Dieulafoy lesion is an uncommon cause of gastrointestinal bleeding, reported to be only 2% of acute or chronic upper gastrointestinal bleeding episodes. Bleeding occurs from a small mucosal erosion involving an unusually large submucosal artery in an otherwise normal mucosa. It is associated with massive, life threatening hemorrhage and is difficult to diagnosis. In most cases the lesion is encountered in the proximal stomach, antrum, duodenum, colon and rectum. In particular, extragastric Dieulafoy lesion is an extremely rare source of intestinal bleeding. In Korea, no case of bleeding from a Dieulafoy lesion of the small intestine has been previously reported. We experienced one case of bleeding from a jejunal Dieulafoy lesion, which was confirmed by the pathologic examination of the resected specimen, and report here.
Adult ; Arteries/abnormalities* ; Case Report ; Female ; Gastric Mucosa/blood supply* ; Gastrointestinal Hemorrhage/etiology* ; Human ; Intestinal Mucosa/blood supply*

AIMTo investigate the effects of calcitonin gene-related peptide (CGRP), gastrin 17 (G17), bombesin (Bom), met-enkephalin (Met-enk), neuropeptide Y (NPY) and somatostatin (SS) on GMBF and the role of endogenous NO in increased GMBF induced by neuropeptides in rats.

METHODSBy hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and arterial infusion close to stomach or intracerebroventricular (icv) to microinject neuropeptides.

RESULTS(1) Arterial infusions of CGRP and G17 (5, 50 and 100 pmol x min(-1)) increased GMBF significantly in dose-dependent manners. CGRP had more effective effect on increasing GMBF than that of G17. Intravenous pretreatment of L-nitro-L-arginine methyl ester (L-NAME) to inhibit the synthesis of endogenous NO could abolish completely or partially the increases in GMBF response to CGRP or G17 respectively. (2) Arterial infusions of Bom and Met-enk (50 and 100 pmol x min(-1)) increased GMBF significantly. The increases in GMBF induced by Bom or Met-enk were abolished completely or partially by pretreatment of L-NAME respectively. (3) Arterial infusion of NPY (5, 50 and 100 pmol x min(-1)) led to reduction of GMBF significantly in a dose-dependent manner. SS (50 and 100 pmol x min(-1)) also reduced GMBF significantly. (4) icv microinjection of CGRP (10 microg) and G17 (10 Microg) increased GMBF significantly. The increases in GMBF induced by icv microinjection of CGRP or G17 were blocked completely or partially respectively by pretreatments with L-NAME. (5) icv microinjection of NPY (10 microg) decreased GMBF significantly.

CONCLUSIONNeuropeptides play important roles in the regulation of GMBF in rats and NO is involved in the increase of GMBF induced by some neuropeptides.

Animals ; Gastric Mucosa ; blood supply ; drug effects ; Male ; Neuropeptides ; pharmacology ; physiology ; Nitric Oxide ; physiology ; Rats ; Rats, Sprague-Dawley

AIMTo observe the degree of gastric mucosal injury following limb ischemia/reperfusion (LI/R), and to investigate the mechanism of gastric mucosal injury and the protection of ischemic preconditioning (IPC) on gastric mucosal injury.

METHODSThe model rats which underwent 4 hours of ischemia and 4 hours of reperfusion of hind limbs were made. Then we respectively observed and determined the histologic lesion score after I/R and IPC + I/R. The gastric barrier mucus in mucus were measured in different groups. The values of MPO, SOD, MDA and XOD in gastric mucosa and the values of MDA, XOD, SOD, LDH in plasma were detected.

RESULTSIn the LI/R group, the histologic lesion score increased significantly. The content of gastric barrier mucus in mucus decreased significantly. The value of MPO, MDA, XOD in gastric mucosa and the values of MDA, XOD, LDH in plasma increased remarkably and SOD activity in gastric mucosa and in plasma decreased. However in the IPC group, the histologic lesion score decreased significantly and the content of gastric barrier mucus in mucus increased significantly and the value of MPO MDA XOD LDH in gastric mucosa or in plasma decreased remarkably and the SOD activity increased compared to LI/R group.

CONCLUSIONLI/R will lead to the development of stress ulcer, oxygen free radicals play an important role in it. IPC can alleviate the damage of gastric mucosa following ischemia/reperfusion of hind limbs. The decrease of OFR is one of the protection mechanism of IPC.

Animals ; Extremities ; blood supply ; Gastric Mucosa ; metabolism ; pathology ; Ischemic Preconditioning ; Male ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology

AIM AND METHODSBy hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and a high dose of capsaicin to ablate the capsaicin-sensitive afferent fibers, the roles of capsaicin-sensitive afferent fibers and endogenous NO in the gastric acid secretion and hyperemic response to intragastric distention were studied in rats.

RESULTS(1) There was an increase in acid secretion associated with the increase in GMBF to intragastric distention. (2) Pretreatment with a high dose of capsaicin to ablate afferent fibers completely abolished the GMBF and partially inhibited the acid secretion during the intragastric distention. (3) The increase in GMBF to intragastric distention was completely blocked by pretreatment with L-NAME, whereas the acid secretion was significantly attenuated.

