Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are conflicting views on the pathogenesis of the intestinal malfunction seen in infants with gastroschisis. It has been variously ascribed to abnormalities of ganglion cells and smooth muscle elements, intestinal ischemia, and the "peel" which invests the serosa of the intestine. Review of the clinical and experimental literature showed only limited information on the histology of the eviscerated human intestine. In order to add to this data base, and to further investigate the pathogenesis of the intestinal malfunction from a histologic standpoint, we reviewed surgical and autopsy material from our experience with 105 neonates with gastroschisis. Ten specimens were satisfactory for evaluation from a standpoint of tissue integrity. The specific mural components of mucosa, submucosa, muscularis, and ganglion cells were examined and found to be either normal, or to show nonspecific abnormalities that varied from case to case, and were related mostly to intestinal infarction due to compromise of the gut at the site of the gastroschisis defect. In six patients, this progressed to atresia formation. The most consistent abnormalities were found in the serosal layer with its peel. Using special stains, the peel was found to be composed largely of fibrin and collagen. Based on this study, we feel that edema and ischemic changes, though often present, are much less prominent than the peel, as the leading histologic abnormality of the intestine of gastroschisis. Squamous epithelial cells were seen in the peel in four cases, suggesting that the peel had been "appliqued" onto the serosa of the herniated fetal gut.
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PMID:Histology of the intestine in human gastroschisis--relationship to intestinal malfunction: dissolution of the "peel" and its ultrastructural characteristics. 297 19

Vasoactive intestinal peptide (VIP), first isolated from the gut, was originally considered a candidate gastrointestinal hormone. Since about 1975, however, it has become increasingly clear that it is primarily a neurotransmitter or neuromodulator and that it exerts its functions mainly by local release from nerve endings. VIP plays a hormonal role only when it is released in large amounts from a tumor, with a consequent overflow into the circulation and grossly elevated plasma concentrations of the peptide. Moderately increased VIP plasma and tissue concentrations that cause mainly local effects are found in intestinal ischemia. Crohn's disease and some other chronic inflammatory diseases of the bowel. VIP is also measured in increased amounts in the normal fetus and neonate, where it may play an important physiological role. Such an increase of VIP levels in the circulation could enhance perfusion and metabolic activity of tissues during their rapid-growth period. On the other hand, disorders with a disturbed VIP function such as achalasia and Hirschsprung's disease and possibly also asthma and cystic fibrosis seem to be characterized mainly by a derangement of smooth muscle activity and/or exocrine secretion. Considering this list of disorders where VIP has either a proven or suspected role, it is easy to imagine the significance of this peptide in pediatric pathophysiology.
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PMID:[Vasoactive intestinal polypeptide (VIP)--possible importance in diseases of childhood]. 299 82

In the normal digestive tract, interaction of the mucosa with a large and varied microbial flora is inevitable. In fact, the "normal" state of the digestive tract reflects the impact of the resident flora to a significant degree. The pathogenesis of various infectious conditions encountered by the surgical pathologist in the gut is understood more readily when the gastrointestinal tract is viewed as a complex ecosystem. Significant disease may result from perturbation of the normal flora, as well as from exogenous infection, and susceptibility of the host may vary with disturbances of the digestive ecosystem. An ecologic perspective is essential in the consideration not only of the "infected" gut, but of conditions as diverse as ischemia or even carcinogenesis in the gastrointestinal mucosa.
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PMID:Surgical pathology of the infected gut. 302 89

Continuous jejunal feeding through needle catheter jejunostomy is generally well tolerated with minimal morbidity. Small bowel ischemia or infarction has not been reported in association with jejunal feedings. We describe five patients, each of whom had grossly normal small bowel at the time of insertion of needle catheter jejunostomy. All had episodes of hypotension during continuous jejunal feedings, and subsequently had abdominal distention. Upon abdominal exploration, two patients were found to have infarction of the jejunum and three had infarction of the entire small bowel. No evidence of major vascular occlusion or mechanical obstruction was found. Patients at high risk for hypoperfusion may not tolerate jejunal feedings during such episodes. It appears possible that feeding may increase the susceptibility of the gut to hypoperfusion.
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PMID:Small bowel ischemia: a consequence of feeding jejunostomy? 308 Aug 12

