A healthy young patient with hepatic portal vein gas due to acute gastric dilatation: a case report.

Hepatic portal vein gas (HPVG) is caused by the influx of gastrointestinal gas into the intrahepatic portal vein as a result of gastrointestinal wall fragility due to ischemia or necrosis. Gastrointestinal tract necrosis is fatal in severe cases. We observed a case of food intake-induced acute gastric dilatation (AGD) in a healthy young male who developed HPVG and underwent conservative treatment. A 25-year-old male presented to our hospital with epigastric pain and nausea the day after excessive food intake. Computed tomography (CT) revealed gas along the intrahepatic portal vein and marked gastric dilatation with large food residue. AGD-induced HPVG was considered. Esophagogastroduodenoscopy (EGD) was not performed at this stage because of the risk of HPVG and AGD exacerbation, and the patient was followed up with intragastric decompression via a nasogastric tube. Food residue and approximately 2 L of liquid without blood were vomited 1 h after the nasogastric tube placement. His symptoms improved after the vomiting episode. An EGD was performed 2 days after undergoing CT. Endoscopic findings revealed extensive erosions and the presence of a whitish coat extending from the fornix to the lower body of the stomach, indicating AGD. HPVG disappeared on the CT scan taken during EGD. Thereafter, symptom relapse and HPVG recurrence were not observed.

Correlation analysis of gastric mucosal lesions with Helicobacter pylori infection and its virulence genotype in Guiyang, Guizhou province, China.

Background: Helicobacter Pylori (H. pylori) infection is the most important factor affecting clinical outcome in patients with gastric mucosal lesions. This study aimed to investigate H. pylori infection in patients with gastric mucosal lesions and their virulence genotype in Guiyang, China. Methods: Pathological examinations of 1,364 biopsies from patients with upper gastrointestinal symptoms and H. pylori infection were analyzed according to different pathological types. The bacterial genome DNA was extracted from H. pylori strains isolated from gastric biopsies, and the cagA, vacA, and iceA virulence genes were detected and typed to analyze the correlation of their genotypes between different pathological lesions. Results: The positive rate of H. pylori infection was approximately 19.9% (272/1,364), as determined by histopathological examination (HPE). It was more frequently detected in men than in women. A total of 85 H. pylori isolates were obtained from 280 clinical samples (positive rate 30.4%, 85/280). Of these 85 strains, cagA, vacA, and iceA genes were identified in 85.9%, 100%, and 83.5% of samples, respectively. Approximately 74.1% of strains were cagA East Asian type (cagA-ABD), and 11.8% of were cagA Western strains (cagA-AB, cagA-ABC), only present in patients with chronic non-atrophic gastritis. Gastric intraepithelial neoplasia and gastric cancer harbored both Asian strains. A total of 7 combinations of vacA genotypes were noted, among which s1c/m1b (30.6%) and s1c/m2 (41.2%) were the dominant genotypes. The predominant iceA genotype was iceA1 (64.7%). Conclusions: We observed that the positive rate of H. pylori infection was related to the pathological type of patients' gastric mucosal lesions. Isolated H. pylori strains showed a unique genotype, mainly East Asian type cagA (ABD), vacA s1c/m2 genotype, and iceA1. These results provide an important reference for further studies of H. pylori in Guizhou province, China.

A Rare Case of COVID-19 Pneumonia Concomitant with Bleeding from Acute Gastric Mucosal Lesions.

A 70-year-old man was diagnosed with coronavirus disease 2019 (COVID-19) pneumonia. Twenty-six days after admission, he experienced hematemesis despite improvement in his respiratory symptoms. Contrast-enhanced computed tomography revealed edematous stomach wall thickening with neither ischemic findings in the gastric wall nor obstruction of the gastric artery. Emergent esophagogastroduodenoscopy showed diffuse dark-red mucosa accompanied by multiple easy-bleeding, irregularly shaped ulcers throughout almost the whole stomach without active bleeding or visible vessels. The clinical course, including the endoscopic findings, progressed favorably with conservative treatment. COVID-19 pneumonia can present with acute gastric mucosal lesion, which may be induced by microvascular thrombosis due to COVID-19-related coagulopathy.

Phlegmonous gastritis: a case series.

