K. Segawa

Distribution of Epithelial Dysplasia in the Cancerous Esophagus

A total of 114 cases, consisting of 20 non-cancerous esophagi, 48 non-irradiated cancerous esophagi, and 46 irradiated cancerous esophagi, were investigated with semiserial sections to evaluate the role of epithelial dysplasia as a precursor of esophageal cancer. The incidence of dysplasia was higher in cancerous esophagi than in non-cancerous esophagi and in non-irradiated cancerous esophagi than in irradiated cancerous esophagi. The difference in distribution pattern of dysplasia made it possible to classify the esophagi into three types: extensive, multifocal, and scanty. In the extensive type the main tumor tended to have an ill-defined margin and large diameter. In the multifocal type it tended to be superficial and small, and in the scanty type it usually had a well-defined margin. A possible relationship of epithelial dysplasia to the origin of esophageal cancer and its growth was shown by at least two thirds of the esophageal cancers.

The Role of H2 Receptors in Gastric Mucosal Blood Flow

To determine the relation between H2 receptors and gastric mucosal blood flow, we measured the latter in rats by the electrolytically generated hydrogen gas clearance technique. The blood flow increased significantly after intravenous injection of 0.1 mg/kg of impromidine, a very potent and specific agonist of H2 receptors. On the other hand, gastric mucosal blood flow decreased significantly after intravenous administration of 5 or 20 mg/kg of cimetidine or 2 mg/kg of famotidine. However, 2 or 20 rng/kg of omeprazole, whose anti-secretory effect is as strong as that of H2 blockers such as cimetidine and famotidine, caused no significant change in the gastric rnucosal blood flow. This indicates that H2 receptors regulate gastric mucosal blood flow in rats.

The effect of motilin on the gastrointestinal propulsion in rats.

SummaryWe studied the gastrointestinal propulsion in unanaesthetized rats by51Cr method that permits the simultaneous determination of two functions of the gastric emptying and the intestinal propulsion. The results obtained are as follows:1)The semi-logarithmic presentation of the gastric emptying showed a linear relationship with the time.2)When synthetic motilin was subcutaneously injected at the dose of 1µg/kg, the gastric emptying was promoted to a statistically significant extent.

The role of prostaglandin D2 in the genesis of indomethacin-induced gastric lesions in rats.

Four kinds of prostaglandins (PGs), 6-keto-PGF1 alpha, PGF2 alpha, PGE2 and PGD2, in rat gastric mucosa were decreased at 1 or 6 h after oral administration of indomethacin (2 or 12 mg/kg). With 2 mg/kg of indomethacin, the PG levels had slightly recovered 6 h later. Gastric lesions were observed 6 h after administration of indomethacin (12 mg/kg), but not with 2 mg/kg. Omeprazole (20 mg/kg, i.p.) prevented ulcer formation caused by indomethacin, without improvement of the reduced gastric mucosal PG levels. PGD2 (0.5 mg/kg, p.o.) reduced indomethacin-induced gastric lesions and considerable amounts of PGD2 existed in the gastric mucosa. We conclude that H+ is a determining factor in the genesis of indomethacin-induced gastric lesions and persistent decreases in tissue PG levels also participate in ulcer formation.

Fluctuation of the Mucosal Hydroxyproline Content in Compound 48/80-Induced Gastric Lesions in Rats

Extensive gastric mucosal lesions were observed after i.p. administration of compound 48/80 (0.75 mg/kg) for 3 days to rats. The mucosal hydroxyproline content was significantly increased at 4 h after the last injection of compound 48/80 and subsequently decreased as the lesions were healed. Treatment with cimetidine (50 mg/kg, i.p.) did not prevent compound 48/80-induced gastric lesions. The increase in the mucosal hydroxyproline content was significantly reduced by treatment with cimetidine. This fact suggested that cimetidine might have an inhibitory effect on the regeneration of connective tissue.

A new method for experimental study on gastric mucosal damage

SummaryWe have demonstrated development of mucosal damage in rats maintained in a hypoxic condition. The gastric lesions were observed only in the corpus ventriculi in almost all cases, and they were rated as U1-1 erosions histopathologically. The method has proven to facilitate the induction of long-sustained, stable hypoxemia of any desired degree in animals and is concluded to be appropriate for an experimental model of ulceration designed for the study of defensive mechanisms.

Experimental gastroduodenal ulcer induced by synthesized tetragastrin in rats. (VI)

ConclusionsMost case of gastrin induced ulcers were observed predominantly in duodeuum and, therefore, especially in duodenal ulcer the role of gastroduodenal motility may be not evident as a causative factor.

