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

Stress ulcers are multiple, superficial erosions which occur mainly in the fundus and body of the stomach. They develop after shock, sepsis, and trauma and are ofter found in patients with peritonitis and other chronic medical illness. Stress ulcers should be differentiated from reactivation of chronic duodenal or gastric ulcers. Cushing's ulcer following head injury, or drug-induced gastritis. Digestive symptoms are usually absent, hemorrhage is the most common manifestation, and perforation and obstruction are rare. The presence of luminal acid and ischemia are necessary for the production of stress ulcer, while disruption of the gastric mucosal barrier by refluxed duodenal content may contribute to the pathogenesis. Endoscopy is the mainstay of the diagnostic procedure, and angiography should be used if endoscopy fails to identify the bleeding lesions. Medical management should include volume replacement, nasogastric aspiration, and the use of antacid. Selective intraarterial infusion of pitressin has shown encouraging preliminary results. Surgical treatment is reserved only for those patients who continue to bleed despite all medical management. The operation of choice is open to question. We prefer vagotomy, pyloroplasty, and oversewing the ulcers as an initial operation. Since the result of all forms of therapy has been poor, it seems resonable to try to prevent ulcer development. The use of vitamin A, hyperalimentation, and growth hormones is still in an experimental stage. Large clinical studies with case control are necessary before recommendations can be made. The use of potent and frequent antacid to buffer the gastric content has shown promising results; however, these observations need to be confirmed in a properly controlled and randomized study.
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PMID:Stress ulcers: their pathogenesis, diagnosis, and treatment. 79 64

The influence of the proximal selective vagotomy (PSV) on the origin and the extent of experimental gastric ulcer were investigated in rats. The lesions of the gastric mucosa were caused in three groups: by stress through swimming-test, by application of phenylbutazone, and by ischemia (ligature of the left gastric and the right gastroepiploic vessels). The PSV practised a protective influence on the pharmacodynamic etiology, however, not on the stress ulcer. The areas of the ischemic gastric ulcers were larger on an average of 40% after PSV than in the control animals. The difference was not statistically significant. In case the PSV caused besides hyposecretion and hypo-acidity even passive hyperemia caused in the denervated part of the stomach then these did not produce any sufficient defence against the origin of stress ulcers and ischemic lesions.
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PMID:[The effect of proximal selective vagotomy on experimental gastric mucosal lesions in the rat]. 222 3

Virtually all patients who are under the physiologic stress of an intensive care unit (ICU) are vulnerable to stress-related mucosal damage and ulceration. Although clinically significant hemorrhage from stress ulceration occurs in only 5-20 percent of patients in the ICU, the associated mortality is greater than 50 percent. The pathophysiologic mechanisms of stress ulcer are not well understood; however, a number of risk factors such as intraluminal gastric acidity and mucosal ischemia have been implicated. To prevent the development of stress ulcers and subsequent complications, it is important to identify and correct these underlying risk factors. Improving mucosal blood flow (i.e., fluid resuscitation and low-dose dopamine) and providing adequate nutritional support are invaluable adjuncts in minimizing the risk of stress ulcer formation. The use of pharmacologic prophylaxis controls the gastric acidity and prevents the formation of stress ulcers. The potential for drug-induced adverse effects and drug-drug interactions are of particular concern in the care of critically ill patients. Multiple organ system dysfunction or failure, malnutrition, fluid and electrolyte abnormalities, as well as the use of multiple pharmacologic agents predispose these patients to alterations in drug pharmacokinetics, drug-induced adverse effects and drug-drug interactions. These changes may alter the pharmacodynamic response to therapy and must be considered when designing drug dosage regimens for critically ill patients.
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PMID:Pathophysiologic changes in the critically ill patient: risk factors for ulceration and altered drug metabolism. 227 Jun 97

Gastric ulceration has been induced after stress, combining 24 h of fasting and 48 h of restraint in 9 groups of 20 rats with or without a pyloroplasty or a pylorojejunostomy combined with atropine and gastric infusion of NaHCO3 or taurocholic acid. After death or sacrifice at 48 h, ulcer index and blood in the jejunum were determined. Gastric mucosal blood flow was measured semi-continuously by a laser Doppler velocimeter. There were 45% deaths after 48 h of restraint alone, and 70% in the group combining pylorojejunostomy with taurocholic acid. Mortality was lower (p less than or equal to 0.01) pylorojejunostomy alone and more significantly so (p less than or equal to 0.001) when associated with NaHCO3. There was no death when NaHCO3 and atropine were combined with restraint. The mucosal blood flow increased significantly during the first 12 h of restraint in the taurocholic acid group. Both groups with NaHCO3 had mucosal blood flows similar to the controls. Gastric acid and gastric emptying, mucosal ischemia and bile reflux are joint factors inducing gastric stress ulcer. The 100% survival and the low ulcer index after a treatment by atropine and gastric infusion of NaHCO3 suggest that these well-known drugs should be used more frequently.
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PMID:Gastric stress ulcer of the rat: relative contribution of the pyloric sphincter, HCO3- bile reflux and mucosal blood flow. 301 38