BACKGROUND: Phlegmonous gastritis is a rare and fatal infectious disease of the stomach, presenting varied and nonspecific endoscopic images, which are therefore difficult to diagnose. This report discusses three cases of phlegmonous gastritis, each with unique endoscopic images, and considers the differential diagnosis of this disease. These cases were initially suspected of scirrhous gastric cancer, gastric syphilis, and acute gastric mucosal lesion. CASE PRESENTATION: Case 1 A 32-year-old Asian man visited our hospital complaining of upper abdominal pain. Endoscopy raised suspicion of scirrhous gastric cancer. However, a histopathological examination showed no malignant cells, thus leading to the diagnosis of phlegmonous gastritis. The patient was started on antibiotic therapy, which was effective. Case 2 A 33-year-old Asian man visited our hospital complaining of epigastralgia. Endoscopy raised suspicion of gastric syphilis. However, the serum test for syphilis was negative, and Streptococcus viridans was detected in the biopsy specimen culture, which led to the diagnosis of phlegmonous gastritis. The patient was started on antibiotic therapy, resulting in significant improvement in the endoscopic image after 2 weeks. Case 3 A 19-year-old Asian man visited our hospital complaining of epigastric pain. Endoscopy raised suspicion of acute gastric mucosal lesion. A gastric juice culture showed Pseudomonas aeruginosa and Streptococcus viridans, thus leading to the diagnosis of phlegmonous gastritis. The patient was started on antibiotic therapy, resulting in the disappearance of the gastric lesions. CONCLUSION: In severe cases of phlegmonous gastritis, immediate surgical treatment is generally required. However, the endoscopic images are varied and nonspecific. These three cases suggest that clinicians need to consider the differential diagnosis of phlegmonous gastritis and make accurate diagnoses at an early stage.

Nervous mechanisms of restraint water-immersion stress-induced gastric mucosal lesion.

Stress-induced gastric mucosal lesion (SGML) is one of the most common visceral complications after trauma. Exploring the nervous mechanisms of SGML has become a research hotspot. Restraint water-immersion stress (RWIS) can induce GML and has been widely used to elucidate the nervous mechanisms of SGML. It is believed that RWIS-induced GML is mainly caused by the enhanced activity of vagal parasympathetic nerves. Many central nuclei, such as the dorsal motor nucleus of the vagus, nucleus of the solitary tract, supraoptic nucleus and paraventricular nucleus of the hypothalamus, mediodorsal nucleus of the thalamus, central nucleus of the amygdala and medial prefrontal cortex, are involved in the formation of SGML in varying degrees. Neurotransmitters/neuromodulators, such as nitric oxide, hydrogen sulfide, vasoactive intestinal peptide, calcitonin gene-related peptide, substance P, enkephalin, 5-hydroxytryptamine, acetylcholine, catecholamine, glutamate, γ-aminobutyric acid, oxytocin and arginine vasopressin, can participate in the regulation of stress. However, inconsistent and even contradictory results have been obtained regarding the actual roles of each nucleus in the nervous mechanism of RWIS-induced GML, such as the involvement of different nuclei with the time of RWIS, the different levels of involvement of the sub-regions of the same nucleus, and the diverse signalling molecules, remain to be further elucidated.

Dynamic observation and analysis of metabolic response to moxibustion stimulation on ethanol-induced gastric mucosal lesions (GML) rats.

BACKGROUND: Gastric mucosal lesion (GML) is the initiating pathological process in many refractory gastric diseases. And moxibustion is an increasingly popular alternative therapy that prevents and treats diseases. However, there are few published reports about developing pathology of GML and therapeutic mechanism of moxibustion treatment on GML. In this study, we investigated pathology of GML and therapeutic mechanism of moxibustion treatment on GML. METHODS: The male Sprague-Dawley (SD) rats were induced by intragastric administration of 75% ethanol after fasting for 24 h and treated by moxibustion at Zusanli (ST36) and Liangmen (ST21) for 1 day, 4 days or 7 days. Then we applied 1H NMR-based metabolomics to dynamic analysis of metabolic profiles in biological samples (stomach, cerebral cortex and medulla). And the conventional histopathological examinations as well as metabolic pathways assays were also performed. RESULTS: Moxibustion intervention showed a beneficial effect on GML by modulating comprehensive metabolic alterations caused by GML, including energy metabolism, membrane metabolism, cellular active and neurotransmitters function. CONCLUSIONS: Moxibustion can effectively treat gastric mucosal damage and effectively regulate the concentration of some related differential metabolites to maintain the stability of the metabolic pathway.

Protective effect of Corchorus capsularis L. leaves on ethanol-induced acute gastric mucosal lesion in rats.

