body fluids and tissues

The levels of gastrin in all samples tested from Group B (treated with reserpine alone) were 20%-60% less than Group A (controls). Levels of gastrin in Group D (treated with reserpine, the water) were also less than in Group A, though higher than in Group B. Levels of somatostatin were 50%-200% higher the Group B than in Group A. Levels of somatostatin were also higher than in Group A, though not as high as in Group B (Table 1, Table 2, Table 3, Table 4).

Table 1 Gastrin in body fluids (n = 10, -x±s, ng/L).
GroupPlasmaGastric juiceIntestinal juice
A168.40 ± 38.0148.72 ± 12.55147.36 ± 31.47
B109.46 ± 40.88a30.78 ± 6.81a96.58 ± 14.36a
C150.38 ± 31.7551.17 ± 7.56b171.19 ± 25.28b
D119.48 ± 30.21a33.03 ± 6.64ac122.57 ± 31.61bc
E179.84 ± 64.77bd54.29 ± 7.05bd79.01 ± 33.31abd
Table 2 Somatostatin in body fluids (n = 10, -x±s, ng/L).
GroupPlasmaGastric juiceIntestinal juice
A17.93 ± 4.469.70 ± 2.1413.43 ± 3.08
B32.56 ± 7.91a29.21 ± 4.58a25.74 ± 4.16a
C18.24 ± 4.02b11.69 ± 2.53b15.30 ± 3.31b
D20.87 ± 4.68b22.56 ± 4.99abc24.16 ± 4.50ac
E16.98 ± 3.53b7.64 ± 2.26bcd13.85 ± 2.19bd
Table 3 Gastrin in tissues (n = 10, -x±s, ng/g).
GroupGastric antrumJejunumHypothalamus
A503.77 ± 74.3238.57 ± 8.14107.85 ± 16.36
B232.61 ± 53.88a22.47 ± 3.02a68.09 ± 13.40a
C493.75 ± 91.20b35.76 ± 6.41b102.79 ± 12.29b
D372.31 ± 54.35abc28.46 ± 5.48abc89.95 ± 11.11abc
E535.67 ± 57.58bd41.31 ± 7.27bd110.03 ± 12.94bd
Table 4 Somatostatin in tissues (n = 10, -x±s, ng/g).
GroupGastric antrumJejunumHypothalamus
A175.19 ± 26.2423.50 ± 6.3643.96 ± 6.45
B367.15 ± 42.30a47.31 ± 10.97a66.76 ± 6.55a
C207.23 ± 34.08b21.00 ± 5.66b45.56 ± 5.57b
D327.94 ± 46.68abc25.88 ± 7.57b59.45 ± 6.02abc
E184.94 ± 57.58bd17.61 ± 5.12b39.98 ± 5.40bd

Levels of both gastrin and somatostatin in Groups C (treated concurrently with reserpine Si Junzi Tang) and E (treated first with reserpine then Si Junzi Tang) were similar to those in Group A, indicating that Si Junzi Tang may provide a protective effect against the functional disturbance caused by reserpine.

Expression of G cells and D cells in gastroduodenal mucosa

G cells of gastric antrum were mainly located in the lower 2/3 of the mucosa and rarely in the upper 1/3. G cells appeared round, elliptical, fusiform, triangular or irregular. They differed from the typical endocrine cells of gastroduodenum in that they produced long cytoplasmic and processed the end with small bulbous expansions on the putative effector cells. G cells gave off long cytoplasmic and processed terminate on D cells and also on enterochromaffin cells (Figure 1 and Figure 2). D cells of gastric antrum were mainly located in the lower 1/3 of the mucosa and rarely in the upper 2/3 (Figure 3). Appearance of D cells was similar to that of G cells. G cells and D cells of the duodenum were mainly distributed in the intestinal glands and their appearances were similar to those of the gastric antrum. The number and even square of G cells and D cells declined, whereas the even grey of G cells and the ratio of the number and square on G/D increased in functional disturbance of gastrointestinal tract (Table 5, Table 6, Table 7).

