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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) is thought to be secondary to mucosal ischemia. Because blood flow to the submucosal plexus is derived from vessels traversing three separate layers of visceral smooth muscle (longitudinal, circular, and muscularis mucosa), we investigated whether an increase in their tone might elicit mucosal ischemia. The intestinal intraluminal pressure (IIP) and the superior mesenteric artery (SMA) blood flow were evaluated in 23 dogs before and after either ligation of the SMA or neostigmine infusion into the SMA. Changes in vascularity were assessed by silicone rubber casting, India ink, or arteriography. Ten minutes after ligation of the SMA, there was a considerable increase in peristalsis, IIP, and inability to fill the intestinal microcirculation by the three methods described. Mucosal necrosis was present three hours later. In the neostigmine infusion group after a transient increase in mesenteric flow, the IIP rose 750%, while the mesenteric flow fell by 40%, mucosal necrosis occurred in one hour. When myotomy was performed on the antimesenteric border, mucosal necrosis was prevented. In a third group, neostigmine infused (femoral artery) in the hind limb demonstrated vasodilating effects. The data indicate that an increase in the myogenic tone and frequency of contraction of intestinal smooth muscle can produce mucosal ischemia, thus, intestinal hypertonicity may be an important factor in the pathogenesis of intestinal ischemia and possibly NEC. The effects of neostigmine in these experiments raise questions regarding its use during anesthesia in neonates with intestinal low flow states.
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PMID:Hypertonicity of intestinal smooth muscle as a factor of intestinal ischemia in necrotizing enterocolitis. 349 12

There is growing evidence that colonic blood flow is controlled by both intrinsic and extrinsic factors. The existence of intrinsic vascular control mechanisms is evidenced by pressure-flow (and oxygen uptake) autoregulation, reactive hyperemia, vascular responses to acute venous hypertension, and a functional hyperemia. Although myogenic factors have long been considered to be solely responsible for the intrinsic ability of the colon to regulate its blood flow, recent developments indicate that metabolic mechanisms may be of equal importance in this regard. Both parasympathetic and sympathetic nerves play an important role in regulating colonic blood flow. The influence of circulating vasoactive agents and ischemia on colonic oxygenation are largely explained in terms of the relationship between oxygen uptake and blood flow. Colonic vascular dysfunction appears to be a major factor in the pathogenesis of inflammatory bowel diseases, chronic portal hypertension, and neonatal necrotizing enterocolitis. Future progress in this area will require the development of techniques for the measurement of colonic blood flow in man.
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PMID:Physiology and pathophysiology of the colonic circulation. 353 16

Pathologic studies of the visceral smooth musculature in humans are scant despite the relatively frequent occurrence of alterations in these muscles in autopsy material. We investigated the different types of lesions of this musculature observed in various conditions associated with ischemia--acute tubular necrosis, congenital heart disease (low output syndrome due to open heart surgery), and necrotizing enterocolitis in premature babies. Control cases included normal rat tissue undergoing autolysis and rigor mortis and bowel resected from patients with ulcerative colitis and Hirschsprung's disease. Four histologically distinct lesions were present on hematoxylin--eosin staining in the ischemic group: contraction bands, wavy fibers, thick waves, and coagulation necrosis. These lesions were absent in the control groups. We conclude that myofibrillar degeneration and necrosis of the visceral musculature are common in disorders associated with visceral ischemia. These changes are not artifacts produced by autolysis, rigor mortis, or technical handling, nor are they induced by nonischemic inflammatory conditions. Catecholamines may play a role in their genesis.
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PMID:Myofibrillar degeneration and necrosis of the visceral smooth musculature: an ischemic visceral myopathy. 361 Jan 32