The finding of FDS, especially of descending duodenum

The endoscopy for the digestive tract has achieved marked advance in these days, permitting to carry out the direct visual observation and the biopsy at almost every site of the whole canal. In the duodenum, it is possible even to take the backward Vr However, most of these techniques have been applied to the morphological examination, giving little consideration to the functional or physiological aspects. The authors have developed a new technique for the functional examination of the Vaters papilla and its surroundigns, by recording, under the direct visual control, the smooth muscle electromyogram with a pair of electrodes atached to its tip and grounding wire and lead wires sealed within, inserted through the forceps channel of the duodenoscope. As the electrode, a silver wire coated with silverchloride of 0.3 mm diameter and 5 mm lentgh was soldered to an enamel-coated wire of diameter approximately 0.3 mm. A pair of such electrodes were fixed in parallel at a space of 0.5 mm and sealed in a vinyl tube of 2 mm diameter. The bioelectrical signals picked up by this electrode were fed into a recorder. For the pretreatment, the mucosa was anesthetized with xylocaine and buscopan. After the insertion of F. D. S. and the application of electrodes, the state of reduced noises and stabilization was considered as the reference, and the drug reaction was checked with buscopan, morphine chloride, and atropine, which had been previously evaluated. Among 30 cases examined, the duration of discharge, the number of discharge bursts and the number of discharges in a burst were measured in two cases each derived from the papilla and a point approximately 1 cm away from it and a case of choledocholithiasis. The result of drug reaction was in accord with the general property of smooth muscle electromyogram, since morphine augmented the discharge activity of Oddis sphincter. The present method of E. M. G. lead will supposedly provide a stride beyond the existing technique for electromyogram study of the human smooth muscles in which the lead electrode was positioned surgically or radiographically.

The thermometry of gastric mucosa

related to the fa te of any bleeding gas t r ic lesion, the re fo re knowing the c h a n g e in the gas t r ic blood flow which occurs wi th gas t r ic b leeding or wi th blood t r an s fu s s ion is cl inically wor thwhi le . In th is regard , an e x p e r i m e n t a l s t udy was conduc t ed in the dogs. Blood in the a m o u n t equ iva len t to 3.0% of the body weight was d r a w n f rom a b r anch of the left gas t r ic a r te ry and t h e n th is blood was t r a n s f u s e d into the s a m e dog. D u r i n g these procedures , the blood flow of the left gastroepiploic a r t e ry was m e a s u r e d by an e l ec t romagne t i c flow me te r and the f emora l a r te r ia l p res su re was checked as well. As resul t , a t r end was observed t ha t the ra te of gas t r ic blood flow s l ight ly inc reases du r ing and af te r (1 hour) gas t r i c b leeding and t ha t it t h e n keeps gross ly c o n s t a n t du r ing and af ter (1 hour) blood t r an s fu s i on . T h u s , it is unl ike ly tha t gas t r ic b leeding m i g h t r educe the func t iona l act ivi ty of the s t o m a c h or tha t blood t r a n s f u s i o n m i g h t p romote the gas t r ic blood flow and cause r ecu r rence of gas t r ic b leeding.

Clinical study on gastric acid and pepsin relation between caffeine and gastrin method

Male albumino rats, weighing between 200 and 400 g, were fasted for 48 hours and divided into two groups. A group of rats were anesthet ized with ure thane and another group were given stress by confinement. Stomach was drained with a canula and perfused with saline at a cons tant flow rate. The fluid was collected every 30 minites. Gastrin was given by a continuous intravenous infusion at a rate between 5 and 160 microgram/kg/hr for 24 hours. Secretion of gastric acid at a cons tant rate was obtained at least for 24 hours in these conditions. In anesthetized rats, the acid secretion in response to gastr in increased with increasing doses of gastr in from 5 to 40 microgram/kg/hr . Maximal response was produced by 40 microgram/kg/hr and followed by a decline of the secretion with fur ther increase in the dose of gastr in f rom 40 to 100 microgram, After minimal response to gastr in was obtained, the acid secretion increased again with increasing doses from 100 to 160 microgram/kg/hr . Thus , two phases of st imulation, the initial and the late phase, were obtained in the dose-response curve, and the response to gastr in 160 microgram/kg/hr was almost the same as the response to gastr in 40 microgram/kg/hr . Ulcerative lesions in the gastric mucosal membrane were reported previously by us in the rats following infusion of large amount of gastr in. These lesions seem to have relation to the increase in the output of gastric acid in the late phase of the dose response curve in the present experiment. In the s tress group, the basal secretion of gastric acid was higher than in the anesthetized group. Maximal response was obtained by gastr in at a dose between 20 and 40 microgram/kg/hr . The acid output at the maximal response was almost the same in the anesthetized group. The high level of acid output in the stress group with 0 and submaximal doses of gastr in mus t be due to the endogenous gastr in secretion caused by nervous st imulation.