T. Ogihara

Gastric Blood Flow in Ulcer Diseases

BACKGROUND Gastric blood circulation maintains the structure and functions of the stomach, and thereby is closely associated with the pathogenesis and the healing of gastrointestinal lesions. Gastric mucosal blood flow, regulated by systemic neural and humoral factors, is also modified by local metabolic factors such as prostaglandins, leukotrienes. PAF and other endogenous chemical mediators in mucosa. Endothelium-derived factors that are produced by vascular endothelial cells, inducing relaxation or contraction of the blood vessels, are also recognized as basic mediators that regulate the circulation in the stomach. RESULTS The regionally disturbed gastric circulation in combination with the presence of acid is closely associated with the pathogenesis of NSAIDs and ethanol-induced gastric lesions. Blood flow and oxygenation in the surface mucosa surrounding the peptic ulcer change during healing, depending on the quality of the ulcer healing process: an increased blood circulation with increased oxygen supply to the ulcer margin is important for rapid ulcer healing shown by reflectance spectrophotometry. Factors altering the blood flow during the ulcer healing are discussed.

Different Effect of Helicobacter pylori on the Human Gastric Antral and Body Mucosal Intracellular Mucin

To elucidate the role of Helicobacter pylori infection in the pathogenesis of gastric ulcer, we investigated the intracellular mucin content by measuring the periodic acid-Schiff-Alcian blue (PAS-AB)-stained substances, by means of computer, in the biopsy sample of gastric mucosa from patients with and without H. pylori infection. In the antral mucosa the intracellular PAS-AB-stained mucin content was significantly smaller in patients with infection than in patients without infection, whereas in the oxyntic gland mucosa the intracellular mucin content showed no significant change between patients with and without infection. In an animal study we investigated the effect of ammonia, which might be produced by H. pylori in the presence of urea. The ammonia, administered orally, caused a greater decrease of intracellular PAS-AB-stained mucin content in the gastric antral mucosa than in the body mucosa, in a dose-dependent manner. The results suggested that H. pylori infection had a different effect on the gastric mucosal intracellular PAS-AB-stained mucin and lowered specifically the antral intracellular PAS-AB-stained mucin content, possibly due to generation of ammonia by H. pylori.

Effect of cigarette smoking on the gastric mucosal blood volume index and hemoglobin oxygenation in man.

SummaryThe acute effect of cigarette smoking on the gastric mucosal blood volume index and the oxygen saturation of hemoglobin (SO2) in the gastric mucosa was investigated in 12 young male volunteers using reflectance spectrophotometry during endoscopy. Six of these volunteers were habitual smokers who had smoked more than 20 cigarettes a day for more than five years. The others were non-habitual smokers who smoked less than 20 cigarettes a year. The indices of mucosal blood volume and the mucosal blood SO2 level were calculated from the spectra obtained at the lesser curvature of the lower corpus of the stomach before and after cigarette smoking. The indices of mucosal blood volume and mucosal blood SO2 decreased significantly after one to three puffs of cigarette smoking in all subjects as compared to the value before smoking, and the degree of decrease in these parameters was significantly greater in the non-habitual smokers than in the habitual smokers. These results suggest that only one to three puffs of cigarette smoking causes a decrease in the mucosal blood volume and the mucosal blood SO2 which might be related to weakening of mucosal defensive factors.

Changes in the Intracellular Calcium Ion Concentration in the Gastric Mucosa in a Rat Ischemia-Reperfusion Model

To investigate the role of the intracellular calcium ion in the development of acute gastric mucosal lesions, phosphorylase a activity was measured as an index of the intracellular calcium ion concentration ([Ca2+]i), using Lowrys method, in the rat ischemia-reperfusion model. [Ca2+]i increased significantly at the end of the ischemic state without acute mucosal lesions (AGML). After reinfusion, [Ca2+]i showed a slight increase and AGML developed. Continual intravenous infusion of the calcium channel blocker, diltiazem (1 mg/kg/hr), inhibited the increase in [Ca2+]i in the ischemic state and reduced the development of AGML after reinfusion. These results suggest that the increase in [Ca2+]i in the ischemic state plays an important role in the development of AGML.

The Effect of DQ-2511, a Newly Synthesized Anti-Ulcer Drug, on the Gastric Mucosal Hemodynamics and Ulceration in Rats

DQ-2511, which is a dopamine derivative, is a newly synthesized anti-ulcer drug. Pretreatment with DW-2511 in the hemorrhagic shock-reperfusion model in rats significantly prevented the decreases of gastric mucosal blood volume, mucosal blood oxygenation index and the ulcer formation. The decrease in gastric mucosal blood oxygenation index in hemorrhagic shock state has a linear correlation with the size of the mucosal ulcers both in DQ-2511 and control groups. The results suggested that DQ-2511 exerts its anti-ulcer activity by improving mucosal hemodynamics in hemorrhagic shock-reperfusion rat model.