The authors report a case of necrotizing enterocolitis which appeared in the first hours of life of a full-term neonate without signs of sepsis. This neonate presented with a severe hypoplasia of the horizontal aorta and very tight coarctation responsible for hepatic, renal and mesenteric ischemia. Reports of enterocolitis as a complication of congenital heart disease are rare and related most often to hypoplastic left heart than to coarctation of the aorta.
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PMID:[A rare cause of neonatal ulcero-necrotizing enterocolitis: aortic coarctation syndrome]. 361 70

This study was undertaken to evaluate the relative contribution of ischemia, bacteria, and luminal substrate, the pathogenetic components of necrotizing enterocolitis (NEC), to the development of intestinal necrosis. Sprague-Dawley rats, either germ-free (No. = 25) or conventionally colonized (No. = 20) underwent laparotomy. Isolated ileal segments were created, two per rat. Ischemia was produced in one segment by application of a microaneurysm clip; the other segment served as a control. Segments were injected with 1 mL of either normal saline, dilute Similac formula, or standard formula. Groups were as follows: Group I (germ-free), received saline; Group II (germ-free), dilute formula; Group III (germ-free), standard formula; Group IV (conventional), saline; Group V (conventional), dilute formula; Group VI (conventional), standard formula. At 48 hours, the rats were evaluated for survival, gross bowel integrity, histologic severity of necrosis (graded 0 to 4+), and bacteriology. Gross analysis of bowel integrity showed no lesions in the ischemic segments of the germ-free rats (Groups I, II, and III) and necrosis in 75% of conventionally colonized animals (Groups IV, V, and VI; P less than 0.001). Microscopic necrosis was more common (P less than 0.001) in ischemic segments of conventional rats than in ischemic segments of germ-free rats. There was no difference in necrosis attributable to ischemic time or to the presence of either standard or dilute formula. Of the three pathogenetic factors evaluated, the presence of bacteria was most crucial to the development of bowel necrosis in this model. Improved treatment and prevention of NEC may depend upon suppression and/or modification of the gut flora.
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PMID:Comparative effects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis. 372 7

Acute primary ulcer of the small intestine is an exceptional occurrence. Diagnosis is established only after a complication occurs. In most instances, this complication is perforation of the gut. Acute primary ulcer of the small intestine is accurately defined by specific histologic criteria. It can be unequivocally distinguished from the many other causes of spontaneous perforation of the small intestine. Experimental studies, although numerous, have not improved understanding of pathophysiology. Nosologic classification remains unclear. Many features are similar to those encountered in acute peptic ulcer but stress is usually absent. Other features resemble those of transient necrotizing enterocolitis ; acute primary ulcer of the small intestine may be a very localized form of this latter condition. Ischemia seems to be the most significant factor. However, for an ulcer and finally perforation to occur, ischemia must probably be associated with a number of other factors.
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PMID:[Acute primary ulcer of the small intestine. Present concepts (author's transl)]. 628 93

The hypothesis is, that necrotizing enterocolitis (NEC) of the neonate occurs by the coincidence of two of three pathologic events: (1) intestinal ischemia, (2) colonization by pathogenic bacteria, and (3) excess protein substrate in the intestinal lumen. NEC is more likely to appear following quantitative extremes, ie, severe ischemia highly pathogenic flora, or marked excess of substrate. NEC develops only if a threshold of injury, sufficient to initiate intestinal necrosis, is exceeded. The hypothesis is derived from previous theories by Santulli, which implicated all three events, and by Lawrence, in which a single event, abnormal bacterial colonization, was considered sufficient to induce NEC. This hypothesis may explain both typical occurrences of NEC among high-risk premature infants in neonatal intensive care units (NICUs), and atypical occurrences among infants considered at low-risk, eg, previously healthy term infants, infants fed breast milk exclusively, and infants never fed. It may further explain why NEC fails to develop in most high-risk infants in NICUs. Preventive measures might include: (1) pharmacologic stabilization of intestinal perfusion, (2) modification of the intestinal flora, or (3) feeding colostrum or other protective substances. Each theoretical benefit is accompanied by potential risks. The prevention of NEC may require favorable intervention in two of the three pathologic events.
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PMID:Pathogenesis and prevention of necrotizing enterocolitis: a hypothesis based on personal observation and a review of the literature. 639 Mar 30

