[Effect of a meal on electrocardiographic features in patients with coronary artery disease]. / Wplyw posilku na obraz elektrokardiogramu u osób z choroba niedokrwienna serca.

The aim of the study was to assess the relationship between gastric motility and extent of coronary insufficiency in males with and without stabile coronary artery disease (CAD). The study group consisted of 30 males with CAD (mean age 56 +/- 12 years) and 10 healthy males in control group (mean age 52 +/- 14 years). In both groups we performed exercise treadmill test (ETT) in interdigestive period (IP) and postprandially after ingestion of a standard meal (775 kcal) after 30 and 120 min. Gastric emptying was determined as antral area evaluated in ultrasonography before, 30 and 120 min. after meal. A period of time to ST depression > or = 1 mm, mean time of exercise, and a maximal voltage of ST depression were measured and compared between studied group of patients in t-test. In healthy individuals there was no influence of meal on ETT, thus in men in CAD group postprandially we observed shortening of time to ST depression > or = 1 mm (p < 0.001) and mean time of exercise (p < 0.001). These findings were parallel to observed enlarged gastric antral area reflecting gastric filling in postprandial period. ST depression during ETT 30 min. after meal was deeper than in interdigestive period (p < 0.001). In contrast to healthy individuals intake of standard meal in CAD group increased symptoms of coronary insufficiency during stress testing. Relationship between exercise-induced coronary insufficiency and degree of gastric filling appears as increasing of coronary insufficiency connected with gastric filling and graduate decreasing during digestion.

Impact of Helicobacter pylori and nonsteroidal anti-inflammatory drugs on gastric ulcerogenesis in experimental animals and in humans.

Helicobacter pylori (H. pylori) and nonsteroidal anti-inflammatory drugs (NSAID) are the most common pathogens in the gastroduodenal mucosa in animals and humans, but their relationship in ulcerogenesis has been little studied. According to some authors, H. pylori infection in humans does not act synergistically with NSAID on ulcer healing, therefore, there is no need to eradicate the germ. This notion is supported by the finding that the eradication of H. pylori does not affect NSAID-induced gastropathy treated with omeprazole and that H. pylori infection induces a strong cyclooxygenase-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandins, which should in turn counteract NSAID-induced gastropathy and heal the existing ulcer. Other investigators claim that H. pylori infection acts synergistically with NSAID on ulcer development, therefore, H. pylori should be eradicated, particularly at the start of long-term NSAID therapy. Maastricht 2-2000 consensus also recommends eradication prior to NSAID treatment, but this eradication does not appear to accelerate ulcer healing or to prevent the recurrent ulcers in NSAID users. Our studies in almost 6,000 dyspeptic patients undergoing upper endoscopy and [(13)C]-urea breath test (UBT) revealed that about 70% of these patients are H. pylori (+) and about 30.6% of these develop gastroduodenal ulcers. Of these ulcers, over 70% were H. pylori (+) positive, 12% NSAID (+), 8% were both H. pylori (+) and NSAID (+), while 22% ulcers were H. pylori (-) and NSAID (-) or "idiopathic" ulcers. Basically, our results support Hawkey's concept and this also agrees with our findings in the rat model showing that: (1) there is no synergistic interaction between H. pylori infection and NSAID on gastric ulcer development, (2) H. pylori and NSAID are independent risk factors for peptic ulceration, and (3) NSAID therapy in H. pylori positive patients attenuates the ulcer development possibly due to direct inhibitory action of these drugs on H. pylori.

Case presentation of gastrinoma combined with gastric carcinoid with the longest survival record -- Zollinger-Ellison syndrome: pathophysiology, diagnosis and therapy.

BACKGROUND: Zollinger-Ellison syndrome is a very rare disease caused by tumor with gastrin producing cells accompanied by hypergastrinemia leading to gastric hypersecretion and peptic ulcers and their complications. CASE STUDY: Female case of gastrinoma (Zollinger-Ellison syndrome; Z-E) with a record of 38 yrs of survival. Acute gastro-duodenal ulcers started at 28 yr of age and Z-E was diagnosed by using gastrin assays. Basal and maximal acid outputs and ratio of basal/maximal outputs were away over normal limits. Because of ulcer recurrence and complications, patient was subjected to several gastric surgeries but refused total gastrectomy. She was also treated with many H2-receptor (R) antagonists and proton-pump inhibitors (PPI), each new drug being initially highly effective but then showing declining efficacy except when PPI, lansoprazole was used. The gastrin level rose in the course of disease from initial high value of 2000 pg/mL to the extreme 4500 ng/mL at present. During the last 2 yrs, metastasis mainly to liver developed and they were successfully treated by synthetic octapeptide derivative of somatostatin and, as a result, metastatis partly reduced and plasma gastrin drasticly decreased. Biopsy taken from liver metastasis showed the presence of typical gastrinoma cells with gastrin and chromogranin, while that from oxyntic mucosa revealed the ECL-cell hyperplasia with carcinoid tumors and unexpected gastric atrophy. CONCLUSIONS: This phenomenal case described in this article might be the new proven evidence needed by gastroenterologists to overturn the traditional treatment using total gastrectomy as a treatment of choice to the partial gastrectomy combined with proton pump inhibitors.

[Exogenous nitric oxide and gallbladder contractility in humans]. / Kurczliwosc pecherzyka zólciowego a egzogenny tlenek azotu.

The physiological function of the gallbladder (GB) is to deliver concentrated bile to the duodenum after a meal. This requires a complex coordination of the motor, secretory, and absorptive functions of the gallbladder. Control of GB motor functions involves a constant interplay between a large number of stimulatory and inhibitory hormones and neurotransmitters. With regard to intrinsic neurotransmitters, nitric oxide (NO) acts as a neurotransmitter in nonadrenergic, noncholinergic (NANC) pathways of the gallbladder. This compound has been found to inhibit GB tone and contraction in both animal and human studies. The Purpose of the present study was to examine the effects of exogenous NO donors such as glyceryl trinitrate (GTN), molsidomine (MO) and L-arginine (L-Arg) on fasting GB volume and on meal-stimulated gallbladder contraction expressed as ejection fraction (EF). The healthy subjects (13 men and 17 women), age range 19-41 years participated in this study. GB volume was examined by means of an ultrasonographic method. Volumes of GB were calculated using the sum of cylinders method as described by Dodds. EF was measured every 15 min up to a total observation period of 2 h. After recording of control values, 0.5 mg GTN was administered sub-lingually, or 4 mg MO orally or L-Arg (12.63 g of L-Arg in 300 ml of 0.9% NaCl) was infused i.v. over 120 min. It was found that the fasted GB volume was increased after GTN by 22 +/- 10% and after MO by 28 +/- 4% (p < 0.05). Post-prandial EF was reduced maximally by 22 +/- 9% (p < 0.05) after pretreatment with GTN and by 32 +/- 8% (p < 0.01) after MO. Whereas L-Arg was without any effect on resting GB, however it reduced significantly stimulated EF. These findings support the earlier knowledge that NO, released from its exogenous donors has the potent inhibitory effect on human gallbladder motor activity.