In Taiwan, Corchorus capsularis L. has long been cultivated and the leaves are consumed as edible vegetable. This study is to investigate the protection effect of extract of C. capsularis leaves (ECC) on ethanol-induced acute gastric mucosal lesion (AGML) in rats. The results of phytochemical determination in ECC for total polyphenol, flavonoid and polysaccharide were 59.88 ± 0.61 mg/g, 86.39 ± 18.0 mg/g and 320.89 ± 6.99 mg/g, respectively. ECC showed significant activity of 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging with IC50 of 0.25 mg/ml. In vivo studies, Sprague-Dawley (SD) rats were randomly divided into five groups: sham, vehicle (control) and low-, medium-, and high-dose ECC (LECC, MECC, HECC; 200, 400, and 1,000 mg/kg/day, respectively). ECC was able to decrease significantly the ulcer index (UI) caused by 80% ethanol in a dose dependent manner. There was no significant effect on growth trend and food intake rate after the administration of ECC in the experimental period. The serum lipid parameters in ECC groups revealed significant increase in glutathione peroxidase (GPx), superoxide dilmutase (SOD) and catalase (CAT), and a decrease in malondialdehyde (MDA). Significant amelioration on pathological lesion score was found in ECC groups compared with the control group (P<0.05). The overall results indicate that ECC has protective effects on ethanol-induced AGML in rats, which could be associated with its antioxidant activity.

Transient Receptor Potential Ankyrin 1 and Substance P Mediate the Development of Gastric Mucosal Lesions in a Water Immersion Restraint Stress Rat Model.

BACKGROUND: Activation of substance P (SP) contributes to the development and maintenance of gastric lesions, but the mechanisms underlying the release of SP and SP-mediated damage to the gastric mucosa remain unknown. Transient receptor potential ankyrin 1 (TRPA1) is expressed in SP-positive neurons in the dorsal root ganglion (DRG) and stomach of rats. We hypothesized that water immersion restraint stress (WIRS) may activate and sensitize TRPA1 in DRG neurons, subsequently inducing the release of SP from DRG and stomach cells, causing the development of acute gastric mucosal lesions (AGML). METHODS: Changes in TRPA1 and SP expression in T8-11 DRG sensory neurons and the stomach in an AGML rat model were determined by reverse transcription polymerase chain reaction, western blotting and immunohistochemistry. The SP levels of serum and gastric mucosa were measured by using an enzyme-linked immunosorbent assay (ELISA). Gastric lesions were evaluated by histopathological changes. The TRPA1 antagonist HC-030031 and TRPA1 agonists allyl isothiocyanate were used to verify effect of TRPA1 and SP on AGML. RESULTS: SP and TRPA1 in the DRG and stomach were upregulated, and the serum and gastric mucosa levels of SP were increased after WIRS, which are closely associated with AGML. The release of SP was suppressed and AGML were alleviated following a selective TRPA1 antagonist HC-030031. TRPA1 agonists AITC increased release of SP and led to moderate gastric lesions. We confirmed that WIRS induced the release of SP in the DRG, stomach, serum and gastric mucosa, and in a TRPA1-dependent manner. CONCLUSIONS: Upregulated SP and TRPA1 in the DRG and stomach and increased serum and gastric mucosa SP levels may contribute to stress-induced AGML. TRPA1 is a potential drug target to reduce stress-induced AGML development in patients with acute critical illnesses. This study may contribute to the discovery of drugs for AGML treatment.

Mechanism of apoptosis involved in gastric mucosal lesions in Tibetans with high-altitude polycythemia.

The Tibetan high plateau is a low-oxygen environment, which may cause the pathogenesis of high-altitude polycythemia (HAPC). Gastric mucosal lesions (GML) are a common complication of HAPC. The molecular mechanisms involved in HAPC-induced GML have remained to be fully elucidated and were therefore investigated in the present study. Gastric tissues of patients with heavy, HAPC-induced GML and healthy controls were assessed by ultrastructural and histopathological analysis. In addition, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis were used to detect cell apoptosis in the gastric mucosa tissues. Moreover, the expression of genes associated with the phosphoinositide-3 kinase (PI3K) pathway was assessed by RT-qPCR to investigate the mechanism of cell apoptosis in HAPC-induced GML. The results revealed a significant increase in the number of red blood cells, gastric vessels and the diameter of gastric mucosal vessels in HAPC-induced GML patients compared with those in healthy controls. In addition, more red blood cells were distributed in gastric tissue not only at the vascular level but also in the tissue space. The number of vacuoles was increased in the gastric mucosal cells. Furthermore, a significant increase in apoptosis of the gastric mucosal cells was identified. The expression of phosphatase and tensin homolog was significantly higher in gastric mucosa from patients with HAPC-induced GML compared with that in the healthy controls. All of the pathologic changes suggested that significant cell apoptosis occurred in the HAPC-induced GML tissues, which may be associated with the PI3K pathway. These findings may provide novel insight for the treatment of gastric lesions caused by HAPC in the future.

