Occurrence of Helicobacter pylori in dental plaque and saliva of dyspeptic patients.

BACKGROUND: Helicobacter pylori infection in the stomach is associated with gastric and duodenal ulcers, gastric cancers and gastric lymphoma. The organism is transmitted by ingestion, but the oral-oral route and the fecal-oral route are also suggested. The prevalence of infection with H. pylori in developing countries, including Brazil, is higher than in developed countries. PURPOSE: This study aimed to evaluate the role of the oral cavity as a reservoir of this species, by evaluating the occurrence of H. pylori in supragingival dental plaque and in saliva of Brazilian dyspeptic patients, whether harboring the organism or not in the stomach. MATERIAL AND METHODS: Forty-nine patients reporting dyspeptic symptoms were subjected to oral clinical examination and collection of saliva and supragingival dental plaque samples prior to the endoscopic examination. The detection of H. pylori in oral samples was performed by PCR using 16S rRNA primers. The bacteria were detected in stomach by means of the rapid urease test. RESULTS: Helicobacter pylori was detected in the stomach of 20 of 49 subjects reporting dyspeptic symptoms. The organism was detected in only one supragingival plaque sample, obtained from a patient positive for the urease test in the stomach and in none of the salivary samples. CONCLUSION: Supragingival dental plaque and saliva may not be relevant reservoirs of H. pylori.

Detection of Helicobacter pylori in gastric cancer.

BACKGROUND AND OBJECTIVES: Considering the high prevalence of stomach cancer in the northern region of Brazil and the recognized relationship between chronic gastric inflammation caused by Helicobacter pylori, and its carcinogenic potential, the objective we had with this study was to investigate the presence of the microorganism in macro and microscopic presentations of neoplasm in different regions of the stomach, and in non-malignant lesions concomitant to the adenocarcinoma in patients originating from the metropolitan area of Belém (State of Pará, Brazil). METHODS: Examinations were made on 172 patients divided into two groups: group I, formed by 75 patients with gastric carcinoma, and group II, formed by 97 patients with mild enanthematic gastritis, considered control group. The diagnosis was obtained during endoscopic examination and the respective biopsy. Gastric neoplasms were classified macroscopically in accordance with Borrmann's classification, and microscopically in accordance with Laurén's classification. In group I, 54 patients were male and 21 female while in group II, 22 patients were male and 75 female. The average age in group I was 61.2 years (range 27 to 86 years), while in group II it was 37.5 years (range 16 to 69 years). Thin sections were prepared and stained using the hematoxylin-eosin method. In the Helicobacter pylori research, the modified Gram stain was utilized. Statistical analysis was done by utilizing the chi-squared (chi 2) test, Mann-Whitney test (U), and Fisher's exact test. RESULTS: The results showed the detection of Helicobacter pylori were significantly greater in patients with mild enanthematic gastritis than in patients with gastric carcinoma. The presence of Helicobacter pylori in patients with gastric carcinoma and mild enanthematic gastritis was significantly greater in the antral region than in other gastric regions. Helicobacter pylori detection in patients with gastric carcinoma did not present a significant difference in relation to the macroscopic aspect of the tumor either intestinal or diffuse histological types. CONCLUSIONS: These data suggest the presence of the bacteria is predominant in the antral region and it does not show relation with the macroscopic types or histological intestinal or diffuse types of gastric carcinoma.

Cisplatin impairs fluid and electrolyte absorption in rat small intestine: a role for 5-hydroxytryptamine.

BACKGROUND: The antineoplastic drug cisplatin has been widely used for the treatment of cancer in humans but its use has been limited by vomiting and diarrhoea. Cisplatin releases 5-hydroxytryptamine into the gut which is thought to be the major mediator of cisplatin induced vomiting. AIM: To determine whether cisplatin affects fluid and electrolyte transport in rat jejunum and whether this change can be modulated by the 5-hydroxytryptamine3 receptor antagonist, ondansetron. METHODS: Jejunal perfusion in rats in vivo was performed one hour after intraperitoneal cisplatin (5 and 10 mg/kg) administration. The effect of pretreatment with subcutaneous ondansetron 300 microg/kg was investigated. RESULTS: Median net fluid absorption after cisplatin 10 mg/kg (67 microl/min/g dry intestinal weight (interquartile range 46 to 100); n = 15) was reduced compared with controls (120 (107 to 151) microl/min/g; n = 13; p<0.001). Ondansetron reversed the impairment of jejunal fluid absorption produced by cisplatin to normal (161 (130 to 176) microl/min/g; n = 11; p<0.001). Electrolyte movement paralleled fluid movement. Jejunal histological examination of sections from cisplatin treated animals showed villus damage, which was not prevented by pretreatment with ondansetron. CONCLUSION: These findings suggest that diarrhoea during cisplatin therapy may be due to altered fluid transport in the small bowel. The reversal of fluid transport to normal in the presence of a 5-hydroxytryptamine3 receptor antagonist suggests that 5-hydroxytryptamine is a local mediator in the small intestine.

