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Query: UMLS:C0022116 (
ischemia
)
91,303
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
There is a broad spectrum of presentations and severity of
necrotizing enterocolitis
. Because it may have several different causes, ncerotizing enterocolitis may be a syndrome rather than a specific disease. The triad of formula feeding, intestinal
ischemia
, and bacterial growth may be part of the pathogenesis of
necrotizing enterocolitis
. Bacteria are of central importance for the production of pneumatosis, a prerequisite of which is formula feeding. Bacteria may also contribute to the intestinal injury seen after
ischemia
. However, the disease in the low risk patient seen during an epidemic associated with a single organism is probably caused by a primary gastrointestinal infection. On the other hand, in the stressed newborn infant with mucosal injury the presence of the appropriate bacteria may be all that is needed to initiate the chain of events leading to
necrotizing enterocolitis
. Figure 2 illustrates the importance of bacteria in all the causes proposed to be involved in the pathogenesis of
necrotizing enterocolitis
. Whether bacteria are primary or secondary agents,
necrotizing enterocolitis
should always be approached therapeutically as an infectious disease.
...
PMID:Neonatal necrotizing enterocolitis: implications for an infectious disease. 37 77
Apparently there are different causes for
necrotizing enterocolitis
(NEC) in the newborn infant. Besides it may be that NEC only is caused by the interaction of several factors such as perinatal complications, medical measures, an aggressive oral alimentation and an adverse colonization of the bowel and that a critical degree of stress is required to initiate enterocolitis. This assumption would help to explain, why one newborn infant can stand an episode of perinatal stress without falling ill, while the other develops the disease a short time later. Probably NEC starts with an intestinal mucosa damage caused by
ischemia
or local noxae, and only subsequent invasion by the bowel flora into the damaged tissue and gas formation within the bowel wall lead to the picture of necrotizing inflammation and pneumatosis intestinalis.
...
PMID:[The etiology of necrotizing enterocolitis in the newborn]. 43 60
The clinical course of 54 patients with
necrotizing enterocolitis
has been compared to a matched group of 98 control patients. On the day of life that NEC occurred, all 54 NEC patients and 63% of controls were receiving standard formula feedings, both at 80/cal/kg/day. Stool cultures at the time revealed a significantly increased frequency of Klebsiella in NEC as compared to control patients. Our data suggest that the combined presence of certain intestinal bacteria and enteric feedings, perhaps requiring a background of mucosal
ischemia
, may be of etiologic significance in the development of NEC and its radiologic hallmark, pneumatosis intestinalis.
...
PMID:Necrotizing enterocolitis. 80 85
During a one-year prospective survey to determine the incidence of hyperviscosity in small-for-gestational age infants, we found a significant increase in the incidence of
necrotizing enterocolitis
in SGA infants with HV. Of the 14 SGA infants with HV, five developed NEC, and of 65 SGA infants with normal blood viscosity,one had NEC (p less than 0.005). Comparison of clinical features of the five HV infants with NEC with those reported in the literature showed that the infants with HV and NEC had had longer gestational periods and higher weights and, in contrast to those reported in the literature, were free of clinical evidence of asphyxia distress. The respiratory disorders have been proposed as the clinical events that might lead to
ischemia
of the intestine and subsequently to NEC. It is proposed that HV may be another factor leading to
ischemia
in the gastrointestinal tract with subsequent development of NEC.
...
PMID:Necrotizing enterocolitis and hyperviscosity in the newborn infant. 83 41
Necrotizing enterocolitis
continues to be a perplexing problem in the newborn and, in particular, the premature. Its pathogenesis is controversial, although there are well established clinical risk factors. Three patients had
necrotizing enterocolitis
while under close clinical observation and monitoring, despite the fact that these patients were not at high risk for
necrotizing enterocolitis
. All three had
necrotizing enterocolitis
after hypothermia and total circulatory arrest--a complication which until now has not been reported. Because of the close monitoring, these patients provide a unique clinical setting which eliminates most of the etiologic factors that have been implicated in the pathogenesis of
necrotizing enterocolitis
. The onset of
necrotizing enterocolitis
shortly after total circulatory arrest and the selective ischemic organ damage observed suggest local perfusion inadequacy. The authors postulate that splanchnic vasoconstriction as a result of marked sympathetic stimulation contributes to this local
ischemia
and subsequent
necrotizing enterocolitis
.
...
PMID:Necrotizing enterocolitis after cardiac surgery: a local ischemic lesion?. 84 68
Three cases of double left colic stenosis revealed at one month of age by subobstruction are reported. Recovery was obtained by surgery. The evolution of radiological data in one case, and of histological changes observed on the resected sigmoid colon in the two other cases favor the assumption that cicatricial stenosis occurred likewise. These cases also confirm the existence of a benign expression of necrotising enterocolitis, most common with a colonic localization. Such stenosis due to submucous connective sclerosis strengthens the hypothesis that a transitory mesenteric
ischemia
is responsible for the
necrotizing enterocolitis
in newborns.
...
