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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study determined which nutrient component of formula may be responsible for changes in ischemia/reperfusion-induced mucosal permeability, as quantitated by the plasma-to-lumen clearance of 51Cr-ethylenediaminetetraacetic acid, in newborn piglets. Loops of jejunoileum in 1-day-old and 1-month-old piglets were perfused with predigested and bile acid-solubilized solutions of formula, lipid, protein, carbohydrate, delipidated formula, or fatty acid during 1 hour each of control, ischemia, and reperfusion. Luminal perfusion with formula or lipid led to significantly greater increases in mucosal permeability during reperfusion in newborn intestine than did carbohydrate or protein, whereas mucosal permeability in older animals was not different among solutions. Removal of all lipids from the formula abolished the increased mucosal permeability associated with reperfusion in newborn animals. Perfusion with oleate, a monounsaturated dietary fatty acid, led to still greater increases in reperfusion-associated permeability in newborn but not older intestine. The oleate and lipid perfusions also caused significantly increased mucosal permeability in the absence of ischemia. Thus, it appears that a lipid component of formula, probably a fatty acid, is responsible for the increase in mucosal permeability induced by ischemia/reperfusion in newborn intestine and also leads to increased mucosal permeability in the absence of ischemia/reperfusion. Investigation of the mechanism of these lipid-associated changes in mucosal permeability may provide a rationale for dietary modifications that may decrease the risk of mucosal injury during feeding and ischemic stress in immature intestine.
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PMID:The role of lipids in ischemia/reperfusion-induced changes in mucosal permeability in developing piglets. 156 79

Reactive oxygen metabolites have been implicated in the pathogenesis of mucosal injury induced by ischemia-reperfusion in adult animals, with recent interest centering on the capacity of polymorphonuclear neutrophil-derived oxidants to mediate this injury. A role for oxidants has also been postulated in the etiology of neonatal necrotizing enterocolitis. Based on evidence that the intrinsic capacity of the neonatal piglet intestine to detoxify hydrogen peroxide (H2O2) is minimal relative to that of older piglets, we characterized the changes in mucosal permeability induced by luminal perfusion with H2O2 and hypochlorous acid at concentrations that can be produced physiologically by activated neutrophils (0.05 mmol/L, 0.1 mmol/L, and 0.5 mmol/L), in the distal ileum of 1-d- and 1-mo-old piglets. Mucosal permeability was quantitated by measurement of blood-to-lumen clearance of 51-labeled chromium EDTA. Luminal perfusion with either H2O2 (0.05 mmol/L and 0.1 mmol/L) or hypochlorous acid (0.1 mmol/L and 0.5 mmol/L) significantly increased mucosal permeability in newborn piglets but did not affect mucosal permeability in 1-mo-old animals. Perfusion with 0.5 mmol/L H2O2 significantly increased mucosal permeability over control values in both age groups, but injury in the newborn intestine was significantly greater than that observed in 1-mo-old animals. Thus, as predicted by the reduced intrinsic capacity of the mucosa of neonatal piglets to detoxify H2O2, the ileum of newborn piglets is more vulnerable to oxidant-induced mucosal injury than is the ileum of older animals.
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PMID:Oxidant-induced increases in mucosal permeability in developing piglets. 216 84

Luminal gastric acid is essential for the formation of acute gastric mucosal lesions during ischemia. The mechanism by which luminal acid promotes gastric injury is, however, unclear. We investigated the effect of exogenous luminal acid on gastric mucosal blood flow using the radiolabeled microsphere technique. In rats with intact gastric blood supply application of exogenous luminal acid increased blood flow to the mucosa of the corpus and antrum. However, after ligation of the left gastric artery, which compromised mucosal blood flow to the corpus, application of luminal exogenous acid further decreased blood flow to the corpus. This indicates that the ability of the normal stomach to respond to luminal acidification with an increase in blood flow, which is thought to support clearance of back diffusing H+, is reversed in the ischemic stomach. The exposure to high luminal H+ concentrations may therefore promote gross injury in the ischemic stomach by further compromising nutritional mucosal blood flow.
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PMID:Luminal acid reduces gastric mucosal blood flow in the ischemic stomach. 273 21

To evaluate the place of intravenous digital subtraction angiography (IV-DSA) in the investigation of patients with carotid territory ischemia, we have compared the IV-DSA and conventional angiographic (CA) findings in 40 patients in a prospective study. Arterial disease was assessed by grading stenosis from zero (normal artery) to six (complete occlusion) and recording any luminal ulceration. In 59 of 66 bifurcations imaged by both techniques, the IV-DSA evaluation of any internal carotid artery origin disease was within one grade of the CA assessment, with three false negatives and four false positives. Luminal ulceration was less reliably predicted, and two clinically important middle cerebral artery lesions were missed by IV-DSA. In 11 patients who had carotid endarterectomy, there was a good correlation between surgical, CA, and IV-DSA findings, although some ulcerations were not detected by either angiographic technique. These results suggest that IV-DSA is a sensitive technique for detection of carotid bifurcation stenosis when the study is of good quality, but that intracranial lesions may be missed.
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PMID:Intravenous digital subtraction angiography in patients with carotid territory ischemia: a prospective trial. 386 36

