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)

1. We evaluated changes in contractility of the guinea-pig isolated ileum, using intact segments and myenteric plexus-longitudinal muscle (MPLM) preparations, after several times (5-160 min) of ischemia in situ. 2. Intestinal ischemia was produced by clamping the superior mesenteric artery. Ischemic and nonischemic segments, obtained from the same guinea-pig, were mounted in organ baths containing Krebs-bicarbonate (K-B) solution, maintained at 37 degrees C and gassed with 95% O2/5% CO2. The preparations were allowed to equilibrate for 60 min under continuous superfusion of warm K-B solution and then electrically stimulated at 40 V (0.3 Hz, 3.0 ms). Thereafter, complete noncumulative concentration-response curves were constructed for acetylcholine (ACh), histamine (HIS), potassium chloride (KCl), and barium chloride (BaCl2). Mean Emax (maximal response) values were calculated for each drug. 3. Our study shows that alterations of chemically and electrically evoked contractions are dependent on ischemic periods. It also demonstrates that contractile responses of ischemic tissues to neurogenic stimulation decreases earlier and to a significantly greater extent than the non-nerve mediated responses of the intestinal smooth muscle. Contractile responses to smooth muscle stimulants were all similarly affected by ischemia. Electron microscopy images indicated necrotic neuronal death. The decrease in reactivity of ischemic tissues to electrical stimulation was ameliorated by dexrazoxane, an antioxidant agent. 4. We consider the guinea-pig isolated ileum as a useful model system to study the processes involved in neuronal ischemia, and we propose that the reduction in maximal responses to electrical stimulation is a useful parameter to study neuroprotection.
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PMID:Altered responsiveness of the guinea-pig isolated ileum to smooth muscle stimulants and to electrical stimulation after in situ ischemia. 1634 Dec 32

Intestinal ischemia/reperfusion (I/R) may induce bacterial translocation (BT). Glutamine (GLN)-enriched nutrition decreases BT. However, little is known about the effect of glucan (GL) in BT. This study investigated the combined effect of GL/GLN on BT, intestinal damage, and portal blood cytokines in animals under I/R. Four groups of 10 rats each were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. The control group (group 1) received only rat food/water, group 2 received glutamine via gavage, group 3 received subcutaneuos soluble (1, 3)-d-glucan, and group 4 received GL + GLN. A sham group (group 5) served as a normal control. Bacterial cultures of ileum, mesenteric lymph nodes (MLN), liver and lung biopsies, histological changes of ileum, and serum cytokines variables were examined after I/R. Data were analyzed by analysis of variance (ANOVA) and the Newman-Keuls test. Results showed that GLN, GL, and GL/GLN significantly reduced BT to MLN, liver, and lung. BT was more attenuated after GL treatment than GLN (P < .05). Rats treated with both GL and GLN exhibited lower bacterial colony counts than the ones treated only with GLN or GL. Severe mucosal damage on histological findings was shown in group 1, but these findings were significantly ameliorated (P < .05) in groups 3 and 4. Tumor necrosis factor (TNF)-a and interleukin (IL)-6 levels in portal serum were significantly reduced and IL-10 was increased by GL and GLN treatment. In conclusion, the use of GL was more effective than GLN in reducing BT, intestinal damage, and cytokine levels after I/R. Additionally, the combination of GL and GLN improved results.
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PMID:Glucan and glutamine reduce bacterial translocation in rats subjected to intestinal ischemia-reperfusion. 1654 28