The timing of weaning alters the vulnerability to stress-induced gastric erosion in adult rats.

BACKGROUND AND PURPOSE: Weaning is an important period of life and its timing may influence the resilence for later stress. One of the most important stress-related disorder is gastric ulceration. METHODS: Therefore we aimed to investigate the sensitivity of gastric mucosa to cold (at 16°C) water immersion stress (WIS for 3h) in adult (75-day-old) female and male rats after weaning them at different timepoints (at 17, 21, 30, 36 or 42 postnatal days). The connection with stress was studied by comparing control groups to those underwent WIS at the time of weaning and measuring corticosterone levels at the time of collecting the stomach samples. RESULTS: The timing of weaning has strong impact on all studied parameters. Stress-induced erosion development was the smallest in rats weaned at 36-day independently from preconditioning with WIS at weaning, or sex, despite a clear sex-effect on blood corticosterone levels and body weight. WIS at weaning influenced only the body weight in adult rats weaned at 30-day, being higher in stressed than in control groups. There was no clear overall correlation between erosion area and blood corticosterone measures. CONCLUSION: Taken together our results confirm that the timing of weaning has long-lasting impact on the resiliance of gastric mucosa to ulcerogenic stressful events. In rats the postnatal day 30-36 seems to be optimal for weaning in both sexes as both earlier and later weaning increased vulnerability. Females seems to be more vulnerable to the effect of weaning than males.

[Comparison of electroacupuncture at lower he-sea points on HMGB 1 and nAchR α7 in rats with acute gastric mucosal lesion].

OBJECTIVE: To observe the influence of electroacupuncture (EA) at lower he-sea points of stomach, large intestine, small intestine and gallbladder on interleukin-1ß (IL-1ß), high mobility group protein 1 (HMGB 1) and alpha 7 nicotinic acetylcholine receptor (nAchR α7) in rats with acute gastric mucosal lesion (AGML), so as to explore whether there is relative specificity in treating gastric viscera disease by stimulating Zusanli (ST 36). METHODS: Sixty healthy SD rats were randomly assigned into a blank group, a model group, a Zusanli group, a Shangjuxu group, a Xiajuxu group and a Yanglingquan group, ten rats in each one (half male and half female). The WRS method was applied to induce the AGML model except the rats in the blank group. The rats in the blank group were treated with routine diet; the rats in the model group were treated with immobilization at rat platform, 30 min per time; the rats in the Zusanli group, Shangjuxu group, Xiajuxu group and Yanglingquan group were treated with acupuncture and connected with EA device (dilatational wave 10 Hz/50 Hz, positive electrode on the left side and negative electrode on the right side, intensity was appropriate when rat hind leg slightly shook), 30 min per time. The treatment was given once a day. After consecutive 10-day treatment, the gastric tissue was collected and the damage of gastric mucosa was evaluated; ELISA method was applied to measure the content of serum IL-1ß and tissue HMGB 1; the Western blot method was applied to measure the expression of nAchR α7 receptor. RESULTS: (1) Compared with the model group, the ulcer index (UI) of gastric mucosa, serum IL-1ß and tissue HMGB 1 were lower, and the expression of nAchR α7 was increased in the remaining groups (P<0.05, P<0.01). (2) Compared with the Zusanli group, the UI of gastric tissue, serum IL-1ß and tissue HMGB 1 were higher in the Shangjuxu group, Xiajuxu group and Yanglingquan group (P<0.05, P<0.01), and the expression of nAchRα7 was reduced in the Yanglingquan group (P<0.01). CONCLUSIONS: (1) EA at digestive system-related lower he-sea points, through IL-1ß, HMGB 1 and nAchR α7, could regulate immune response, lighten inflammatory reaction and reduce mucosal injury, which could realize the intervention effect on AGML rats. (2) From the comparison, it is concluded the intervention effect of Zusanli group is superior to the other groups, partly indicating the relative specificity between Zusanli and stomach.

Prevalence and risk factors for clinically significant upper gastrointestinal bleeding in patients with severe acute pancreatitis.