In vivo effects of the 5-HT3 antagonist alosetron on basal and cholera toxin-induced secretion in the human jejunum: a segmental perfusion study.

BACKGROUND: 5-hydroxytryptamine type 3 receptor antagonists have been shown to reduce fluid and electrolyte secretion or promote absorption in experimental models of small intestinal secretion. The aim of this study was to compare the effects of a single dose (4 mg) of the 5-hydroxytryptamine type 3 receptor antagonist alosetron and placebo on jejunal fluid and electrolyte movement in humans under basal conditions (n = 7) and following cholera toxin-induced secretion (n = 5) in a randomized, double-blind, crossover design over two separate study periods. METHODS: One hour after oral alosetron or placebo, jejunal intubation was performed. A 30 cm segment of jejunum, isolated by two occluding balloons, was exposed to 15 microg of purified cholera toxin for 2 h prior to triple lumen perfusion with a plasma electrolyte solution containing [14C]-polyethylene glycol as a nonabsorbable volume marker. In the basal study, intestinal perfusion was performed without exposure to cholera toxin. Collection and analysis of the effluent from the jejunal segment allowed fluid and electrolyte movement to be calculated. RESULTS: Alosetron treatment increased basal jejunal fluid absorption (median 5.1 mL/cm/h [interquartile range 4.2 to 7.1] compared with placebo (3.8 [3.6 to 4.3] P = 0.028, two sided Wilcoxon matched pairs signed rank test)). However, following establishment of a secretory state by cholera toxin, alosetron failed to significantly promote absorption or reduce secretion (0.3 [-1.2 to 1.2] compared to placebo (-4.3 [-7.7 to -1.3] P = 0.14)). Adverse events during the study, which included anorexia, nausea, dizziness and loose bowel movements, were not considered to be clinically important. There were no clinically significant changes in laboratory parameters. CONCLUSION: The 5-hydroxytyptamine type 3 receptor antagonist, alosetron, increased basal fluid absorption in normal human small intestine but failed to have a beneficial effect in cholera toxin-induced secretion.

L-Arginine, nitric oxide, and intestinal secretion: studies in rat jejunum in vivo.

BACKGROUND: L-Arginine has been shown to induce fluid secretion in human jejunum. Nitric oxide, a derivative of L-arginine is thought to have an important role as an intestinal secretagogue. AIM: To determine the effect of L-arginine and the nitric oxide synthase inhibitor, nitro L-arginine methyl ester (L-NAME), on fluid and electrolyte movement in rat jejunum. METHODS: A 25 cm segment of rat jejunum was perfused in situ with iso-osmotic solutions containing either (1) saline, (2) D-arginine 20, (3) L-arginine 20, (4) L-NAME 0.1, 1, or 20 mmol/l, or (5) a combination of L-arginine 20 and L-NAME 0.1, 1, or 20 mmol/l. In further groups the effect of a subcutaneous injection of L-NAME 100 mg/kg was examined in rats pretreated with either D-or L-arginine 500 mg/kg. RESULTS: L-Arginine, unlike D-arginine, induced fluid secretion despite being better absorbed (mean -7.3 v 17.0 microliters/min/g; p < 0.01). L-NAME at 0.1 mmol/l had no effect on basal fluid movement but reversed L-arginine induced secretion (7.8; p < 0.05). L-NAME at 1 and 20 mmol/l induced fluid secretion (-15.4 and -28.4, respectively), which was enhanced by the addition of L-arginine (-30.0 and -41.0, respectively; both p < 0.05). A subcutaneous injection of L-NAME resulted in marked fluid secretion (-39.9) and histological evidence of intestinal ischaemia. These changes were attenuated or reversed by pretreatment with subcutaneous L- but not D-arginine. CONCLUSIONS: L-arginine induces intestinal fluid secretion through production of nitric oxide. There is a delicate balance between the effect of nitric oxide as a secretagogue and its effect on maintaining blood flow and thus preventing intestinal ischaemia.

Changes in capillary permeability during severe experimental acute pancreatitis in rats.

Abnormalities of microcirculation are thought to have an important role in the pathogenesis of severe acute pancreatitis (SAP) and in the associated multiple organic failure. We studied changes in capillary permeability during experimental SAP in rats. Necrotizing acute pancreatitis was induced by retrograde injection of sodium taurocholate in pancreatic ducts in rats (n = 30). The animals were distributed in three groups in which the spaces of compartmental distribution as well as the tissue distribution of labeled tracers were evaluated with the use of erythrocytes and albumin tagged with radioactive chromium, apart from determining the volume of total body water. All the studies were carried out four hours after the induction of acute pancreatitis and the administration of radioactive tracers.

