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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the results of the Ticlopidine Aspirin Stroke Study, a blinded trial at 56 North American centers that compared the effects of ticlopidine hydrochloride (500 mg daily) with those of aspirin (1300 mg daily) on the risk of stroke or death. The medications were randomly assigned to 3069 patients with recent transient or mild persistent focal cerebral or retinal ischemia. Follow-up lasted for two to six years. The three-year event rate for nonfatal stroke or death from any cause was 17 percent for ticlopidine and 19 percent for aspirin--a 12 percent risk reduction (95 percent confidence interval, -2 to 26 percent) with ticlopidine (P = 0.048 for cumulative Kaplan-Meier estimates). The rates of fatal and nonfatal stroke at three years were 10 percent for ticlopidine and 13 percent for aspirin--a 21 percent risk reduction (95 percent confidence interval, 4 to 38 percent) with ticlopidine (P = 0.024 for cumulative Kaplan-Meier estimates). Ticlopidine was more effective than aspirin in both sexes. The adverse effects of aspirin included diarrhea (10 percent), rash (5.5 percent), peptic ulceration (3 percent), gastritis (2 percent), and gastrointestinal bleeding (1 percent). With ticlopidine, diarrhea (20 percent), skin rash (14 percent), and severe but reversible neutropenia (less than 1 percent) were noted. The mean increase in total cholesterol level was 9 percent with ticlopidine and 2 percent with aspirin (P less than 0.01). The ratios of high-density lipoprotein and low-density lipoprotein to total cholesterol were similar in both treatment groups. We conclude that ticlopidine was somewhat more effective than aspirin in preventing strokes in this population, although the risks of side effects were greater.
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PMID:A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. Ticlopidine Aspirin Stroke Study Group. 230 95

The authors report an initially successful left gastric artery embolization performed because of massive upper gastrointestinal bleeding; the procedure was complicated by focal gastric and hepatic infarctions. These complications occurred in the absence of underlying factors known to predispose to ischemia. Low-grade gastric bleeding persisting after seemingly successful embolization of the left gastric artery may indicate ischemic gastritis and is an indication for endoscopy. In addition, the presence of a left hepatic artery completely replaced to the left gastric artery should alert one to the potential for hepatic necrosis.
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PMID:Gastric and hepatic infarction following embolization of the left gastric artery: case report. 278 92

True stress ulcers are primarily superficial gastric fundic lesions that occur in the clinical setting of severe shock, trauma, burns, and sepsis, especially peritonitis. They are to be clearly differentiated from Cushing's ulcers, exacerbation of pre-existent chronic ulcers, and drug-induced gastritis, all of which have completely different pathogenetic mechanisms. The etiology of true stress ulcers is most importantly related to ischemia and tissue acidosis, although luminal acid and pepsin are requisite for ulceration to occur. The sole clinical manifestation of stress ulcers is hemorrhage. Prophylaxis with antacids alone, or with a combination of antacids and H2 receptor antagonists is highly efficacious if luminal pH is carefully monitored. The treatment of exsanguinating hemorrhage, once established, carries with it an extremely high morbidity and mortality.
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PMID:The clinical problem of stress ulcers. 288 24

Stress ulcers are multiple, superficial erosions of the proximal stomach that develop in the setting of severe physiological stress. Evidence suggests that the mechanism of cytoprotection may be impaired in settings conducive to their development. The two most critical elements in the pathogenesis of the disease are the presence of some luminal acid and some degree of associated mucosal ischemia. The probable endpoint is reduction of intramucosal pH below acceptable physiological limits. In the absence of effective prophylaxis, 30% of patients with stress ulcer disease will develop hemorrhage of life-threatening severity--acute hemorrhagic gastritis--a condition difficult to treat both nonoperatively and operatively. Mortality remains high irrespective of the capacity to control hemorrhage. Prevention is the best treatment. Both H2- receptor antagonists and intragastric titration with antacids have been proposed in prophylaxis. Current evidence suggests that each is equally efficacious for moderately ill patients. However, for the severely ill, antacid titration is superior to cimetidine. A small group of critically ill patients are not effectively treated by either modality. It seems likely that prostaglandins may prove efficacious in this patient population.
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PMID:Prostaglandins. A surgeon's perspective. 394 55

The critical care environment may be characterized by invasive monitoring, vasoactive drugs, and major interventions which may have adverse effects on gastrointestinal function. Furthermore, conditions such as heart failure or sepsis may compromise oxygen delivery to gastrointestinal organs. Life threatening illness from a variety of causes may produce endoscopically evident gastritis or ulceration in up to 100% of patients, and clinically evident bleeding in 20%. Clinical studies suggest that antacids or H2 receptor blockers may reduce the frequency of this complication. Other conditions are associated with a spectrum of hepatic dysfunction ranging from the cholestatic jaundice of reactive hepatopathy during sepsis to centrilobular necrosis and hepatitis of shock liver. Additionally, many drugs used in the critical care setting may adversely affect mesenteric oxygen delivery and result in ischemia or infarction of the bowel. An increased awareness and understanding of these and other gastrointestinal complications in critically ill patients will, it is hoped, lead to earlier detection and better therapy than is now available.
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PMID:Gastrointestinal complications in critically ill patients: the intensivists' overview. 396 47

