Interdigestive small bowel motility and duodenal bacterial overgrowth in experimental acute pancreatitis

The objective of this study is to investigate the effects of an acute necrotizing pancreatitis (ANP), without biliary obstruction, on the migrating motor complex (MMC), small bowel bacterial overgrowth (SBBO), bacterial translocation (BT) and infection of the pancreas simultaneously. Rats were divided into four groups: mild pancreatitis, control, ANP and sham operated control. Jejunal myoelectrodes were used to measure MMCs. Blood, peritoneal fluid, bile, and abdominal organs were harvested for microbial culturing 72 h after induction of pancreatitis. The splenic portion of the pancreas was taken for histology. During ANP the MMC cycle length was significantly increased from 14.1 +/- 0.2 to 22.4 +/- 1.9 min (P < 0.05). The duodenum of ANP rats was in contrast with the other groups characterized by Enterobacteriacae (> 3 log 10 CFU g-1 in seven of 12 rats, P < 0.05). A positive correlation (r = 0.78, P < 0.01) existed between duodenal Gram-negative and anaerobic flora and the MMC cycle. Correlation between MMC cycle length and BT to the pancreas was positive as well (r = 0.70, P < 0.01). A positive correlation (r = 0.85, P < 0.01) was found between the severity of pancreatitis and duodenal bacterial overgrowth. During ANP without biliary obstruction, the jejunal MMC is disturbed and consequently SBBO occurs. The correlation between the severity of pancreatitis, the disturbance of the MMC and SBBO suggests an important pathophysiological role of the proximal small bowel in the infection of pancreatic necrosis.     

Relationship between the mechanism of gastro-oesophageal reflux and oesophageal acid exposure in patients with reflux disease

Abstract  This study investigated the relationship between the oesophageal acid exposure time and the underlying manometric motor events in patients with gastro-oesophageal reflux disease (GORD). In 31 patients, 3-hour oesophageal motility and pH were measured after a test meal. Ten patients underwent 24-hour ambulatory manometry and pH recording. In the 3-hour postprandial study, of 367 reflux episodes 79% was associated with a transient lower oesophageal sphincter relaxation (TLOSR), 14% with absent basal lower oesophageal sphincter (LOS) pressure and the remaining 7% with other mechanisms, representing 62, 28 and 10% of the acid exposure time, respectively. Acid reflux duration per motor mechanism was longer for absent basal LOS pressure than for TLOSR (189 ± 23 s and 41 ± 5 s, respectively, P  < 0.001). In the 24-hour ambulatory study, the contribution of TLOSRs to reflux frequency vs acid exposure time were 65 vs 54% interprandially and 74 vs 53% after the meal. During the night, absence of basal LOS pressure accounted for 36% of reflux events representing 71% of acid exposure time. In conclusion, the duration of oesophageal acid exposure following a TLOSR is shorter than reflux during absent basal LOS pressure. TLOSRs are, the major contributor to oesophageal acid exposure during the day. At night, however, reflux during absent basal LOS pressure is the major contributor to acid exposure.     

Relationships between air swallowing, intragastric air, belching and gastro-oesophageal reflux

BACKGROUND: With each swallow a certain amount of air is transported to the stomach. The stomach protects itself against excessive distention by swallowed air through belching (gas reflux). The mechanism of belching (transient lower oesophageal sphincter relaxation) is also one of the mechanisms underlying gastro-oesophageal reflux. AIM: To investigate whether swallowing of air leads to an increase in size of the intragastric air bubble and to gastro-oesophageal reflux. METHODS: Multichannel intraluminal impedance measurement was used to quantify the incidence of swallowing of air in 20 healthy volunteers before and after a meal. Radiography was used to measure the size of the intragastric air bubble. Gastro-oesophageal reflux was assessed by concurrent impedance and pH measurement. RESULTS: The rate of air swallowing was correlated to the size of the intragastric air bubble postprandially and to the rate of gaseous gastro-oesophageal reflux. The number of air swallows and the size of the intragastric air bubble did not correlate with the number of liquid acid and non-acid reflux episodes. CONCLUSIONS: In healthy subjects, air swallowing promotes belching but does not facilitate acid reflux.