Morphological change of endoneurial and perineurial vessels accompanied severe loss of myelinated axons in peripheral nerves of each of 17 patients with diabetic neuropathy. Vascular mural thickening averaged 18.9 +/- 9.9 micron2 in diabetic capillaries (n = 11) vs. 6.9 +/- 4.1 micron2 in controls (n = 7). Electron microscopy revealed vigorous endothelial proliferation as well as thickening and reduplication of basal lamina in each instance. Particular attention was paid to vessels which penetrate the perineurium en route to the endoneurial interstitium, since they provide a major portion of the endoneurial blood supply. Luminal narrowing and mural thickening of these vessels was compounded by basal laminar thickening of the perineurium. Fenestrated endoneurial capillary endothelium was noted in one case. Both demyelination and axonal degeneration were observed with intra-axonal glycogen accumulation in some axons. Morphometric analysis revealed extensive myelinated nerve fiber loss in diabetic nerves. These morphological findings emphasize the impact of diabetic microangiopathy on specialized endothelium and suggest that local anatomic factors in the perineurial sheath render the nerve vulnerable to chronic ischemia.
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PMID:Microangiopathy in human diabetic neuropathy. 409 Sep 41

Ischaemia of the small intestine leads to the destruction of the intestinal mucosa. The capacity of the epithelium to regenerate is proportional to the duration of revascularization. The aim of this work was to analyze the kinetic aspects of intestinal epithelial regeneration after destruction due to prolonged ischaemia. This study was conducted in 44 animals (swine) after development of an ischaemia-revascularization protocol of a jejunal loop and bipolar secondary cutaneous exteriorization. After a first series with ischaemia times of 1, 2, 3 and 4 hours, the 4 hour period of ischaemia was chosen for further analysis of the regeneration kinetics over a period of 21 days since it leads to regular and total destruction of the epithelium compatible with regeneration. This analysis included (1) a histological examination (semi-thin slices), (2) immunofluorescent detection of intestinal brush border proteins on frozen slices (villin, saccharase-isomaltase, aminopeptidase N, dipeptidylpeptidase-IV) and mucines, (3) measurement of specific intestinal hydrolase activities (saccharase, aminopeptidase N, dipeptidylpeptidase-IV and alkaline phosphatase) in enriched brush border fractions, and (4) an analysis of variations in intestinal flora. After the 4 hour ischaemia, total destruction of the epithelium with disappearance of the villin and intestinal hydrolases and disorganization of the mucosa invaded by mucosal lacks was observed. Epithelial regeneration was rapid and two days later the histological aspect of the mucosa showed apical expression (still discontinuous), villin and intestinal hydrolase activity. Luminal apical expression of the markers became continuous on day 4, demonstrating the total recovery of the intestinal barrier as confirmed by stable microbial flora. Mucine expression also returned to normal. This regeneration was however incomplete since the mucosa was seen to be flat, without villosities. Immunofluorescence showed the weak intensity of brush border activity and the very low specific activity of hydrolase. Values were below normal and did not start to rise again until day 21. If serum levels and associated brush border markers could be measured and were significant, they could be specific markers of regeneration in double stomy ischaemic-revascularized intestine and thus eliminate the need for early second look laparotomy.
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PMID:[Effects of ischemia and revascularization on the epithelium of the small intestine: study on swine]. 798 9

The authors investigated whether amelioration of intestinal mucosal injury, due to ischemia-reperfusion (I/R), with oxygenated perfluorocarbon (PFC) would reduce an oxidant-generated lung injury. The small intestine is increasingly recognized as a primary effector of distant organ injury. Clinical and experimental studies suggest oxidant species and activated neutrophils as the agents responsible for lung injury after intestinal I/R. The role of intestinal mucosal injury has not been defined. Oxygenated PFC was perfused through the lumen of the intestine during periods of I/R. Portal venous effluent was examined for reactive oxygen species and lung tissue was examined for lipid peroxidation. Luminal perfusion of oxygenated PFC during intestinal I/R reduced oxidant species in the portal blood. This correlated with a reduction in lung lipid peroxidation. Oxygenated PFC prevented intestinal mucosal injury resulting from induced I/R. Amelioration of mucosal injury reduced oxidant generation in the portal venous circulation that was proportional to the reduction in measured lung injury. Protection of the mucosa with intraluminal oxygen may prevent I/R-associated lung injury.
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PMID:Mucosal protection from intestinal ischemia-reperfusion reduces oxidant injury to the lung. 944 91

