| Gastrin has been detected by John in the sinus ventriculi mucosa first time in 1905, which has been believed that it has relation with the stimulation of gastric acid secretion. In 1964, the gastrin has been separated and purified by Gregory and Tracy, which be affirmed one kind of gastrointestinal peptide hormones.At present, it is known to all that gastrin is synthesized in the G cell of the sinus ventriculi, which has the active molecules G-17 and G-34. G-17 and G-34 are the 17and 34 amino acid polypeptides. Gastrin can go into the blood, tissue fluid and the gastric fluid through the way of the endocrine, paracrine and the cavity secretion, and then it has the function of stimulating the gastric acid secretion and the mucosa cells nutrition through the combination with its receptors.Recently, along with the developing and the investing deeply, scientists believed that gastrin can prompt the occurrence and development of the gastric mucosa affection including the gastric carcinoma, and the blood is one of the main routes. The investigation displayed that the homeostasis of gastrin can change along with the different stages of the gastric carcinomatous process, and it is the important indictor of precancerous lesion serum diagnosis. However, it has no reports in details about the possibility of the gastrin serum level to the function in the gastric mucosa carcinomatous change. In order to explore the dynamic relation and meaning between the gastrin express and serum gastrin level and then to reveal the mechanism of the changes of serum gastrin, we have detected immunehistochemical reaction and ELISA through the investigation of the 336 biopsyand serum samples which included control 33 samples, superficial gastritis 53 samples, gastric ulcers 36 samples, atrophic gastritis 85 samples, atypical hyperplasia 49 samples and gastric carcinoma 80 samples.In result, gastrin positive cells distribute in the middle and lower parts of the gastric mucosa glands in the control groups, but it in cluster distribution in the superficial gastritis and the gastric ulcer samples, and there are light dying, degranulation phenomenons, and the scatter and disperse distribution in the atrophic gastritis. The gastrin positive cells has the lamella distribution in the gastric mucosa atypical hyperplasia, and in the gastric carcinoma tissues, less gastrin positive cells can be seen, and then it can be cluster in the paracarcinoma tissues. So in the investigation results, along with the changes of the G cells secretionstation and the distribute forms, the protein of gastrin changed fluctuatly.Having analysed the gastrin positive cells and the serum gastrin level in the process of the normal mucosa→superficial gastritis→gastric ulcer→atrophy gastritis→gastric mucosa atypical hyperplasia→gastric carcinoma, the results manifested that the gastrin positive cells and the serum gastrin level increased from the normal gastric mucosa to the superficial gastritis. And the gastrin positive cells decreased and the serum gastrin level increased evidently from the superficial gastritis to the gastric ulcer, but they are decreased evidently from the gastric ulcer to the atrophic gastritis, and then they all increased lightly from the atrophic gastritis to the atypical hyperplasia, and from the atypical hyperplasia to the gastric cancer, gastrin positive cells increased and the gastrin level is decreased. This is a evidence about the separation between the gastrin protein changes and the serum gastrin level in the process of the gastric mucosa canceration, and the gastrin secretion route can be adjust to in the different stages of mucosa canceration.The gastric mucosa canceration is a chronic pathology process with many stages, at the same time it is a pathology process of changes alternatively. The gastrin positive cells and the serum gastrin level increased from the normal gastric mucosa to the superficial gastritis. And the gastrin positive cells decreased and the serum gastrin level increased evidently from the superficial gastritis to the gastric ulcer. These results manifested that the gastrin protein and the gastrin serum level are separated in this stage. It is maybe because inflammatory factors and the cell factors can prompt the gastrin synthesis and release and then the gastrin can accelerate this pathology process result to gastrin release accordingly in the gastric gastritis. Gastrin can compensated secretion and nourished the gastric mucosa through the endocrine route in the gastric ulcer stage. The gastrin positive cells and gastrin serum level becomes decrease in the gastric mucosa atrophic stage, but they become increased in the atypical hyperplasia, which means the gastrin parallel to the gastrin serum level. This result pace to the G cells diminished in the atrophic gastritis and to the G cells damaged lightly in the slight atypical hyperplasia which is the gastrin homeostasis in the physiological condition. In the experiments, gastrin positive cells increased in the gastric canceration but gastrin serum level decreased. Scientists believed that the gastrin secreted by the gastric positive cells and G cells in the gastric canceration tissues or theparacanceration tissues, which can combine with its receptor and then prompt a series of proliferation reactions. Above all are the reasons of separation phenomenon between the gastrin changes and gastrin serum level.In a word, there is the separation between the gastrin and the gastrin serum level in the early and late stages of the gastric mucosa canceration, but they are paralleled in the middle stage of middle stages. So the dynamic balance during the gastrin and serum gastrin level is the important indictor in the gastric mucosa canceration. |