Role of 5-hydroxytryptamine type 3 receptors in rat intestinal fluid and electrolyte secretion induced by cholera and Escherichia coli enterotoxins.

Cholera toxin and Escherichia coli heat labile toxin (LT) induced intestinal secretion has in the past been attributed exclusively to an increase in intracellular cAMP whereas E coli heat stable toxin (ST) induced secretion is mediated through cGMP. Evidence is accumulating on the importance of 5-hydroxytryptamine (5-HT) in cholera toxin induced secretion, but its role in LT and ST is not well established. This study therefore investigated in vivo the effect of 5-HT3 receptor antagonist, granisetron, on intestinal fluid and electrolyte secretion induced by cholera toxin, LT, and ST. Granisetron (30, 75, 150, or 300 micrograms/kg) was given subcutaneously to adult male Wistar rats 90 minutes before instillation of 75 micrograms cholera toxin or 50 micrograms LT in isolated whole small intestine. In situ small intestinal perfusion was performed with an iso-osmotic plasma electrolyte solution (PES) to assess fluid movement. In a second group of animals, granisetron (300 micrograms/kg) was given subcutaneously and two hours later small intestinal perfusion with PES containing 200 micrograms/l ST was performed. Cholera toxin induced net fluid secretion (median -50.1 microliters/min/g (interquartile range -59.5 to -29.8)) was found to be dose dependently decreased or abolished by granisetron (plateau effect at 75 micrograms/kg: 18 (-7.8 to 28), p < 0.01). Granisetron in high dose (300 micrograms/kg), however, failed to prevent LT or ST induced secretion (-52 (-121 to -71) v -31 (-44 to -18), and (-39 (-49 to 17) v (-22 (-39 to -3)), respectively). Sodium and chloride movement paralleled that of fluid. In conclusion, these data show that 5-HT and 5-HT3 receptors play an important part in cholera toxin induced secretion but are not involved in E coli heat stable or heat labile toxin induced secretion.

Modifications of tissue blood flow in acute pancreatitis.

1. Acute pancreatitis (AP) was induced by ductal injection of 2.5% sodium taurocholate saline solution. Plasma and red blood cell (RBC) volume and visceral organ blood flow were evaluated by a radioisotopic method (51Cr tracers) in 45 adult male Wistar rats (22 submitted to AP and 23 controls) 4 h after AP induction. 51Cr-albumin was used to measure plasma volume and 51Cr-RBC was used to measure RBC volume. 2. Changes in tissue hematocrit reflect alterations in tissue blood flow, since reduction in blood flow increases microvascular erythrocyte sequestration. To evaluate the tissue blood flow, we introduce a "tissue hematocrit index" calculated by relating 51Cr-RBC and 51Cr-albumin specific activities measured in visceral organ biopsies. Application of this index to the control and AP groups showed a decrease in blood flow in all visceral organs of the AP group which was reflected by an increase in tissue hematocrit index (2.5-fold for kidneys, 2-fold for pancreas and lungs, 1.6-fold for liver, and 1.2-fold for spleen). 3. As expected, there was an increase in blood hematocrit and a decrease in plasma volume in the AP group, but there were no significant alterations in RBC volume. However, an unequal decrease in blood flow in various tissues such as kidneys, lungs, pancreas and liver was detected in the AP group. 4. This approach provides an easy and simple way to evaluate possible therapeutic protocols for the treatment of acute pancreatitis by measuring effects on visceral blood flow and plasma and blood volumes.

Modifications of tissue blood flow in acute pancreatitis

I.Acute pancreatitis (AP) was induced by ductal injection of 2.5% sodium taurocholate saline solution. Plasma and red blood cell (RBC) volume and visceral organ blood flow were evaluated by a radioisotopic method (51Cr tracers) in 45 adult male Wistar rats (22 submitted to AP and 23 controls) 4 h after AP induction. 51Cr-albumin was used to measure plasma volume and 51Cr-RBC was used to measure RBC volume. II.Changes in tissue hematocrit reflect alterations in tissue blood flow, since reduction in blood flow increases microvascular erythrocyte sequestration. To evaluate the tissue blood flow, we introduce a "tissuehematocrit index" calculated relating 51Cr-RBC and 51Cr-albumin specific activities measured in visceral organ biopsies. Application of this index to the control and AP groups showed a decrease in blood flow in all visceral organs of the AP group which was reflected by an increase in tissue hematocrit index (2.5-fold for kidneys, 2-fold for pancreas and lungs, 1.6-fold for liver, and 1.2-fold for spleen). III.As expected there was an increase in blood hematocrit and a decrease in plasma volume in the AP group, but there were no significant alterations in RBC volume. However, an unequal decrease in blood flow in various tissues such as kidneys, lungs, pancreas and liver was detected in the AP group. IV.This approach provides an easy and simple way to evaluate possible therapeutic protocols for the treatment of acute panreatitis by measuring effects on visceral blood flow and plasma and blood volumes