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)

The total activities of sucrase, trehalase, amino-peptidase, and gamma-glutamyltransferase in the isolated brush border of the entire small bowel are reduced to 35, 55, 33, and 21 per cent, respectively, of control values (p less than 0.001) 2 hours after a 45 minute occlusion of the superior mesenteric artery. Since brush border proteins are also reduced by ischemia to 42 per cent of control, enzymatic activity when expressed as U/mg protein is significantly reduced only in the case of gamma-glutamyltransferase, to 48 per cent of control.
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PMID:Intestinal brush border enzymes after short-term mesenteric ischemia. 1 65

Ischaemia of the dog intestine lasting 1 h causes desquamation of the epithelium at the villus tips and congestion in the villus capillaries. The crypt cells are relatively undamaged. These changes are associated with a loss of active transport of organic solutes, determined in vitro, a reduction in mucosal sucrase activity and an abolition of glucose absorption in vivo. A profuse net loss of water and electrolytes into the lumen in vivo develops. The net sodium loss is due primarily to an inhibition of the lumen-blood flux of this ion, the blood-lumen flux being relatively unchanged. In uraemic dogs, the loss of urea into the lumen is the same in control and ischaemic loops, testifying to the lack of change in the unidirectional water flow from blood to lumen. Perfusion of the dog intestine with 1% Triton X-100 leads to morphological changes that have certain similarities with those provoked by ischaemia. Damage was restricted to the villus tips, protection from further alterations apparently being provided by a mucus layer that forms on the mucosal surface; the crypt region remained unchanged. After 10 min exposure, organic solute transport in vitro and glucose absorption in vivo were both reduced by not abolished; sodium and water absorption in vivo were suppressed, but no net secretion occurred. To account for these observations, we have suggested that the normal crypt cell is a secretory element with respect to sodium and water. During maturation, its absorptive properties develop such that the mature enterocyte, possessing both absorptive and secretory mechanisms, is capable of net absorption of sodium. After destruction of the villus tips, net secretion continues in the crypts; if there are insufficient villus cells remaining to ensure reabsorption, a net secretory capacity is observed.
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PMID:Source of net water and electrolyte loss following intestinal ischaemia. 736 61

We have followed the time-course of the morphological and functional recovery of intestinal mucosa after 90 min of mesenteric vascular occlusion. At the end of the ischemic period the villi were smashed, but crypts were preserved. Microvillous hydrolase activities showed a dramatic drop when compared with sham-operated controls. Reperfusion was followed by an immediate upsurge of ornithine decarboxylase activity and a significant (p < 0.01) enhancement of putrescine and N1-acetyl-spermidine concentrations, while spermidine and spermine concentrations in mucosal cells decreased. This indicated that, both, de novo synthesis and degradation rates of the polyamines were increased. Treatment with alpha-difluoromethyl-ornithine, a selective inactivator of ornithine decarboxylase prevented the accumulation of active enzyme, but did not prevent morphological healing. It delayed however the recovery of sucrase and aminopeptidase-specific activities. Our results suggest that in addition to de novo synthesis, other sources of polyamines are mobilized to an extent that growth at a normal rate is supported. This indicates that the presence of active ornithine decarboxylase enzyme is not a prerequisite for the restitution of intestinal integrity after ischemia. We suggest that in a situation of inadequate polyamine supply the restoration of vital processes (mucosal regeneration) has priority over the restoration of specific functions.
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PMID:Polyamines and the recovery of intestinal morphology and function after ischemic damage in rats. 817 30

Oxygen-derived free radicals are known to be generated during ischemia/reperfusion injury and biomembranes are the prime target of these active species. In order to study the effect of in vivo generated free radicals on intestinal mucosal membrane, brush border membranes (BBM) were isolated from rat small intestine after subjecting to ischemia (I) and ischemia/reperfusion (I/R) injury and their lipid composition and marker enzyme activity were compared with BBM prepared from control animals. No significant alteration in the lipid composition of BBM was observed after I or I/R as compared to control. Membrane fluidity measurements showed that I/R increased the fluidity of BBM. Activity of alkaline phosphatase, one of the marker enzymes for BBM was reduced by I or I/R whereas activity of another BBM enzyme, sucrase was not altered. The decrease in alkaline phosphatase activity was more after reperfusion. In vitro fluidization of BBM using benzyl alcohol indicated that the inactivation of alkaline phosphatase was not due to change in fluidity. These results suggest that free radicals generated during I/R inactivate BBM alkaline phosphatase partially without altering the membrane lipid composition.
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PMID:Effect of ischemia/reperfusion on intestinal brush border membrane lipid composition, fluidity and enzyme activities. 874 34