Prostaglandins stimulate repair of the ischemia-injured intestinal barrier in the porcine ileum through a mechanism involving cAMP-dependent Cl- secretion and inhibition of electroneutral Na+/H+ exchanger (NHE) activity. In the present study, we focused on the role of individual NHE isoforms in the recovery of barrier function. Ischemia-injured porcine ileal mucosa was mounted on Ussing chambers. Short-circuit current (I(sc)), transepithelial electrical resistance (TER), and isotopic fluxes of 22Na were measured in response to PGE2 and selective inhibitors of epithelial NHE isoforms. Immunoassays were used to assess the expression of NHE isoforms. Forty-five minutes of intestinal ischemia resulted in a 45% reduction in TER (P < 0.01). Near-complete restitution occurred within 60 min. Inhibition of NHE2 with HOE-694 (25 microM) added to the mucosal surface of the injured ileum stimulated significant elevations in TER, independent of changes in I(sc) and histological evidence of restitution. Pharmacological inhibition of NHE3 or NHE1 with mucosal S-3226 (20 microM) or serosal cariporide (25 microM), respectively, had no effect. Ischemia-injured tissues treated with mucosal S-3226 or HOE-694 exhibited equivalent reductions in mucosal-to-serosal fluxes of 22Na+ (by approximately 35%) compared with nontreated ischemia-injured control tissues (P < 0.05). Intestinal ischemia resulted in increased expression of the cytoplasmic NHE regulatory factor EBP50 in NHE2 but not in NHE3 immunoprecipitates. Selective inhibition of NHE2, and not NHE3, induces recovery of barrier function in the ischemia-injured intestine.
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PMID:Prostaglandin-mediated inhibition of Na+/H+ exchanger isoform 2 stimulates recovery of barrier function in ischemia-injured intestine. 1657 91

The purpose of the present study was to investigate whether mibefradil can reduce oxidative stress and histologic damage in the rat small bowel subjected to mesenteric ischemia and reperfusion injury. Thirty Sprague-Dawley rats weighing between 210 and 220 g were divided into three groups, each containing 10 rats: group 1, sham operation; group 2, untreated ischemia-reperfusion; and group 3, ischemia-reperfusion plus mibefradil treatment group. Intestinal ischemia for 45 min and reperfusion for 60 min were applied. Ileal specimens were obtained to determine the tissue levels of MDA, CAT, SOD, and GSH-Px and histologic changes. In group 2, MDA values were significantly increased compared to those in groups 1 and 3. In addition, SOD, CAT, and GSH-Px values decreased significantly in group 2 compared to groups 1 and 3. The intestinal injury score increased significantly in group 2 and 3 rats compared to group 1 rats. However, this increase was reduced in group 3 rats compared to group 2. Histopathologically, the rats in group 1 had essentially normal testicular architecture. In group 2 rats, the lesions varied between grade 3 and grade 5. In contrast, most of the specimens in the mibefradil-treated group 3 showed grade 1 injury. Mibefradil plays a role in attenuating reperfusion injury of the small intestine by depressing free radical production and mucosal injury score and regulating postischemic intestinal perfusion while restoring intestinal microcirculatory blood flow and encountered histologic injury.
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PMID:Mibefradil, a T-type Ca2+ channel blocker, protects against mesenteric ischemia-reperfusion-induced oxidative injury and histologic alterations in intestinal mucosa in rats. 1686 26

Growing number of studies implicate that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, have beneficial effects on ischemia/reperfusion injury that are unrelated to their cholesterol-lowering action. In the present study, we aimed to evaluate possible effects of atorvastatin on oxidative stress, neutrophil accumulation, and contractile response of terminal ileum segments in rats subjected to intestinal ischemia/reperfusion. Intestinal ischemia/reperfusion model was generated by clamping the superior mesenteric artery for 30 min followed by reperfusion for 3 h. Oral administration of atorvastatin at a dose of 10 mg/kg/day lasted 3 days just before induction of intestinal ischemia. At the end of reperfusion period, terminal ileum samples were removed to determine the concentrations of malondialdehyde, reduced glutathione, and myeloperoxidase. Samples were collected also to assess histopathological alterations and contractile response to agonists. Ischemia/reperfusion significantly decreased contractile responses, and this decrease was attenuated by atorvastatin. Pretreatment with atorvastatin caused remarkable decrease in both oxidative stress and neutrophil accumulation. Atorvastatin appeared to be restoring amount of reduced glutathione back to about control level. Furthermore, the pretreatment lowered mucosal damage at histopathological level. Our results suggested that pretreatment with atorvastatin attenuated intestinal muscle dysfunction associated with ischemia/reperfusion. This remarkable effect of atorvastatin is accomplished at least by decreasing oxidative stress and neutrophil accumulation as well as preventing the depletion of reduced glutathione.
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PMID:Attenuation of contractile dysfunction by atorvastatin after intestinal ischemia reperfusion injury in rats. 1733 1