A previous study demonstrated that continuous enteric luminal perfusion of fetal bovine serum (FBS) protects the small intestine from total ischemia/reperfusion injury (IRI) and increases the intestinal mass. In this study, we further investigated the changes in plasma interleukin-8 (IL-8) level caused by total ischemia/reperfusion of the small intestine and the effect of FBS on plasma IL-8 levels. A 3-h total ischemia was induced in a 15-cm segment of terminal ileum and then reperfusion was instituted. Luminal perfusion of FBS was conducted via an osmotic minipump connected to the stomach through a fine polyethylene tube, starting 3 days prior to total ischemia. The rats were killed after 10 and 30 min and 1 and 3 h of total ischemia, and 1, 6, and 12 h or 1, 2, and 3 days after initiation of reperfusion. Plasma IL-8 was measured by enzyme-linked immunosorbent assay. The results were compared among the FBS-treated and untreated groups. The plasma IL-8 level was elevated from 1 h of total ischemia to 6 h after initiation of reperfusion ( P< 0.05) with a peak of 641.5 +/- 36.9 pg/ml in the untreated group and 471.6 +/- 42.2 pg/ml in the treated group. Luminal perfusion of FBS significantly suppressed plasma IL-8 levels after 1 h of total ischemia and 1 h after initiation of reperfusion ( P< 0.05). The results suggest that FBS might play a role in the treatment of total IRI of the small intestine.
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PMID:Suppression of elevated plasma interleukin-8 levels due to total ischemia and reperfusion of the small intestine by luminal perfusion with fetal bovine serum. 1195 73

Although edaravone (3-methyl-1-phenyl-pyrazolin-5-one), a newly developed radical scavenging agent, has been widely used for protection against ischemia-reperfusion (I-R) injury in patients with cerebral infarction, its effects on gastrointestinal I-R injury have not been evaluated. In the present study, we examined the effects of edaravone on experimental intestinal I-R damage in rats. In male Wistar rats with and without edaravone treatment, intestinal damage was induced by clamping the superior mesenteric artery for 30 min, followed by reperfusion. Edaravone was administered via intravenous infusion at 5 min before reperfusion was achieved by removal of the clamp. The rats were sacrificed after 60 min of reperfusion. Luminal protein and hemoglobin concentrations were measured as an index of mucosal injury and histological examination of hematoxylin and eosin-stained sections was performed. Thiobarbituric acid (TBA)-reactive substances and tissue-associated myeloperoxidase (MPO) activity were measured in the mucosa as indicators of lipid peroxidation and neutrophil infiltration, respectively. The mucosal concentration of cytokine-induced neutrophil chemoattractant (CINC)-1 (a member of the IL-8 family) was determined by enzyme-linked immunosorbent assay (ELISA). Additionally, CINC-1 messenger RNA (mRNA) was measured by the reverse-transcription polymerase chain reaction (RT-PCR). As a result, the levels of luminal protein and hemoglobin, TBA-reactive substances, and MPO activity were all increased significantly by I-R injury, and these increases were significantly inhibited by treatment with edaravone. Multiple erosions and bleeding were observed macroscopically after the small intestine was exposed to I-R injury, and these changes were inhibited by administration of edaravone. Microscopic I-R damage was also reduced by treatment with edaravone. CINC-1 protein and CINC-1 mRNA were both increased by I-R injury, while edaravone markedly reduced the levels of both protein and mRNA. In summary, these results suggest that edaravone can protect the small intestine against I-R injury by scavenging oxygen-derived free radicals.
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PMID:Edaravone, a newly developed radical scavenger, protects against ischemia-reperfusion injury of the small intestine in rats. 1465 79

Luminal acidity is a physiological challenge in the foregut, and acidosis can occur throughout the gastrointestinal tract as a result of inflammation or ischemia. These conditions are surveyed by an elaborate network of acid-governed mechanisms to maintain homeostasis. Deviations from physiological values of extracellular pH are monitored by multiple acid sensors expressed by epithelial cells and sensory neurons. Acid-sensing ion channels are activated by moderate acidification, whereas transient receptor potential ion channels of the vanilloid subtype are gated by severe acidosis. Some ionotropic purinoceptor ion channels and two-pore domain background K(+) channels are also sensitive to alterations of extracellular pH.
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PMID:Taste receptors in the gastrointestinal tract. V. Acid sensing in the gastrointestinal tract. 1712 65


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