Figure 1
Figure 1 G cells of gastric antrum were mainly located in the lower 2/3 mucosa and rarely in the upper 1/3 mucosa. Magnification × 400
Figure 2
Figure 2 G cells appeared round, elliptical, fusiform, triangular or irregular. Magnification × 1000
Figure 3
Figure 3 D cells of gastric antrum were mainly located in the lower 1/3 mucosa and rarely in the upper 2/3 mucosa. Magnification × 400
Table 5 G cells and D cells of gastric antrum mucosa (n = 10, -x±s).
GroupG cells
D cells
NumberSquare (± 10-6 m2)Even greyNumberSquare (× 10-6 m2)Even grey
A103.60 ± 12.3398.05 ± 7.06125.41 ± 2.2915.67 ± 5.2170.49 ± 8.96124.04 ± 3.14
B40.33 ± 5.53a93.47 ± 6.55128.24 ± 3.03a5.70 ± 1.32a45.41 ± 5.27a115.38 ± 2.62a
C72.70 ± 10.14ab94.31 ± 5.77125.90 ± 3.13b11.20 ± 2.55ab61.05 ± 7.11ab123.72 ± 3.10b
D50.63 ± 7.54abc87.54 ± 8.92abc123.15 ± 4.09abc8.30 ± 1.86abc43.54 ± 5.06ac123.27 ± 2.26b
E88.03 ± 10.37abcd97.16 ± 6.24d125.39 ± 2.22bd13.83 ± 3.11abcd72.71 ± 5.88bcd124.47 ± 2.46b
Table 6 G cells and D cells of jejunum mucosa (n = 10, -x±s).
GroupG cells
D cells
NumberSquare (× 10-6 m2)Even greyNumberSquare (× 10-6 m2)Even grey
A63.57 ± 10.1681.99 ± 9.75125.44 ± 3.147.80 ± 2.5860.56 ± 7.26125.82 ± 1.70
B29.43 ± 7.11a78.49 ± 6.94130.24 ± 2.01a3.13 ± 1.14a41.80 ± 5.14a111.29 ± 3.26a
C54.83 ± 10.03ab73.63 ± 6.55ab124.58 ± 2.31b6.77 ± 1.98b53.92 ± 6.86ab125.94 ± 2.58b
D35.37 ± 9.16abc62.18 ± 6.07abc122.34 ± 2.56abc5.10 ± 1.92abc44.52 ± 6.02ac123.80 ± 2.96b
E65.10 ± 9.63bcd77.44 ± 7.69ad125.80 ± 2.45bd7.53 ± 2.26bd61.77 ± 10.27bcd125.47 ± 2.76abcd
Table 7 Ratio of the number and square on G/D cells (n = 10, -x±s).
GroupGastric antrum
Jejunum
Number (cells)SquareNumber (cells)Square
A6.48 ± 0.771.42 ± 0.248.43 ± 1.571.39 ± 0.20
B7.20 ± 0.54a2.05 ± 0.37a9.82 ± 2.71a1.87 ± 0.30a
C6.47 ± 0.691.55 ± 0.26b8.25 ± 1.46b1.38 ± 0.21b
D5.95 ± 1.13b2.01 ± 0.30ac7.33 ± 1.16b1.18 ± 0.25bc
E6.81 ± 0.61d1.29 ± 0.13abcd8.53 ± 1.87b1.24 ± 0.25b
DISCUSSION

Gastrin and somatostatin are both important gut hormones[12-21]. Edkins first discovered gastrin in 1905. However, the existence of gastrin was questioned until the middle of the 19th century. Gastrin is mostly distributed in the mucosa of gastric antrum, the mucosa of the jejunum, and the central nervous system. Gastrin has a wide range of biological actions[22-25]. The most potent actions of gastrin are stimulation of gastric acid secretion[26-29] and antral smooth muscle activity.

Somatostatin was originally isolated from extracts of sheep hypothalamus as a growth hormone inhibiting factor. In addition to its marked effect on GH secretion, the peptide[30-33] possesses a surprising range of biological effects paralleled by an equally wide but characteristic anatomical distribution. Somatostatin also appears to inhibit the secretion of many gastrointestinal hormones and may be an important regulator for gastrointestinal functions[34-37].

