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)

Necrotizing enterocolitis (NEC) occurred in 2 neonates with pulmonary atresia and intact ventricular septum. Both infants underwent open heart surgery for the insertion of a right ventricular outflow tract patch under profound hypothermia, surface cooling and a fibrillating heart, without circulatory arrest. In both patients the development of NEC preceded both the cardiac catheterization study and open heart surgery. Urgent repair of the cardiac lesion was undertaken in an attempt at improving the critical bowel wall ischemia. Postoperatively, exacerbation of the NEC reached an advanced stage rapidly leading to the death of the patients. Recommendations regarding the management of future cases exhibiting this potentially lethal combination of disease are presented.
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PMID:Necrotizing enterocolitis in pulmonary atresia with intact ventricular septum. 241 76

A mouse model for the study of necrotizing enterocolitis is presented. It is a model of temporary intestinal ischemia and consists of occluding both superior mesenteric vessels with a bulldog clamp for varying periods of time. The resultant lesions resemble the intestinal lesions seen in necrotizing enterocolitis in respect to the gradual development of the necrotizing lesions and their patchy distribution. We also studied the effect of intravenous saline and low molecular weight dextran in preventing the development of these ischemic lesions. In moderate ischemia, saline and dextran show a similar protective effect, and in severe ischemia, both show a protective effect, with dextran being more effective than saline.
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PMID:A mouse model for the study of necrotizing enterocolitis. 241 91

The pathogenesis of neonatal necrotizing enterocolitis is unknown, but enteral alimentation, infectious agents, and mesenteric ischemia have been frequently invoked as primary initiators of the disease. To define the vulnerability of the intestinal mucosa to ischemia and reperfusion in the developing piglet, we evaluated changes in mucosal permeability using plasma-to-lumen clearance of chromium 51-labeled ethylenediaminetetraacetic acid in the ileum of anesthetized 1-day-, 3-day-, 2-wk-, and 1-mo-old piglets as a function of (a) duration of intestinal ischemia (20, 40, or 60 min of total superior mesenteric artery occlusion), (b) feeding status (fasted or nursed), and (c) composition of luminal perfusate (balanced salt solution vs. predigested cow milk-based formula). Baseline chromium 51-labeled ethylenediaminetetraacetic acid clearance was not significantly altered by ischemia, irrespective of duration, or feeding in all age groups. However, clearances were significantly elevated during reperfusion after 1 h of total intestinal ischemia in all age groups, whether fasted or fed. Reperfusion-induced increases in clearance did not differ among age groups when the bowel lumen was perfused with a balanced salt solution. However, luminal perfusion with formula resulted in higher clearances in 1-day-old piglets compared with all older animals. Thus, the neonatal intestine appears to be more vulnerable to mucosal injury induced by ischemia and reperfusion in the presence of formula than the intestine of older animals.
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PMID:Mucosal injury induced by ischemia and reperfusion in the piglet intestine: influences of age and feeding. 250 2

Necrotizing enterocolitis is the most common gastrointestinal emergency in the newborn. The syndrome strikes premature infants during the first 2 weeks of life. Abdominal distention, lethargy, and feeding intolerance are early signs of NEC that may progress to gastrointestinal bleeding and hemodynamic instability. The radiographic hallmark of NEC is pneumatosis intestinalis (air in the bowel wall). The ileum and colon are the usual sites of crepitant intestinal necrosis, leading frequently to perforation. In spite of appropriate medical therapy, about half of the infants with NEC develop intestinal gangrene or perforation and require surgery, consisting of bowel resection and enterostomy formation. The most common late complication, intestinal stricture, occurs in 15 to 35 per cent of recovered infants. Overall mortality from NEC ranges from 20 to 40 per cent. The etiology of NEC is poorly understood and is considered to be multifactorial, related to ischemia, bacterial colonization, and formula feedings in a susceptible infant. Future progress in the treatment of NEC may be achieved by earlier detection of necrosis, modification of gastrointestinal flora, or by bolstering the deficient gastrointestinal immune mechanisms of the premature neonate.
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PMID:Necrotizing enterocolitis of the neonate. 265 67

Numerous risk factors for necrotizing enterocolitis (NEC) including prematurity, bowel ischemia, pathogenic bacteria, and hyperosmolar feedings have been proposed. Recent studies have demonstrated feeding intolerance and bowel dysfunction in children with hypoalbuminemia. No association between hypoalbuminemia and NEC has been suggested. The records of 45 patients with NEC and complete documentation of prenatal and birth histories were reviewed. A control (CONT) group of 90 children matched for maternal age (+/- 1 year), parity, gestational age (+/- 1 week), birth weight (+/- 20 g), type of delivery, sex, race, type of initial feeding, and perinatal stress was compiled. While all other measured parameters were similar in the two groups, premorbid albumin was significantly lower in the patients who subsequently developed NEC (P less than .001). These data suggest that newborns with hypoalbuminemia may have an increased risk of developing NEC.
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PMID:Hypoalbuminemia may predispose infants to necrotizing enterocolitis. 275 84