Necrotizing enterocolitis (NEC) is a serious condition affecting the neonate that may be responsive to medical management. This study evaluates the efficacy of supplemental oxygen (FiO2 40% and 50%), systemic antibiotics (ampicillin and gentamicin, cephamandole) and oral antibiotics (trimethoprim-sulfamethoxazole, neomycin and gentamicin) in a weanling rat bowel ischemia model induced by a transient (one minute) occlusion of the superior mesenteric artery. Animals were evaluated for overall survival, duration of survival, presence of bowel necrosis or perforation at seven days. Mortality in ischemic controls was 83.8%. This was reduced to 52% by FiO2 of 50%, and 40% with systemic ampicillin and gentamicin (with or without FiO2 50%) (P less than .001). Length of survival was 3.4 days in controls and increased from 5.4 to 5.9 days in rats given FiO2 50% and/or ampicillin and gentamicin (P less than .001). The incidence of bowel necrosis in controls was 60% and was reduced to 25% in rats given systemic ampicillin and gentamicin and 23.3% with 50% FiO2 and the same antibiotics (P less than .001). Systemic cephamandole and oral antibiotics had no beneficial effects.
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PMID:Laboratory basis for the medical management of necrotizing enterocolitis (NEC). 648 78

Detection of intestinal ischemia, prior to necrosis, is a major clinical problem. The lysosomal acid hydrolase, hexosaminidase (HEX), is known to be elevated in intestinal infarction. To determine if this enzyme could differentiate between partial intestinal ischemia and full-thickness intestinal gangrene, the following rat study was designed. Partial segmental intestinal ischemia was created by ligating alternate vascular bundles over a short (6 vessel) segment of the small-bowel mesentery, and complete segmental intestinal vascular occlusion was achieved by ligating the blood supply to the ileocecal segment. Preoperative serum HEX values were obtained from 15 animals. The rats were separated into one sham-operated and two intestinal ischemia groups. At four hours after surgery HEX values were determined. Total HEX activity was significantly elevated four hours after insult in both partial and complete intestinal ischemia, (P less than 0.005 and P less than 0.001 respectively). Total HEX activity was greater in complete intestinal ischemia than in partial ischemia, (P less than 0.05). Three neonates with intestinal perforation, secondary to necrotizing enterocolitis, were evaluated. The mean preoperative HEX activity was 1421 nmol/hr/mL serum and the mean post-resection HEX activity was 808 nmol/hr/mL serum. These data suggest that serum HEX activity may be a good marker for intestinal gangrene in neonates with necrotizing enterocolitis.
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PMID:Hexosaminidase: a marker for intestinal gangrene in necrotizing enterocolitis. 662 88

Gastro-intestinal (G-I) disorders were studied in 95 premature neonates. Each child presented with at least one of the features usually associated with mesenteric ischemia. Nearly all the children had been fed early with tyndallized maternal milk. No certain necrotizing enterocolitis (NEC) was observed; however, it was suspected in 4 children (4.2%) and in 7 (7.3%), minor changed occurred. Among the 13 factors examined which might be responsible for inducing NEC, only 2 were correlated with G-I disorders: low birth weight (less than 1,500 gm) and occurrence of secondary apnea or asphyxia incidents during mechanical ventilation. This study led to the following practical conclusion: maintenance of early enteral feeding in prematures theoretically at risk for G-I disorders, taking into account the low incidence of severe G-I impairments and of the advantages of such a feeding method, while carefully supervising intestinal symptoms; preventative and temporary interruption of feeding in low weight prematures, in case of acute asphyxia or hypoxia episodes.
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PMID:[Gastro-intestinal disorders in premature neonates receiving early enteral feeding (author's transl)]. 680 35


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