Upon functional disturbance of the gastrointestinal tract, we inferred[22-25] that the inhibition of the release of gastrin might lead to a decrease of basal and maximal gastric acid secretion and inhibition of the secretion of gastric proteinase and inner factor. We further anticipated a decrease in blood flow to the upper digestive tract mucosa, which would lead to a reduction in nutrition and proliferation of gastric mucosal cells. Somatostatin[30-33] inhibited not only secretion of basal gastric acid and gastric proteinase, but also the effect of gastrin on gastric acid secretion. Some studies have demonstrated that motilin[34] had a potent actions on the smooth muscle of the stomach, the duodenum, and the colon, which could enhance gastric emptying rate, colonic motility and nutrition absorption. We observed that somatostatin inhibited the gastric emptying rate, colonic motility and nutritional absorption by inhibiting motlin secretion following administration of reserpine. We inferred that decrease of gastrin release, increase of somatostatin release, and mutual regulatory disturbance can lead to a functional disturbance of gastrointestinal tract. Treatment with Si Junzi Tang, appeared to regulate the levels of gastrin and somatostatin in body fluids and tissues. Following administration of Si Junzi Tang, both gastrin and somatostatin remained or returned to normal level in the experimental functional disturbance of gastrointestinal tract model. This result indicates that Si Junzi Tang may be used to treat disorders of gastrointestinal hormones secretion.

Somatostatin[38] is also produced by endocrine-like (D) cells of the gut and pancreas and by peripheral nerve cells. Its actions are not restricted to the hypothalamo-hypophyseal system, somatostatin may also inhibit the release of several gastrointestinal and pancreatic hormones and affect on gastric HCl and pancreatic enzyme secretion. The bulk of evidence[38-40] suggests that somatostatin is delivered directly onto the membranes of G cells and parietal cells. In agreement with the cytochemical observations of D cells processing termination on G cells. Studies on the isolated perfused stomach have shown that infusion of somatostatin antiserum results in a brisk increase of gastrin release to up to 70 percent of maximally stimulated levels. These data suggest that G cells may be under tonic inhibitory control by somatostatin.

The reserpine-induced functional disturbance caused the number of G cells, D cells, and the even square of D cells to decline, whereas the even grey of G cells evaluated and ratio of the number and square on G/D increased[39-40]. These data suggest that high levels of somatostatin detected in body fluids and tissues were partly due to the release of somatostatin by D cells. High levels of somatostatin resulted in a decrease of gastrin release. This might explain the changes observed in G cells and D cells.

The study confirmed that changes of gastrin and somatostatin are associated with gastrointestinal disorder, which is one of the important causes for pathogenesis of the gastrointestinal tract.

Footnotes

Yong-Li Yao, graduated from First Military Medical University with a master degree in 1998. She now works in the Institute of Gastrointestinal Diseases, Nanfang Hospital as a doctoral candidate majoring gastrointestinal diseases and gastrointestinal hormones, she has published 8 papers.