CONCLUSIONCapsaicin-sensitive afferent fibers and endogenous NO are involved in the increases of gastric acid secretion and GMBF.

Animals ; Capsaicin ; pharmacology ; Gastric Acid ; secretion ; Gastric Dilatation ; metabolism ; Gastric Juice ; secretion ; Gastric Mucosa ; blood supply ; Male ; NG-Nitroarginine Methyl Ester ; Neurons, Afferent ; drug effects ; Nitric Oxide ; physiology ; Rats ; Rats, Sprague-Dawley

The present study aimed to investigate the protective mechanism of N-acetylcysteine (NAC) against gastric ischemia /reperfusion (GI/R) injury in rats. After intravenous injection (IV) of NAC (150 mg/kg) into femoral vein, the rats were subjected to 30 min of ischemia induced by clamping the celiac artery followed by 60 min of reperfusion. After the gastric mucosal damage index (GMDI) had been calculated, gastric mucosal cell in situ apoptosis was detected by TUNEL method. The protein expression of p-ERK, p-JNK and NF-kappaB, and mRNA expression of TNF-alpha and Caspase-3 in gastric mucosa were evaluated by using Western-blot or RT-PCR, respectively. The results showed that NAC not only attenuated the GI-R injury, but also decreased gastric mucosal cellular apoptosis. Furthermore, NAC increased the protein expression of p-ERK, while inhibited protein expression of p-JNK, NF-kappaB in gastric mucosa. NAC also decreased the expression of TNF-alpha mRNA and Caspase-3 mRNA in gastric mucosa. Capsazepine (CPZ) (400 mg/kg, IV) reversed the protective effect of NAC against GI/R injury in rats. These results suggest that NAC can protect rats against GI/R injury. This protective effect is possibly mediated by the up-regulation of p-ERK and down-regulation of p-JNK and NF-kappaB. In addition, vanilloid receptor subtype 1 may be involved in the protective mechanism of NAC against GI/R injury.
Acetylcysteine ; pharmacology ; Animals ; Apoptosis ; Gastric Mucosa ; pathology ; Male ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology ; prevention & control ; Stomach ; blood supply

AIMTo investigate the effect of paraventricular nucleus (PVN) stimulation and the c-fos expression within PVN and nucleus tractus solitarius (NTS) of the rat following gastric ischemia/reperfusion injury (GI/RI).

METHODSThe rat celiac artery was clamped for thirty minutes and reperfused for sixty minutes, using Fos immunohistochemical method (ABC method) examined the c-fos expression within PVN and NTS.

RESULTS(1) Both electrical and chemical stimulation of the PVN obviously attenuated the GI/ RI. (2) Bilateral electrolytic lesion of NTS could eliminate the protective effect of electrical stimulation of the PVN. (3) The Fos-like immunoreactive neurons were increased in bilateral PVN and NTS by GI/RI.

CONCLUSIONThe function of PVN and NTS could be affected by the GI/RI noxious stimulation. PVN, NTS were involved in the regulation of GI/RI.

Animals ; Gastric Mucosa ; pathology ; Male ; Paraventricular Hypothalamic Nucleus ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; Solitary Nucleus ; metabolism ; Stomach ; blood supply

The present study aimed to investigate the protective effect and mechanism of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) in rats. GI-R injury was induced by clamping the celiac artery of adult male SD rats for 30 min and followed by reperfusion for 1 h. The rats were randomly divided into sham group, GI-R group, NaHS group, glibenclamide group and pinacidil group. Gastric mucosal damage was analyzed with macroscopic injured area, deep damage was assessed with histopathology scores, and the hydrogen sulfide concentration in plasma was determined by colorimetric method. The results showed that pretreatment of NaHS significantly reduced the injured area and deep damage of the gastric mucosa induced by GI-R. However, NaHS did not significantly alter the levels of hydrogen sulfide in plasma 14 d after NaHS administration. The gastric protective effect of NaHS during reperfusion could be attenuated by glibenclamide, an ATP-sensitive potassium channel (K(ATP)) blocker. However, K(ATP) opener pinacidil inhibited the GI-R-induced injury. These results suggest that exogenous hydrogen sulfide plays a protective role against GI-R injury in rats possibly through modulation of K(ATP) channel opening.
Animals ; Gastric Mucosa ; pathology ; Hydrogen Sulfide ; metabolism ; Ischemic Preconditioning ; methods ; KATP Channels ; metabolism ; physiology ; Male ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Stomach ; blood supply ; Sulfides ; pharmacology