OBJECTIVE: To investigate the prevalence and risk factors of upper gastrointestinal bleeding (UGIB) in patients with severe acute pancreatitis (SAP). METHODS: Altogether 101 patients were admitted to the Department of Gastroenterology, Changhai Hospital, Second Medical Military Hospital from July 2006 to June 2010 due to SAP. Their prevalence and risk factors of UGIB were retrospectively analyzed. RESULTS: In total, 18 (17.8%) patients developed UGIB and 13 received endoscopic examination, which yielded six cases of acute gastric mucosal lesions (AGML), five of peptic ulcers (PU) and two of pancreatic necrotic tissue invading the duodenal bulb and presenting as multilesion, honeycomb-like ulcer. The mortality rate of UGIB patients was much higher than that of non-UGIB patients (44.4% vs 10.8%, P = 0.0021). Univariate analysis revealed that the risk factors for UGIB included the Acute Physiology and Chronic Health Evaluation II (APACHE II) score, computed tomography severity index (CTSI), Ranson score, arterial blood pH and PaO2 , serum blood urea nitrogen and creatinine concentrations, platelet count, shock, sepsis and organ failure, mechanical ventilation, heparinized continuous renal replacement therapy and total parenteral nutrition. Multivariate logistic regression revealed that APACHE II score and CTSI were significant risk factors while PaO2 was the protective factor for UGIB in SAP. CONCLUSIONS: UGIB is a common complication with poor prognosis due mainly to PU and AGML. Patients having SAP with high APACHE II scores and CTSI or low PaO2 should be considered to be at high risk for UGIB.

Orally given gastroprotective capsaicin does not modify aspirin-induced platelet aggregation in healthy male volunteers (human phase I examination).

Capsaicin is a well-known component of red pepper. Recent studies have shown that capsaicin could prevent gastric ulcer provoked by various NSAID-s like acetylsalicylic acid (ASA). Primary objective of this human clinical phase I trial was to investigate whether two different doses of capsaicin co-administered with ASA could alter the inhibitory effect of ASA on platelet aggregation. 15 healthy male subjects were involved in the study and treated orally with 400 µg capsaicin, 800 µg capsaicin, 500 mg ASA, 400 µg capsaicin+500 mg ASA and 800 µg capsaicin+500 mg ASA. Blood was drawn before and 1, 2, 6 and 24 hours after the drug administration. After that epinephrine induced platelet aggregation was measured by optical aggregometry. Between treatments, volunteers had a 6-day wash-out period. Our results showed that capsaicin had no effect on platelet aggregation, while as expected, ASA monotherapy resulted in a significant and clinically effective platelet aggregation inhibition (p ≤ 0.001). The combined ASA-capsaicin therapies reached equivalent effectiveness in platelet aggregation inhibition as ASA monotherapy. Our investigation proved that capsaicin did not influence the inhibitory effect of ASA on platelet aggregation, thus the capsaicin-ASA treatment would combine the antiplatelet effect of ASA with the possible gastroprotection of capsaicin.

Role of the nucleus tractus solitarii in the protection of pre-moxibustion on gastric mucosal lesions.

Previous studies have shown that somatic sensation by acupuncture and visceral nociceptive stimulation can converge in the nucleus tractus solitarii where neurons integrate signals impacting on the function of organs. To explore the role of the nucleus tractus solitarii in the protective mechanism of pre-moxibustion on gastric mucosa, nucleus tractus solitarii were damaged in rats and pre-moxibustion treatment at the Zusanli (ST36) point followed. The gastric mucosa was then damaged by the anhydrous ethanol lavage method. Morphological observations, enzyme linked immunosorbent assays, and western immunoblot analyses showed that gastric mucosa surface lesion and the infiltration of inflammatory cells were significantly ameliorated after pre-moxibustion treatment. Furthermore, the gastric mucosal damage index and somatostatin level were reduced, and epidermal growth factor content in the gastric mucosa and heat-shock protein-70 expression were increased. These results were reversed by damage to the nucleus tractus solitarii. These findings suggest that moxibustion pretreatment at the Zusanli point is protective against acute gastric mucosa injury, and nucleus tractus solitarii damage inhibits these responses. Therefore, the nucleus tractus solitarii may be an important area for regulating the signal transduction of the protective effect of pre-moxibustion on gastric mucosa.

Effects of pre-moxibustion at Zusanli (ST36) on heat shock protein 70 expression in rats with gastric mucosal lesions after neurotomy.