Edited by Jason Carr

References
1.  Nauck MA. Is glucagon-like peptide 1 an incretin hormone. Diabetologia. 1999;42:373-379.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 81]  [Cited by in F6Publishing: 80]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
2.  Pan XZ, Cai LM. Current status of Gastrointestinal hormones. Shijie Huaren Xiaohua Zazhi. 1999;7:464-466.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Rehfeld JF. The new biology of gastrointestinal hormones. Physiol Rev. 1998;78:1087-1108.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Straus E. Gastrointestinal hormones. Mt Sinai J Med. 2000;67:54-57.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  MacIntosh CG, Andrews JM, Jones KL, Wishart JM, Morris HA, Jansen JB, Morley JE, Horowitz M, Chapman IM. Effects of age on concentrations of plasma cholecystokinin, glucagon-like peptide 1, and peptide YY and their relation to appetite and pyloric motility. Am J Clin Nutr. 1999;69:999-1006.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Zaĭtsev VT, Boĭko VV, Savvi SA, Taraban IA, Belozerov IA, Butkevich AIu. [The meaning of duodenostasis in the intestinal phase gastric secretion disorders in bleeding duodenal ulcer]. Klin Khir. 1999;5-6.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Coll P, Guttormsen AB, Berstad A. [Gastrointestinal disease with elevated plasma homocysteine level]. Tidsskr Nor Laegeforen. 1999;119:3577-3579.  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Yao YL, Zhang WD, Song YG. Relationship between Spleen deficiency and gastrointestinal hormones. Xin Xiaohuabingxue Zazhi. 1997;5:728-729.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Elson CO, Ealding W, Lefkowitz J. A lavage technique allowing repeated measurement of IgA antibody in mouse intestinal secretions. J Immunol Methods. 1984;67:101-108.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 184]  [Cited by in F6Publishing: 186]  [Article Influence: 4.7]  [Reference Citation Analysis (0)]
10.  Ye FX Experimental zoology in medicine. First edition. Beijing: The People's Medical Publishing House 1995; 227.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Lü XF, Lu RX, Ye XQ. Changes of β-endorphin in hypothalamus of yang insufficiency model and function of restoring yang drug. Zhongyi Zazhi. 1994;35:619-620.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  Sawada M, Dickinson CJ. The G cell. Annu Rev Physiol. 1997;59:273-298.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 29]  [Article Influence: 1.1]  [Reference Citation Analysis (0)]
13.  Larsson LI, Goltermann N, de Magistris L, Rehfeld JF, Schwartz TW. Somatostatin cell processes as pathways for paracrine secretion. Science. 1979;205:1393-1395.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 387]  [Cited by in F6Publishing: 385]  [Article Influence: 8.6]  [Reference Citation Analysis (0)]
14.  Dockray GJ. Topical review. Gastrin and gastric epithelial physiology. J Physiol. 1999;518:315-324.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 109]  [Cited by in F6Publishing: 113]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
15.  de Weerth A, Bläker M, von Schrenck T. [Receptors for cholecystokinin and gastrin]. Z Gastroenterol. 1999;37:389-401.  [PubMed]  [DOI]  [Cited in This Article: ]
16.  Epelbaum J, Dournaud P. [Somatostatin: a ubiquitous peptide]. C R Seances Soc Biol Fil. 1998;192:597-606.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Reubi JC, Schaer JC, Markwalder R, Waser B, Horisberger U, Laissue J. Distribution of somatostatin receptors in normal and neoplastic human tissues: recent advances and potential relevance. Yale J Biol Med. 1997;70:471-479.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Tuo BG, Yan YH, Ge ZL, Ou GW, Zhao K. Ascorbic acid secretion in the human stomach and the effect of gastrin. World J Gastroenterol. 2000;6:704-708.  [PubMed]  [DOI]  [Cited in This Article: ]
19.  Xie B, He SW, Wang XD. Effect of gastrin on protein kinase C and its subtype in human colon cancer cell line SW480. World J Gastroenterol. 2000;6:304-306.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  Lü B, Ye ZY, Zhu XL, Zhang Q, Du WD, Xiang BK. Study on gastrointestinal hormones in tissues and blood of gastric cancer. Shijie Huaren Xiaohua Zazhi. 2000;8:1429-1430.  [PubMed]  [DOI]  [Cited in This Article: ]
21.  Watson SA, Durrant LG, Morris DL. Growth-promoting action of gastrin on human colonic and gastric tumour cells cultured in vitro. Br J Surg. 1988;75:342-345.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 63]  [Cited by in F6Publishing: 70]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