The effects of electrical and chemical stimulation and electrolytic lesion of lateral hypothalamic area (LHA) on gastric ischemia-reperfusion injury (GI-RI) were investigated in rats whose celiac arteries were clamped for 30 min and reperfused for 60 min by removal of the clamp. The results are as follows. (1) Electrical stimulation of LHA could aggravate GI-RI in an intensity-dependent manner by using 0.2, 0.4 or 0.6 mA current respectively. Microinjection of L-glutamic acid into LHA resulted in a similar effect to that of electrical stimulation of LHA on GI-RI. After electrolytic lesion of bilateral LHA, the area of gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) was smaller than that by electrical stimulation of LHA plus GI-R. (2) Dorsal vagal complex (DVC) lesion or vagotomy could eliminate the effect of electrical stimulation of LHA on GI-RI. (3) Electrical stimulation of LHA increased the content of malondialdehyde (MDA) but decreased the activity of superoxide dismutase (SOD) of ischemia-reperfusion (I-R) gastric mucosa. (4) Electrical stimulation of LHA plus gastric I-R increased gastric juice volume and total acid output, but there were no significant changes in acidity, pepsin activity and gastric barrier mucus. These results indicate that the LHA is an area in the CNS exerting aggravate effects on GI-RI. The DVC and vagus may be involved in the regulative effects of LHA on GI-RI. These effects are associated with increases in gastric mucosal MDA content, gastric juice volume, and total acid output, and a decrease in SOD activity.Acidity, pepsin activity and gastric barrier mucus do not seem to play an important role.
Animals ; Electric Stimulation ; Gastric Mucosa ; blood supply ; metabolism ; pathology ; Hypothalamic Area, Lateral ; metabolism ; Male ; Malondialdehyde ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology ; Superoxide Dismutase ; metabolism

The effect of gastric ischemia-reperfusion (GI-R) on gastric mucosal cellular apoptosis and proliferation was investigated using histological, immunohistochemical methods in Sprague-Dawley rats. The GI-R model was established by clamping the celiac artery for 30 min and reperfusing for 0, 0.5, 1, 3, 6, 24, 48, 72 h, respectively. Mild gastric mucosal injury was induced by ischemia alone. However, the injury worsened and reached the maximum at 1 h after reperfusion, almost simultaneously with the gastric mucosal cellular apoptosis increase and cellular proliferation decrease in gastric mucosa. Then, gastric mucosal cells began to repair by increasing gastric cellular proliferation, which achieved the maximum at 24 h after reperfusion. The mucosal lesions were almost completely repaired at about 72 h after reperfusion. These results indicate that the gastric mucosal injury after GI-R is mainly induced by reperfusion. The damaged gastric mucosa could initiate its repairing mechanism immediately through inhibiting cellular apoptosis and increasing the number of proliferative cells, which substitute the damaged cells gradually. The plerosis almost completes in three days after reperfusion showing a strong self-repair ability of gastric mucosa.
Animals ; Apoptosis ; physiology ; Cell Proliferation ; Female ; Gastric Mucosa ; pathology ; physiology ; Ischemia ; physiopathology ; Male ; Rats ; Rats, Sprague-Dawley ; Regeneration ; physiology ; Reperfusion Injury ; physiopathology ; Stomach ; blood supply ; pathology ; physiology

OBJECTIVETo explore the effect of Ang-2 on angiogenesis in gastric cancer.

METHODSThe expression of Ang-2 mRNA was analyzed by RT-PCR and the expression of VEGF and CD34 was detected by immunohistochemistry in 36 cases of gastric cancer tissues and their paired adjacent gastric mucosa.

RESULTSThe expression of Ang-2 mRNA was found both in gastric cancer and their paired adjacent gastric mucosa; the correlationship between the general expression levels of Ang-2 mRNA and microvessel density (MVD) in gastric cancer tissues was not found. However, in 27 cases whose Ang-2 mRNA expression levels in cancer tissues were lower than those in adjacent gastric mucosa. A significant positive correlation between the expression level of Ang-2 mRNA and MVD in the tumor tissues was found (r = 0.411, P < 0.05). In these 27 cases, the MVD in the gastric cancer tissues with positive VEGF expression (45.45 +/- 10.30) was higher than that with negative VEGF expression (30.15 +/- 8.69, P < 0.05), whereas in the other 9 cases whose expression levels of Ang-2 mRNA in cancer tissues were higher than those in adjacent gastric mucosa, a significant negative correlation between expression level of Ang-2 mRNA and MVD in the tumor tissues (r = -0.758, P < 0.05), but without correlation between the MVD and VEGF.

CONCLUSIONUnder the conditions that the expression of Ang-2 mRNA in cancer tissues was lower than that in adjacent gastric mucosa, VEGF could promote the sprouting of new vessels along with Ang-2 upregulation. But under the conditions that the expression of Ang-2 mRNA in cancer tissues was higher than that in adjacent gastric mucosa, Ang-2 inhibited angiogenesis. Angiopoietin-2 may play a dual effect on angiogenesis in gastric cancer.

Angiopoietin-2 ; genetics ; physiology ; Female ; Gastric Mucosa ; metabolism ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neovascularization, Pathologic ; etiology ; RNA, Messenger ; analysis ; Stomach Neoplasms ; blood supply ; Vascular Endothelial Growth Factor A ; analysis