This study used the Acute Physiological and Chronic Health Evaluation (APACHE II) system to select two groups of ICU patients with comparable risk of hospital death to evaluate the importance of GI dysfunction, defined as failure to tolerate enteral nutrition (EN), as a prognostic factor. In our ICU, patients who have not undergone recent bowel surgery are treated by EN. Those patients who cannot tolerate EN are treated by total parenteral nutrition (TPN). One hundred and eleven patients who tolerated EN (functioning gut) and 97 TPN patients who failed to tolerate EN (GI dysfunction) were studied. The mean APACHE II scores of the two groups were 17.7 +/- 6.5 (SD) and 17.7 +/- 5.1, respectively. The observed mortality of patients with GI dysfunction (51%) was significantly higher (p less than .0005) than that of patients with a functioning gut (25%). This was associated with significantly poorer APACHE II mean BP, oxygenation, and creatinine scores among the GI dysfunction patients. Our results suggest that shock, ischemia, and hypoxemia, in addition to causing impairment of renal function, may bring about changes in the GI tract, evident clinically only as a failure to tolerate EN, which have an adverse effect on the prognosis of ICU patients so affected.
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PMID:Gastrointestinal dysfunction among intensive care unit patients. 311 78

Interest in the pathogenesis of neonatal necrotizing enterocolitis has prompted study of the intestinal circulation in developing animals. It is conceivable that poorly developed collateral channels may predispose the neonatal intestine to ischemic insults. We therefore characterized intestinal collateral blood flow in anesthetized and ventilated 1-day and 1-month-old piglets. Intestinal blood flow was measured with radioactive microspheres (15 micron diameter) before and after either 1) total occlusion of the superior mesenteric artery (SMA) or 2) occlusion of a distal (jejunoileal) branch of the SMA. After total SMA occlusion in 1-day and 1-month-old piglets, perfusion of the intestine via collaterals from the celiac and inferior mesenteric arteries was not evident. Jejunal, ileal, and colonic (except rectal) blood flows fell to zero 30 min after ligation of the SMA. Ligation of a distal branch of the SMA in 1-month-old animals significantly reduced total wall (by 25%) and mucosal/submucosal (by 25%) blood flows in the occluded segment. Similar experiments in 1-day-old piglets produced significantly greater reduction in total (70%) and mucosa/submucosa (70%) blood flows. Muscle/serosa blood flows in both groups were not significantly different from control values. In conclusion, collateral perfusion of the intestine via the celiac and inferior mesenteric arteries is insignificant during acute SMA occlusion in the developing piglet. Although there is significant collateral blood flow within the SMA vascular network, perfusion between adjacent gut segments is less effective in preventing intestinal ischemia after occlusion of a branch of the SMA in neonates than in 1-month-old piglets.
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PMID:Characterization of intestinal collateral blood flow in the developing piglet. 317 91

Traumatology deals with two different types of shock - the early hypovolemic-traumatic, and the late, so called septic shock, which is often associated with multi-organ failure. Both types of shock are triggered by several mediator systems of humoral and cellular origin, with numerous interactions between each other. In hypovolemic-traumatic shock central events are a perfusion deficit (ischemia with reperfusion injury via the xanthine-xanthine oxidase system) and activation of the humoral axis - of coagulation, of fibrinolysis, of the complement and kallikrein-kinin system by injured tissue. Coagulation and complement are responsible for the activation of platelets and granulocytes respectively. These cells further interact with each other e.g. via platelet activation factor, which finally causes tissue damage. Granulocytes play a central role because of their ability to release oxygen radicals and neutral proteinases, which can be monitored (elastase) and probably used to predict organ failure. The gut area is less resistant to the events of shock and therefore is a "locus minoris resistentiae" for further development of endotoxemia, bacteremia, septic shock and multi-organ failure without a typical septic focus. By this "septic challenge" further mediator systems get involved, especially those of macrophages like interleukin-1 or cachectin. Similar to the activation marker of PMN-elastase, we could demonstrate that it was possible to use neopterin for monitoring macrophage activation in sepsis and organ failure. By the action of these cellular elements in microcirculation at the endothelial and interstitial level tissue damage occurs, which finally leads to individual and multi-organ failure.
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PMID:[Current findings in the pathogenesis of the shock process in traumatology]. 328 34