We report our experience acquired over the last seven years with the management of necrotizing enterocolitis in neonates. This condition occurs mainly in small-for-dates, premature, critically ill infants. Diagnosis rests on the combination of clinical evidence of intestinal obstruction with non-specific signs of a decline in general health and suggestive roentgenographic findings. Mortality has fallen from 80% to 24% over the last eight years as a result of advances in the medical management of low-birth-weight infants, earlier treatment of bowel ischemia suspected on the basis of inconspicuous manifestations, and improvements in neonatal intensive care and surgical techniques.
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PMID:[Primary ulcero-necrotizing enterocolitis of the newborn. Advancements in management. Improvement in prognosis]. 293 Jan 30

Necrotizing enterocolitis is the most common digestive emergency in neonatal units. Several factors are involved in their pathogenesis: intestinal ischemia, bacterial colonization and feeding. To analyse these factors, 25 cases of NEC are compared to a control group of 48 newborns. Results showed an incidence of NEC about 1.6 0/00 live newborns, without a greater mortality in respect to other pathologic newborns. Ischemic factors influence significatively in appearance of ECN (p less than 0.001). None of them received maternal feeding. By this reason it seems to be a protective factor against bottle feeding (p less than 0.05). Enteral feeding its main influence upon mature newborns. No common bacterial findings have been found, but 68% of children developed clinical findings compatible with sepsis. Severity of abdominal sings in clinical examination in the acute phase of NEC is positively correlated with the presence of complications. Individual considerations are needed in sight to the different severity and prognosis of NEC.
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PMID:[Etiopathogenic factors in neonatal necrotizing enterocolitis]. 314 23

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

Cocaine use has increased dramatically in the past several years, and multiple medical complications associated with its use have been reported in adults, including bowel infarction and colitis. Maternal use of cocaine during pregnancy has been associated with complications in the fetus and newborn infant, including spontaneous abortions, preterm labor, cerebral infarctions, seizures, renal anomalies, and neurobehavioral and neurophysiologic abnormalities. This paper presents a case of necrotizing enterocolitis at birth in a term newborn exposed to cocaine antenatally. Cultures of the bowel grew two types of Clostridia organisms, Escherichia coli and group B streptococcus. It is suggested that bowel ischemia was secondary to the vasoconstrictive properties of the maternally abused cocaine and that secondary invasion of the bowel by multiple bacteria ensued. This case presents another possible complication to the newborn of maternal cocaine exposure in utero, namely ischemic infarction of the bowel.
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PMID:Cocaine exposure in a term neonate. Necrotizing enterocolitis as a complication. 326 47

Oxygen-derived free radicals, particularly superoxide anion, are considered important mediators of intestinal injury induced by ischemia/reperfusion based on the protective effects of superoxide dismutase and allopurinol. A role for free radicals was investigated in a model of necrotizing enterocolitis (NEC) which was initiated by a luminal, as opposed to a vascular, insult. Intestinal loops of weanling rabbits received either saline (control loops) or a solution of 10 mg/ml casein and 50 mg/ml calcium gluconate acidified to pH 4 with proprionic acid (treated loops). When the animals were sacrificed 3 hours later, severe damage was noted in the treated loops, which included blunting of villi and edema, with all animals surviving. At 16 hours only 5 of 8 rabbits survived, and 3 had hemorrhagic necrosis. Control loops were normal in each case. Intravenous infusion of superoxide dismutase (4 mg/kg/hr), commencing 15 minutes after NEC induction, totally prevented intestinal injury. On the other hand, pretreatment with allopurinol, an inhibitor of xanthine oxidase, for 2 days (30 and 60 mg/kg by mouth) was not protective against intestinal damage. A cellular infiltration in treated loops was not histologically evident in the majority of animals at 3 hours after treatment, a finding confirmed by the minimal accumulation of 111In-labeled leukocytes in damaged and intact intestinal tissue. These results suggest that superoxide generated locally from sources other than xanthine oxidase play a critical and early role in experimental NEC and that superoxide dismutase may prove to be an effective therapy in this devastating neonatal disease.
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PMID:Contribution of oxygen-derived free radicals to experimental necrotizing enterocolitis. 334 58


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