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Background: Acetylsalicylic acid (ASA)-induced gastric injury is reduced when ASA is administered along with phosphatidylcholine. The hydrolysis of endogenous phosphatidylcholine leads to the production of betaine, which may participate in the maintenance of cellular homeostasis. The present aims were to investigate the effects of exogenous betaine and its palmitic acid complex (betaine-palmitate) in the protection of the gastric mucosa in ASA-induced subacute damage. Methods: Repeated doses of ASA were given intragastrically to male Wistar rats. Control rats were given vehicle only, while treated animals were challenged with ASA or with ASA along with betaine, palmitic acid or betaine-palmitate. The gastric mucosa was examined after 3 days and the nature of any microscopic mucosal injury was assessed by histology. The extent of macroscopic damage, changes in permeability (assessed by Evans blue method) and tissue ATP concentrations were determined in separate series. Results: ASA induced a significant fall in the ATP content of the mucosa, which was not affected by the other drugs used in the study. However, the ASA-induced mucosal permeability increase could be completely reversed by betaine-palmitate supplementation. The extent of severity of the macroscopic and microscopic lesions was 33% and 2.45, respectively, for ASA, as compared with 15% and 2.2 for betaine, 14% and 1.9 for palmitic acid and 3% and 1.4 for betaine-palmitate. Conclusions: Betaine-palmitate affords a significant protective effect against ASA-induced injury, without influencing the ATP synthesis, and this suggests that the defence is due to its ability to prevent secondary damage. [ABSTRACT FROM AUTHOR]

This study was designed to determine whether oxygen-derived free radicals play a role in the pathogenesis of gastric mucosal lesions produced by haemorrhagic shock and reperfusion experimental model in the rat. Ranitidine (H2-receptor blocker) in different doses, allopurinol, an inhibitor of xanthine oxidase and SOD (superoxide dysmutase) pre-treatment were used against haemorrhagic shock and reperfusion induced gastric mucosal lesions. Altogether 67 rats were divided into seven different groups. The area of gastric mucosal lesions was measured, the activity of endogenous peroxidase was examined histochemically and histological grading was made. Evans blue was used to demonstrate the improved permeability of gastric mucosal membranes. Ranitidine, in high dose, allopurinol and superoxide dysmutase significantly protected against haemorrhagic shock-induced gastric mucosal lesions, against improved membrane permeability and peroxidation.

Primary malignant tumors of small bowels are relatively rare among the GIA-tumors. There are no specific methods to find these tumors in an early stage. Only the specific radiological examination (double contrast method or CT-scan) or sometimes the specific jejunoscopy can prove the correct diagnosis before the operation. Usually surgeons have to operate because of the emergency situation caused by primary malignant tumors of small bowel. A total of 21 patients were operated on for malignant tumors of small bowels since 1st January, 1986 till 31st December, 1995 (during 10 years). 13 of the 21 were urgent cases. 3 perforations and 10 mechanical bowel obstructions were the indications of the acute surgical procedures. The preoperative diagnoses were correct in the eight elective operations. Types of operations: 8 jejunal-resection, 11 ileal-resection, 1 Whipple-operation, 1 ileal-resection with right hemicolectomy. Peri-operative mortality rate was zero. Histological reports: 13 adenocancers, 2 leiomyosarcomas, 5 malignant carcinoids, 1 anaplastic cancer. Lymphomas and tumors of papilla Vateri were excluded from this study. Most of the patients had abdominal symptoms earlier than 8 months before the operations. Earlier diagnosis may give a better chance to operate these tumors in earlier stages, and it can give a better chance for the patients for longer survival.

Histamine release have been demonstrated in haemorrhagic shock. There are some observations that oxygen free radicals can cause histamine release. Oxygen free radicals play a role in the pathogenesis of gastric mucosal lesions. The goal of this study was to determine whether ranitidine or SOD and allopurinol pretreatment modify the histamine release during and after the haemorrhagic shock in the rat. In the anaesthetized rat 0.1 N HCl was instilled into the stomach and the rat was bled to reduce the blood pressure to 30 mmHg for 20 min. The shed blood was reinfused. Twenty min later the stomach was removed. The area of gastric mucosal lesions were measured, histological grading was made. Blood samples taken from the carotid artery were examined by radioimmunoassay (IMMUNOTECH) to determine the plasma histamine level. Plasma histamine level did not change significantly during the preparative surgery, but there was a significant increase of histamine level by the end of shock period. After the reinfusion of the blood the plasma histamine remained essentially at the same level for five min. Oxygen free radicals did not cause an important histamine release. By the end of the experiment the histamine level decreased dramatically. Ranitidine, allopurinol and SOD pretreatment provided significant protection against the gastric mucosal lesions. Allopurinol and SOD did not influence significantly the histamine level. Ranitidine caused significant histamine release immediately after the injection and every histamine value was significantly higher in this group except for the final value which was lower than the control one. The oxygen free radicals were not found as endogenous histamine releasers in this study.

This study was designed to determine whether oxygen-derived free radicals play a role in the pathogenesis of gastric lesions produced by hemorrhagic shock in the rat. Allopurinol (Zyloric), an inhibitor of xanthine oxidase (responsible for the formation of superoxide radicals) and MTDQ-DA (Kontrad), a synthetic antioxidant of dihydroquinoline type were used. In the anesthetized rat 0.1 N HCl was instilled into the stomach and the rat was bled to reduce the blood pressure to 30 mmHg for 20 min. The blood shed was retransfused. Twenty min later the stomach was removed. The area of gastric mucosal lesions were measured, the activity of endogenous peroxidase was examined histochemically and a histological grading was made. Both allopurinol and MTDQ-DA significantly protected against hemorrhagic shock-induced gastric lesions and peroxidation. These results suggest that oxygen-derived free radicals play an important role in the formation of gastric lesions produced by ischemia plus 0.1 N HCl.