Jejunal expression of three brush-border membrane (BBM) enzymes, intestinal alkaline phosphatase (IAP), lactose-phlorizin hydrolase (LPH), and sucrase-isomaltase (SI), and a cytosolic protein, ferritin (Ft), was investigated after transient segmental ischemia-reperfusion (I/R). I/R reduced mucosal IAP, LPH, and SI mRNAs to 36%, 11%, and 38% of normal jejunal levels after 3 h of reperfusion and to 22%, 8%, and 51% of normal jejunal levels after 6 h of reperfusion, respectively. Intriguingly, in the internal control jejunum IAP and LPH mRNAs also decreased significantly. LPH and SI mRNA rapidly recovered to levels significantly higher than those of normal jejunum at 12 h, whereas IAP mRNA levels did not recover until 48 h. Enzyme activity paralleled changes in mRNA levels in the ischemic reperfused jejunum. Electrophoretic mobility shift assays showed that I/R significantly increased SI footprinting 1 (SIF1) binding activity. The mobility of one of the DNA-protein complexes was further retarded in the presence of anti-Cdx-2 antibody, suggesting that either Cdx-2 or a related protein was interacting with the SIF1 sequences. Similar to BBM enzymes, cytosolic Ft mRNA and protein were significantly decreased at 3 and 6 h after I/R. By 12 h, Ft mRNA, but not Ft protein, had increased to higher than normal levels. We conclude that a rapid recovery of BBM mRNAs and enzymes occurs in regenerating mucosa after upper villus damage. The increase of SIF1 binding protein activity after I/R may enhance SI, and perhaps LPH, gene transcription. The expression of Ft is regulated at both pretranslational and translational levels.
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PMID:Expression of intestinal brush-border membrane hydrolases and ferritin after segmental ischemia-reperfusion in rats. 972 71

Intestinal ischemia necessitates rapid re-establishment of blood flow to prevent irreversible anoxic tissue damage. However, reperfusion results in additional injury as a consequence of the generation of oxygen free radicals. To date, no clear-cut marker to differentiate between ischemia versus reperfusion injury is available. In this regard, previous studies from our laboratory utilizing a rat in vitro lipid peroxidation model demonstrated that the generation of free radicals resulted in the inactivation of only the intestinal brush border alkaline phosphatase enzyme, with no effect on other membrane-bound digestive enzymes. Current studies were designed to assess the possibility of alkaline phosphatase being a specific marker of the reperfusion injury in canine and human ex vivo ischemia/reperfusion models. Small bowels harvested from canines and organ donors were subjected to ischemia followed by reperfusion. Brush border membrane enzymes, alkaline phosphatase, sucrase, maltase, and gamma-glutamyl transpeptidase were assayed in mucosal extracts from intestines with ischemia versus reperfusion. In both experimental models, there was no change in any enzyme activity with warm ischemia alone. In contrast, alkaline phosphatase activity was significantly decreased in both the canine and human reperfusion models, with no change in specific activities of sucrase, maltase, and gamma-glutamyl transpeptidase. Our data indicate that the alkaline phosphatase enzyme activity may represent a potential marker of intestinal reperfusion injury and may permit quantitative assessments of therapeutic interventions in human intestinal reperfusion injury.
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PMID:Decrease in mucosal alkaline phosphatase: a potential marker of intestinal reperfusion injury. 1021 63

We investigated the effects of jejunoileal denervation with or without ischemia-reperfusion on mucosal characteristics and small intestinal structure. Growing pigs underwent sham laparotomy, jejunal transection, or extrinsic jejunoileal denervation with or without in situ ischemia-reperfusion. Small intestinal morphology, crypt cell proliferation, enterocyte ultrastructure, and disaccharidase activities were analyzed from jejunum and ileum after eight weeks. Immunohistological analysis of the ileum showed no staining of catecholaminergic neurons after extrinsic denervation. Neural isolation of the jejunoileum with or without ischemia-reperfusion injury reduced weight gain and villous enterocyte density in the ileum, abolished the proximodistal gradient of sucrase activity, and increased mucosal thickness, villus height, and villus surface area in the ileum. However, gross jejunoileal morphology, crypt cell proliferation, and enterocyte ultrastructure remained unchanged. In conclusion, jejunoileal denervation in growing pigs selectively modulates constitutional mucosal characteristics in the ileum, presumably due to altered enterocyte turnover, without a decrease in small intestinal absorptive surface area. These changes are independent of short ischemia and subsequent reperfusion.
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PMID:Effects of extrinsic denervation with or without ischemia-reperfusion injury on constitutional mucosal characteristics in porcine jejunoileum. 1131 18