In 7 patients with ulcerative colitis, the energy level in the large intestinal mucosa was investigated. ATP and energy charge in the intestinal mucosa in ulcerative colitis showed lower levels than those of control subjects. Therefore, energy-deficit may exist in the large intestinal mucosa in ulcerative colitis.ulcerative colitis ; energy level ; ATP ; energy charge Energy-deficit in the gastric mucosa is considered one of the factors in the pathogenesis of acute gastric mucosal lesions (Menguy et al. 1974 ;Kameyama et al. 1982). The pathogenesis of acute gastric mucosal lesions and ulcerative colitis may be different. However, we decided to investigate further and have therefore studied the energy level in the large intestinal mucosa in ulcerative colitis, which has not yet been reported.Patients and materials. Seven patients with ulcerative colitis (5 males and 2 females, mean age of 34 years) and 7 control subjects (5 males and 2 females, mean age of 58 years) were studied. Of the 7 patients with ulcerative colitis, 6 were in the active stage, severe colitis and total colitis, and one was in the healed stage, mild colitis and left side colitis. Control subjects included 4 with sigmoid colon cancer, 2 with rectal cancer and one with transverse colon cancer without intestinal stenosis. The large intestine was crushed between two copper paddles precooled to the temperature of liquid N2, soon after laparotomy before the intestinal circulation was disturbed. The specimens were taken from the severe and moderate lesions in ulcerative colitis. For the control, specimens of normal colon from patients with large bowel cancer, from a part of the colon that would later be resected, but as far from the tumor as possible. The harvested specimens were dealt with by the "stopfreeze" method, and ATP, ADP and AMP were determined using coupled enzyme reactions for the assays (Dennemann 1961;Jaworek et al. 1974). Energy charge proposed by Atkinson (1968) calculated from (ATP+1/2ADP)/(ATP+ADP+AMP) was also estimated. In statistical analyses, measured values were expressed as meal +s.D. and the significance of the differences was evaluated by using Student's t-test.Results and comments. ATP levels were 1.65+0.621umol/g•wet wt. in control subjects. In ulcerative colitis, the levels of the severe lesions were 1.12±0.2,umol/g•wet wt., significantly lower than those of control subjects (p <0.05). The levels of the moderate lesions of 1.06+0.13 1umol/g•wet wt. were also lower than those of control subjects. No significant difference was found between the severe and moderate lesions in ulcerative colitis (p>0.05) (Fig. 1, left) (Table 1).Energy charge levels were 0.84+0.03 in control subjects. In ulcerative colitis, the levels of the severe lesions of 0.80+0.05 were lower than those of control subjects. The levels of the moderate lesions were 0.77+0.04, significantly lower than those of controls (p < 0.05). No significant difference was found between the severe and moderate lesions in ulcerative colitis (p>0'.05) (Fig. 1, right) (Tab...
In order to observe the plasma gastrin, secretin and pancreatic polypeptide (PP) levels in an acid hypersecretion state, the pyloric antrum was transposed onto the transverse colon in 4 mongrel dogs with a Heidenhain pouch. The effects of meal and cimetidine on these gut hormones and acid secretion levels were observed for 6 hr after meals. After antrocolic transposition (ACT), hypersecretion of acid and high plasma gastrin levels were observed both in the fasting and stimulated states. Plasma secretin levels were elevated for 6 postprandial hr, but were reduced by cimetidine as a result of marked suppression of acid secretion. Plasma PP levels also increased for 6 postprandial hr, but its responses were not altered with or without simultaneous administration of cimetidine. These findings indicate that acid hypersecretion in basal and postprandial states after ACT may be attributed to hypergastrinemia and that endogenous acid is capable of releasing secretin but not effective on the release of PP. gastric acid ; intraduodenal pH ; gastrin ; secretin ; pancreatic polypeptide It is well known that plasma secretin (Koizumi et al. 1980) and PP (Kayasseh et al. 1978) concentration significantly increases as hydrochloric acid is infused into the duodenum. The effect of physiological stimulus such as meal and gastric acid on plasma secretin and PP release, however, has not been elucidated in detail.It is important to examine the effect of endogenously released gastric acid on plasma secretin and PP response for the elucidation of release mechanism and furthermore of a physiological role of these gut hormones in gastrointestinal
Regulation of Cl- and HCO3- secretion by intramural cholinergic neurons was investigated in guinea pig antrum in vitro. Sheet preparations composed of the mucosa and the submucosa were mounted between Ussing chambers and bathed with buffer-free solution on the luminal surface and with HCO3(-)-CO2 solution on the serosal side. Short-circuit current (Isc), unidirectional fluxes of 36Cl and 22Na, and the luminal alkalinization rate (JOHSL) were determined. Electrical stimulation of the preparations elicited increases in both JOHSL and Isc, which were inhibited by tetrodotoxin (TTX) and atropine. Physostigmine also evoked TTX- and atropine-sensitive increases in JOHSL and Isc. Similar increases in JOHSL and Isc were observed when the muscarinic agonist bethanechol chloride (BCh) was added to the serosal side. The responses to BCh were not affected by TTX. The BCh-induced increase in JOHSL was largely abolished by removal of HCO3- or Na+ and addition of ouabain (serosal side) but was neither sensitive to Cl- removal nor associated with 22Na secretion. The increase in Isc induced by BCh was associated with the increase in 36Cl secretion and was inhibited by removal of Cl- or Na+ and by addition of bumetanide or ouabain (both, serosal side). These results suggest that the submucosal cholinergic neurons are involved via muscarinic receptors in the stimulation of epithelial HCO3- and Cl- secretion. For both HCO3- and Cl-, the cellular and membrane mechanisms of secretion induced by muscarinic stimulation, although not entirely clear, appear to be different from those occurring under baseline conditions.
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