Twenty polypoid lesions at gastroenterostomy stomas (the so-called gastritis cystica polyposa-GCP) were endoscopically removed from gastroenterostomy stomas of 16 male and two female patients previously operated for benign lesions. The interval from surgery ranged from 3 to 40 years (mean: 16.2 years). At light microscopy GCP showed 2 histologic patterns: a) with cystic glands limited to the mucosal layer (gastritis cystica superficialis); b) with cystic glands also spreading into the submucosa (gastritis cystica profunda). Atrophy of specific gastric glands, intestinal metaplasia and dysplastic changes also occurred. Local chronic ischemia and inflammatory reaction as a consequence of gastric surgery and suture at gastroenterostomy together with bile reflux were considered responsible for the development of GCP. The sites and the histologic features of GCP resembled those of experimental stomal polyps preceeding carcinoma in rats after partial gastrectomy. The sites of formation, the sex incidence, the interval from previous operation as well as the histologic findings suggest that GCP is a possible precancerous lesion.
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PMID:Gastritis cystica polyposa: a possible precancerous lesion. 398 43

The purpose of the present study was to elucidate the effect of duodenal juice on development of gastric ulcer, in relation to changes of lipid composition and energy metabolism of the gastric mucosa in dogs. For regurgitation of duodenal juice and stagnation of gastric contents in the stomach, the duodenum was constricted below the papilla of Vater, accompanying with pyloroplasty and upper gastro-jejunostomy. Furthermore, to induce ischemia in the gastric mucosa, 0.5 ml of 1% formalin solution was injected into a descending branch of the left gastric artery. Three weeks later, U1 II-III gastric ulcer developed at the formalin injected area with severe gastritis but not with hyperacidity, and the histologic findings were similar to the one of a human gastric ulcer with hypoacidity. On assay of lipid composition in the gastric mucosa, lecithin decreased and both lysolecithin and NEFA increased, showing that lecithin of the gastric mucosa was decomposed by phospholipase A2 of the duodenal juice. In the gastric mucosa, ATP and energy charge decreased, and AMP and lactate increased, indicating that the energy metabolism was led to anaerobic glycolysis. These results revealed that the gastric mucosa becomes very fragile when duodenal juice regurgitates into the stomach and that gastric ulcer may develop even without hyperacidity when the microcirculation is disturbed in this condition.
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PMID:Effect of duodenal juice on pathogenesis of gastric ulcer. 683 47

Ischemia of the gastric epithelium has emerged as one of the more likely mechanisms for gastric ulceration. Radiolabeled microspheres (15 mu) were used to measure blood flow to exteriorized, chambered stomach segments in eight dogs during the development of aspirin erosions. Flow determinations were made before aspirin (20 mM in 140 mM HCl) exposure and at 2, 10, and 20 minutes after the initiation of the chemical insult. Lesions formed at 30 minutes of acetylsalicylic acid exposure. The epithelium was separated into normal and injured, based on gross discoloration caused by intramucosal hemorrhage. The calculated blood flows to the abnormal and normal mucosa were identical at 2 minutes (0.22 +/- 0.04 versus 0.15 +/- 0.03, NS) and at 10 minutes (0.39 +/- 20 versus 0.17 +/- 0.04, NS) after initiation of aspirin injury (all values in ml/gram-wet weight/min, mean +/- SEM). By 20 minutes of aspirin exposure, mucosal blood flow to areas that eventually became injured was greater than the blood flow to areas that remained normal (0.45 +/- 0.12 versus 0.13 +/- 0.05 P less than 0.05). The data suggest that ischemia does not play a role in chemical erosive gastritis.
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PMID:Focal microcirculatory changes during the production of aspirin-induced gastric mucosal erosions. 746 23

Recent studies have indicated that ammonia is involved in the pathophysiology of Helicobacter pylori-associated gastric mucosal damage. Helicobacter pylori-associated chronic active gastritis is characterized by an invasion of neutrophils. We investigated the interrelationship among hypochlorous acid (oxidant produced by neutrophil), ammonia (product of Helicobacter pylori urease), and monochloramine (product of ammonia and hypochlorous acid) in the development of gastric mucosal damage in rats. Gastric mucosal lesions were produced by exposure of the gastric mucosa to ammonia, urea with urease, or urea with Helicobacter pylori in rats subjected to ischemia. Pretreatment with taurine (scavenger of hypochlorous acid) or antineutrophil serum significantly attenuated gastric mucosal lesions induced by the above test agents. Ammonia-induced gastric mucosal lesions were exacerbated in the presence of hypochlorous acid with concomitant generation of monochloramine. These results suggest that the ammonia, hypochlorous acid, and monochloramine triad may be important in Helicobacter pylori-mediated gastric mucosal damage.
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PMID:Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage. 785 Nov 88

Lower gastrointestinal tract symptoms occur frequently in runners. The most common complaints are bowel urgency and diarrhea. Many etiologies have been proposed, including enteric fluid and electrolyte imbalance, autonomic nervous system stimulation, ischemia and mechanical trauma. The evaluation should include a review of the athlete's training program and diet, as well as a review of any preexisting gastrointestinal disease. A stool examination for occult blood should be performed in the athlete who complains of diarrhea. Treatment begins with a reduction in the intensity of workouts, followed by a gradual return to the previous level of training after the symptoms resolve. In most cases, symptoms do not recur. Dietary manipulation or antimotility agents may be helpful in some athletes. Bloody diarrhea, usually related to hemorrhagic gastritis, can be effectively treated with histamine H2-receptor antagonists.
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PMID:Runner's diarrhea and other intestinal problems of athletes. 837 91


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