PMID:[Colonic stenosis following necrotizing enterocolitis in newborn infants. Apropos of 3 cases]. 93 13
Necrotizing enterocolitis
, a highly lethal disease in the newborn infant characterized by ischemic necrosis of the gastrointestinal tract frequently leading to perforation, is seen primarily in low birth weight infants who have undergone stress, such as hypoxia. In an animal model it was demonstrated that cold stress was as effective as hypoxia in producing the disease in formula-fed newborn rats. Breast milk was completely protective in both cold- and hypoxic-stressed animals. Presumably cold stress produces the same selective circulatory
ischemia
as does hypoxia. The experiment further supports the concept that any insult or stress which decreases mesenteric blood flow may initiate the changes leading to
necrotizing enterocolitis
. It was shown also that the incidence of the disease in formula-fed rats was related directly to the number of episodes of either cold or hypoxic stress. These results suggest that a critical amount of
ischemia
is necessary to initiate these changes and may help to explain the fact that not all infants exposed to hypoxia or cold stress developthe disease.
...
PMID:Importance of multiple episodes of hypoxia or cold stress on the development of enterocolitis in an animal model. 117
Injury to the gastrointestinal tract by oxygen dependent processes is important in
ischemia
, inflammatory bowel disease, and
necrotizing enterocolitis
. The Caco-2 cell line is an important tool in assessing various gastrointestinal functions and offers a unique opportunity to assess gastrointestinal oxidant metabolism on a cellular level. However, some Caco-2 cell functions change with time after confluence. To determine if antioxidant enzyme activity changes during differentiation, Caco-2 cells were grown to confluence, and superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities and specific mRNA content were quantitated. With time after confluence the enzymes demonstrated a small, but statistically significant increase in activity. Neither superoxide dismutase nor glutathione peroxidase mRNA levels correlated with enzyme activity changes. Catalase mRNA levels increased as catalase activity increased. Thus, differentiated Caco-2 cells express superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase activities and the superoxide dismutase, glutathione peroxidase, and catalase genes. Superoxide dismutase activity and glutathione peroxidase activity do not correlate with mRNA levels, and suggest that regulation may be at a level other than transcription. The correlation between catalase activity and catalase mRNA suggests differentiation may occur at transcription. If Caco-2 cells are used to elucidate oxidative metabolism, changes in activities of antioxidant enzymes as a function of cell differentiation should be considered.
...
PMID:Antioxidant enzymes in the differentiated Caco-2 cell line. 142 66
Subclinical intestinal
ischemia
-reperfusion injury (IRI) causes an increase in mucosal permeability and may represent an early event in the pathogenesis of
necrotizing enterocolitis
. The present study was undertaken to determine whether these changes are mediated by local or systemic factors. In 6-week-old weanling rats, the ileum was divided into two isolated loops with separate vascular supplies. The mesentery of the proximal loop was occluded for 30 minutes, following which the bowel was reperfused; permeability to 51Cr EDTA was then assessed in the distal loop 30 minutes after reperfusion. In control groups, the distal loop was subjected to 30-minute IRI ("positive" control) or 30-minute sham operation ("negative" control). Permeability in the distal loop was increased only with IRI to the distal bowel (15.4 +/- 3 counts/min/standard), and not with IRI to the proximal bowel (5.1 +/- 1) or with sham operation (8.5 +/- 2). To determine whether a mild "priming" injury might be necessary for systemic factors to have an effect, the distal loop was subjected to 2-minute IRI and the proximal to 30-minute IRI or sham. Permeability was not increased in the distal loop in either of these groups (5.7 +/- 1 and 7.8 +/- 2, respectively). Thirty-minute IRI in the proximal loop did not increase permeability in the distal loop, with or without a priming injury. Only direct IRI in the distal loop resulted in a significant increase in permeability. We conclude that the permeability changes in this model are mediated through local tissue effects, rather than by systemic factors.
...
PMID:Increased mucosal permeability after intestinal ischemia-reperfusion injury is mediated by local tissue factors. 150 Oct 6
Twelve spontaneously delivered, normally suckled, small-for-gestational-age (weighing 756 to 1,213 g) neonatal piglets were used to assess the role of the mesenteric vasculature in the pathogenesis of neonatal
necrotizing enterocolitis
(NEC) by producing intestinal
ischemia
. Component vessels (arteries, veins, lymphatics) of the mesenteric vascular arcades were variously occluded by ligation for 48 hours. Nine adjacent vessels of the same type or nine adjacent combinations of vessels were occluded in piglets 12 to 18 hours postpartum. Arterial plus lymphatic ligation induced lesions showing the complete histopathological spectrum of NEC (mucosal stripping, hemorrhage, submucosal disruption and destruction, full-thickness necrosis, inflammatory infiltration) including pneumatosis intestinalis. Two of the lowest birth weight animals produced complete NEC in response to lymphatic ligation alone. A condition consistent with "prepneumatosis" was found when lymphatics only were ligated. The distended lymphatic vessels in the submucosa resembled pneumatosis with reference to shape size and distribution, but contained milk-derived lipids, some proteins and lymph but no gas. Arterial ligation alone induced NEC-like lesions without pneumatosis. Venous ligation alone induced minor congestive/hemorrhagic lesions. Pneumatosis appears to originate in the lymphatic vessels of the submucosa in this experimental model of NEC. Lymphatic occlusion alone can cause complete NEC in very SGA neonatal piglets. Arterial plus lymphatic occlusion produces a unique combination of specific pathology resembling human NEC.
...
PMID:The role of lymphatics in the pathogenesis of pneumatosis in experimental bowel ischemia. 150 Oct 8
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