Stress-related gastrointestinal bleeding is known to occur in approximately 25 percent of untreated seriously ill patients, but with appropriate prophylaxis is largely preventable. Since the treatment of stress bleeding is generally unsatisfactory and has a high mortality, routine prophylaxis should be instituted for susceptible patients. Multiple mechanisms contribute to stress ulcer formation, the most important of which appear to be mucosal ischemia and the inability to control back-diffused hydrogen. Antacids and histamine2-blocking agents are presently the cornerstone of effective prophylaxis, but because they have been implicated as contributors to nosocomial pneumonias due to bacterial overgrowth in the stomach, investigation is ongoing into such alternative prophylactic agents as sucralfate and prostaglandins that do not alter the normal gastric acidity. This article presents a review of the literature on the development and prevention of stress ulcer disease.
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PMID:Stress ulcers: current understanding of pathogenesis and prophylaxis. 329 57

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

Ischaemia of the gastric mucosa in haemorrhagic shock appears to be one of the principal factors underlying acute bleeding from the upper gastrointestinal tract. In the present experimental study on dogs the changes of blood flow in the upper gastrointestinal tract were recorded by direct flow measurement in the pertinent vessels. Fourteen mongrel dogs were subjected to haemorrhagic shock lasting for 3 and 4 h. A decline of 46 per cent cardiac output was observed while coeliac artery blood flow decreased by 40 per cent and gastric artery blood flow by 60 per cent. All stages of stress ulcers were documented by light and electron microscopy. In addition, pronounced degranulation of mast cells preceding major tissue damage was observed. In the light of these findings a cascade of events is thought to be present resulting in the development of stress ulcer.
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PMID:Gastric blood flow, mast cell degranulation and micromorphology of gastric mucosa following experimental haemorrhagic shock in dogs. 697 71

Recent observations have suggested that stress ulcer prophylaxis should not routinely be used to prevent upper gastrointestinal hemorrhage in critically ill patients. This is because our understanding of stress ulcer pathogenesis has shifted from a problem limited to back diffusion of acid to a phenomenon of gastric ischemia. The purpose of this article is to review the proposed mechanism of stress ulcer bleeding and to discuss prophylaxis.
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PMID:Stress ulcer: is routine prophylaxis necessary? 773 73

Acute gastric stress ulceration occurs frequently in severely ill patients. Mucosal ischemia is central to the etiology of stress ulceration. The ability of the mucosa to restore continuity when damaged is one of the most important of the local defence mechanisms against injury. The aims of this study were to investigate this restitutive process during stress ulcer formation and to determine the effect of prophylaxis against stress ulceration on gastric mucosal cell kinetics. Nuclear DNA was radiolabeled in vivo with tritiated thymidine, and after autoradiography the position and number of labeled cells along the gastric mucosal gland were determined. Wistar rats were studied immediately and 48 hr after cold restraint stress. The labeling index in the proliferative zone of the gastric mucosa was significantly suppressed immediately after stress (12.58% vs 16.81% for unstressed controls, P < 0.001). This effect persisted for 48 hr after stress (9.89% vs 16.35% for unstressed controls, P < 0.001). Prophylaxis against stress ulceration with cimetidine or allopurinol prevented this suppression of gastric mucosal cell kinetics and promoted early migration of labeled cells towards the surface of the mucosal gland. Allopurinol prophylaxis was associated with migration of mucosal cells immediately following stress greater than that following cimetidine prophylaxis (14.0% vs 9.3% surface layer labeling index, P < 0.01). Allopurinol, a xanthine oxidase inhibitor, reduces oxygen free radical production during ischemia reperfusion injury. These results emphasise the importance of the gastric mucosal defence mechanisms in protection against injury and indicate the role of ischemia in the aetiology of acute gastric stress ulceration.
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PMID:Stress ulceration and gastric mucosal cell kinetics: the influence of prophylaxis against acute stress ulceration. 841 98

Rats were fed diets containing different ratios of linoleate (18:2 n-6) to alpha-linolenate (18:3 n-3), and the severity of gastric injury induced by ethanol, ischemia/reperfusion and water-immersion stress was compared. On decreasing the 18:2 n-6/18:3 n-3 ratios in the diets, the proportion of arachidonic acid (20:4 n-6) decreased and that of eicosapentaenoic acid (20:5 n-3) increased in the phospholipids of the gastric mucosa, which was associated with decreased mucosal prostaglandin E2 content. Mucosal injury in all the three experimental models was exacerbated significantly in the diet group fed 18:2 n-6/18:3 n-3 ratio of 0.25 (perilla oil) as compared with the groups fed dietary oils with 18:2 n-6/18:3 n-3 ratios of 2.7 (mixture of perilla and safflower oils) and 127 (safflower oil). This adverse effect induced by perilla oil diet was not observed when rats were pretreated with a mild irritant (20% ethanol) prior to challenge with a strong irritant (absolute ethanol). Furthermore, an 18:2 n-6/18:3 n-3 ratio of as low as 1 was found to be in a safe range in the water-immersion stress ulcer model. Thus, oils with very low n-6/n-3 ratios, for example perilla oil, could be used without the risk of the observed adverse effects on experimental gastric injury in people of industrialized countries ingesting foods with n-6/n-3 ratios of above 4. A decrease in the n-6/n-3 ratios to 2 or below is still recommended for the prevention of chronic diseases in the elderly related to atherosclerosis and inflammation.
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PMID:Effect of dietary linoleate/alpha-linolenate balance on experimentally induced gastric injury in rats. 988 6


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