22.  Ryberg B, Tielemans Y, Axelson J, Carlsson E, Håkanson R, Mattson H, Sundler F, Willems G. Gastrin stimulates the self-replication rate of enterochromaffinlike cells in the rat stomach. Effects of omeprazole, ranitidine, and gastrin-17 in intact and antrectomized rats. Gastroenterology. 1990;99:935-942.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Eissele R, Patberg H, Koop H, Krack W, Lorenz W, McKnight AT, Arnold R. Effect of gastrin receptor blockade on endocrine cells in rats during achlorhydria. Gastroenterology. 1992;103:1596-1601.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Kusyk CJ, McNiel NO, Johnson LR. Stimulation of growth of a colon cancer cell line by gastrin. Am J Physiol. 1986;251:G597-G601.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Wu P, Rui J, Xia XH, Yuan P, Zhou G, Wu CY. Gastrin stimulated growth of colorectal carcinoma. Shijie Huaren Xiaohua Zazhi. 1999;7:501-503.  [PubMed]  [DOI]  [Cited in This Article: ]
26.  Kovacs TO, Walsh JH, Maxwell V, Wong HC, Azuma T, Katt E. Gastrin is a major mediator of the gastric phase of acid secretion in dogs: proof by monoclonal antibody neutralization. Gastroenterology. 1989;97:1406-1413.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Chuang CN, Tanner M, Chen MC, Davidson S, Soll AH. Gastrin induction of histamine release from primary cultures of canine oxyntic mucosal cells. Am J Physiol. 1992;263:G460-G465.  [PubMed]  [DOI]  [Cited in This Article: ]
28.  Ackerman SH. Ontogeny of gastric acid secretion in the rat: evidence for multiple response systems. Science. 1982;217:75-77.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 23]  [Cited by in F6Publishing: 22]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
29.  Waldum HL, Sandvik AK, Brenna E, Petersen H. Gastrin-histamine sequence in the regulation of gastric acid secretion. Gut. 1991;32:698-701.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 151]  [Cited by in F6Publishing: 161]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
30.  Park J, Chiba T, Yamada T. Mechanisms for direct inhibition of canine gastric parietal cells by somatostatin. J Biol Chem. 1987;262:14190-14196.  [PubMed]  [DOI]  [Cited in This Article: ]
31.  Koerker DJ, Ruch W, Chideckel E, Palmer J, Goodner CJ, Ensinck J, Gale CC. Somatostatin: hypothalamic inhibitor of the endocrine pancreas. Science. 1974;184:482-484.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 378]  [Cited by in F6Publishing: 319]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
32.  Okamoto E, Haruma K, Hata J, Tani H, Sumii K, Kajiyama G. Effects of octreotide, a somatostatin analogue, on gastric function evaluated by real-time ultrasonography. Aliment Pharmacol Ther. 1997;11:177-184.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 17]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
33.  Koop H, Bothe E, Eissele R, Dionysius J, Arnold R. Somatostatin-gastrin interactions in the rat stomach. Res Exp Med (Berl). 1988;188:115-121.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 9]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
34.  Yao YL, Song YG, Zhang WD. Study on the relationship between motilin and enterorrhea of spleen deficiency. Shijie Huaren Xiaohua Zazhi. 1999;7:432-433.  [PubMed]  [DOI]  [Cited in This Article: ]
35.  Yao YL, Song YG, Zhang WD, Zhang DQ. Relationship between gastrin, somatostatin and functional disturbance of gastrointestinal tract. Shijie Huaren Xiaohua Zazhi. 1999;7:1016-1017.  [PubMed]  [DOI]  [Cited in This Article: ]
36.  Yao YL, Song YG, Zhang WD. Experimental study on the relationship between gastrin and somatostatin in body fluid and spleen asthenia syndrome. Zhongguo Zhongxiyi Jiehe Piwei Zazhi. 2000;8:333-335.  [PubMed]  [DOI]  [Cited in This Article: ]
37.  Zhang WD, Yao YL, Song YG. Variation in content of gastrin and somatostatin in experimental model of spleen asthenia syndrome and its significance. Zhongguo Zhongxiyi Jiehe Piwei Zazhi. 1998;6:223-225.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  Glória H, Portela-Gomes M, Grimelius L, Ahlman H, Ferra MA. Effects of adrenalectomy on serotonin-, somatostatin-, and gastrin-immunoreactive cells in rat gastrointestinal tract. Dig Dis Sci. 1997;42:1216-1220.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 4]  [Article Influence: 0.1]  [Reference Citation Analysis (0)]
39.  Yao YL, Song YG, Zhang WD. Variations of G cells and D cells in experimental spleen asthenia and its significance. Zhongguo Zhongxiyi Jiehe Piwei Zazhi. 1999;7:8-11.  [PubMed]  [DOI]  [Cited in This Article: ]
40.  Yao YL, Song YG, Zhang WD. Changes and significance of G cells and D cells of experimental functional disturbance of gastrointestinal tract model. Zhongguo Zuzhi Huaxue Yu Xibao Huaxue Zazhi. 2000;9:293-296.  [PubMed]  [DOI]  [Cited in This Article: ]