Studies have shown that pre-moxibustion protects the gastric mucosa by up-regulating the expression of heat shock protein 70. However, the signaling pathway underlying this effect remains unclear. Rats were intragastrically administered absolute alcohol, causing obvious lesion of the gastric mucosa. Following pre-moxibustion at Zusanli (ST36) for 8 days, the ulcer index decreased to different degrees. The results of an enzyme linked immunosorbent assay and western blotting showed significant upregulation of heat shock protein 70 expression in the gastric mucosa and serum. None out of transection of the spinal cord, damage to the nucleus of the solitary tract, neurotomy of the vagal nerve and neurotomy of the common peroneal nerve affected the decrease in ulcer index or the increase in heat shock protein 70 expression in serum after pre-moxibustion at Zusanli, and heat shock protein 70 expression was obviously decreased in the gastric mucosa. These findings suggest that pre-moxibustion at Zusanli can protect the gastric mucosa against lesioning, and that the mechanism underlying this effect involves its induction of heat shock protein 70 expression. Neural pathways participate in the regulatory effects of moxibustion on heat shock protein 70 expression in the gastric mucosa.

Effects of atractylodis rhizoma pharmacopuncture on an acute gastric mucosal lesion induced by compound 48/80 in rats.

OBJECTIVES: This study was designed to investigate the protective effects of Atractylodis Rhizoma pharmacopuncture (ARP) against acute gastric mucosal lesions induced by compound 48/80 in rats. METHODS: The ARP was injected in Joksamni (ST36) and Jungwan (CV12) 1 hr before treatment with compound 48/80. The animals were sacrificed under anesthesia 3 hrs after treatment with compound 48/80. The stomachs were removed, and the amounts of gastric adherent mucus, gastric mucosal hexosamine, thiobarbituric acid reactive substances (TBARS), xanthine oxidase (XO), and superoxide dismutase (SOD) were measured. Also, histological examination were performed. RESULTS: Gastric adherent mucus, gastric mucosal hexosamine and histological defects of gastric mucosa declined significantly after ARP treatment. Changes in gastric mucosal TBARS were also reduced by ARP treatment, but this result was not statistically significant. ARP treatment did not change the XO and the SOD activities. CONCLUSIONS: ARP showed protective effects for acute gastric mucosal lesions induced by compound 48/80 in rats. These results suggest that ARP may have protective effects for gastritis.

Effects of cimetidine, a histamine type 2 receptor antagonist, on microcirculatory disturbance of the stomach induced by full-thickness burn injuries as a model for surgical stress in rats.

BACKGROUND: We have reported the preventive effect of cimetidine, a histamine type 2 receptor antagonist, on decreased gastric mucosal blood flow induced by burn injury, a model of surgical stress. OBJECTIVE: The present study was performed to assess the effects of cimetidine on gastric microcirculatory disturbance induced by surgical stress. METHODS: Twelve male Wistar rats were anesthetized and a 30% full-thickness dorsal scald burn was inflicted. The total lengths of gastric erosions were measured using stereoscopic microscopy. Microvascular images in the basal region of the gastric mucosa were observed using an intravital microscope, and the diameters of venules and collecting venules were measured. Rolling leukocytes inside and along the venules, an indication of endothelial damage to the microcirculation, were observed. The rats were assigned to the cimetidine group or the control group (both, n = 6). Cimetidine 100 mg/kg was administered 30 minutes before and 2.5 hours after infliction of the burn injury. Animals in the control group were given only isotonic saline. Values are expressed as mean (SD). RESULTS: Contraction of venules was easily observed in all rats in the control group. However, venular contraction was rarely observed in the cimetidine group. The total length of gastric erosions was significantly decreased in the cimetidine group compared with the control group (0.93 [0.58] µm vs 5.98 [5.18] µm, respectively; P < 0.05). The percentages of rolling leukocytes that passed the confluence of a prevenule and a venule were also significantly decreased in the cimetidine group compared with the control group (4.7% [7.3%] vs 22.6% [5.7%]; P < 0.01). The diameters of the venules and collecting venules were significantly larger in the cimetidine group (57.3 [6.8] µm and 75.9 [3.6] µm, respectively) than in the control group (30.9 [9.2] µm and 46.8 [8.0] µm, respectively) (both, P < 0.01). CONCLUSIONS: The present study suggests that cimetidine may have a protective effect against gastric microcirculatory disturbances induced by burn injury, a model of surgical stress.