Enteric free flaps have proven to be useful for reconstructing the cervical esophagus. Although jejunum is favored, the rationale for this is not at all clear. We have postulated that resistance to warm ischemia varies in different regions of the gut. An experiment was carried out in 10 mongrel dogs in which 10-cm segments of proximal, middle, and distal small bowel were isolated on single vascular pedicles. In each portion of the gut there were three segments: a control, a segment subjected to 60 minutes of warm ischemia, and a segment subjected to 120 minutes of warm ischemia. The following day each animal was reexplored, and the viability of bowel segments was assessed visually and with fluorescein. All control segments were viable at 24 hours. Twenty segments were subjected to 1 hour of warm ischemia, and all but two were viable. Nineteen gut segments were subjected to 2 hours of warm ischemia. Seven of eight proximal segments were viable, two of five midsegments were viable, and zero of six distal segments were viable. Survival in the distal portion compared to the proximal portion was significantly less (p less than 0.01). It appears from this study that isolated distal small bowel segments are less resistant to warm ischemia than proximal segments.
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PMID:Ischemic injury to enteric free flaps: an experimental study in the dog. 337 56

Three structurally related peptides, ovine corticotropin-releasing factor, sauvagine, and urotensin I are selective mesenteric vasodilators in dogs. To assess the possible benefit of these peptides in nonocclusive mesenteric ischemia, they were compared with a nonselective vasodilator, sodium nitroprusside, in the anesthetized dog. Mesenteric blood flow was reduced by approximately 30%, without lowering of systemic arterial pressure, by either digoxin or pericardial tamponade. In the digoxin model, i.v. infusions of corticotropin-releasing factor, sauvagine, and urotensin I restored intestinal vascular resistance and mesenteric blood flow to control values, without causing a fall in systemic arterial blood pressure. In the tamponade model, only urotensin I was assessed, and it produced the same restoration of hemodynamic variables. On the other hand, in both models, i.v. infusions of nitroprusside, which were effective in correcting intestinal vascular resistance, produced a fall in arterial blood pressure (presumably because of systemic dilatation), which prevented restoration of mesenteric blood flow. Intestinal oxygen uptake was not altered by tamponade, but was reduced by 23% in the digoxin model, where it was restored to control values by both the peptides and nitroprusside. The increased oxygen extraction seen in both models was corrected by the peptides but not by nitroprusside, suggesting that nitroprusside may have a direct and offsetting metabolic effect on the gut.
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PMID:Use of selective mesenteric vasodilator peptides in experimental nonocclusive mesenteric ischemia in the dog. 348 10

We have developed a simple experimental model for studying reversible intestinal ischemia. The model is based on tenting the mesenteric vessels (artery and vein) to a tied loop of the small bowel in rat and, after a certain time, lowering them down again. Total and partial ischemia (created by tenting 2 and 1 cm, respectively) were demonstrated by laser Doppler flowmetry, as was the revascularization obtained after bringing the vessels down again. Alterations in mucosal permeability after ischemia were determined by depositing fluorescent dextran 3000 in the tied loop and measuring its concentration in the portal blood, and mucosal damage due to ischemia was assessed by measuring the activity of N-acetyl-beta-glucosaminidase, a lysosomal enzyme, in the gut lumen. There was a significant increase in the intestinal permeability to dextran 3000 after total ischemia for 10 min or more, and the permeability was directly related to the duration of the ischemia. After the intestine had been subjected to total ischemia for 30 min or more, the activity of N-acetyl-beta-glucosaminidase in the luminal contents was significantly increased. The permeability after partial ischemia for 30 min was less than that after total ischemia for 30 min. After total ischemia for 10 min followed by revascularization for 30 or 60 min, the permeability did not differ from that in animals not subjected to ischemia. It is concluded that this simple model may be used to study reversible small intestinal ischemia and factors that influence mucosal permeability.
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PMID:An experimental model for studying reversible intestinal ischemia. 355 66


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