Intestinal ischemia in antiphospholipid antibody syndrome (PAPS) could be due to arterial thrombosis from hypercoagulability. A male patient, 45 years old, was admitted to the hospital with symptoms of acute abdomen and after laparotomy he developed sepsis, right kidney infarction, jejunal ischemia, aortic thrombosis, wide necrosis of both gluteus muscles, left subclavian vein thrombosis. Our therapeutic and diagnostic strategy was delineated after demonstration of antiphospholipid antibodies. The patient was treated with total parenteral nutrition in the presence of 5 enteric fistulas with very high outflow, arterial stent insertion and daily changes of medicated dressings. Outcome was excellent with small residual deficit in walking. Continuous nutritional status monitoring and very high nitrogen supply allowed excellent healing of huge wounds and closure of enteral fistulas.
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PMID:[Acute abdomen in antiphospholipid antibodies syndrome (PAPS)]. 1736 35

This study deals with the polyviewed expression of the altered contractility of the isolated ileum of the guinea-pig after ischemia/superfusion (I/S). Intestinal ischemia was produced by clamping the superior mesenteric artery for 40, 80 or 160 min. Ischemic and non-ischemic segments taken from the same guinea-pig were mounted for tension recording in organ baths and superfused (120 min) with an oxygenated Krebs-bicarbonate solution. Data were analyzed by means of the Polyview System software, which allows detecting simultaneously several events of one response. Histopathological changes in myenteric neurons were also examined. We found that ischemia in situ followed by superfusion in vitro (reoxygenation) severely reduces the spontaneous intestine contractile activity, and significantly decreases the maximal contractile response to ACh and to electrical field stimulation (EFS), the maximal rate of tension, and the sensitivity of the tissue to EFS. In addition, these ischemic intestines respond with a long-lasting contracture when electrical stimulation was started at supramaximal voltage. Functional alterations were time dependent. Neurons exhibited features of necrosis. These results provide clear evidence of detrimental effects of I/S on intestine contractile function. Digital analysis allows quantification of additional parameters important for evaluation of functional changes after I/S and of the degree of neuroprotection.
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PMID:Polyviewed expression of the altered contractility of the guinea-pig ileum after ischemia in situ and superfusion in vitro. 1762 97

The aim of this study was to determine the effect of magnesium deficiency on small intestinal morphology and function. Rats were assigned to 4 groups and placed on magnesium sufficient or deficient diet for 1 or 3 weeks. Infiltration of neutrophils and mucosal injury were assessed in stained sections of small intestine. Magnesium deficiency alone induced a significant increase in neutrophil infiltration and increased vascular ICAM-1 expression, in the absence of changes in mucosal injury or expression of proinflammatory mediators. Magnesium deficiency was associated with hyposecretory epithelial cell responses and vascular macromolecular leak in the small intestine and lung, which was attributed partly to reduced expression of NOS-3. To determine the effect of hypomagnesmia on the intestinal responses to a known oxidative stress, groups of rats were randomized to either sham operation or superior mesenteric artery occlusion for 10 (non-injurious) or 30 (injurious) minutes followed by a 1- or 4-hour reperfusion period. In response to mesenteric ischemia/reperfusion, deficient rats showed exaggerated PMN influx, but similar mucosal injury. Intestinal ischemia in sufficient animals induced vascular macromolecular leak in the small intestine and lung at 4 hours of reperfusion, with levels similar to those observed in untreated deficient rats. Acute magnesium repletion of deficient rats 24 h before surgery attenuated the exaggerated inflammation in deficient rats. These data show that magnesium deficiency induced a subclinical inflammation in the small intestine in the absence of mucosal injury, but with significant functional changes in local and remote organs and increased sensitivity to oxidative stress.
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PMID:Intestinal inflammation caused by magnesium deficiency alters basal and oxidative stress-induced intestinal function. 1765 90

Intestinal ischemia is reported to be the most common gastrointestinal complication of renal transplantation and a potential cause of morbidity and mortality. The recent use of more potent immunosuppressive drug regimens has reduced the incidence of acute rejection, increasing the incidence of potentially fatal infectious complications, such as clinically important cytomegalovirus (CMV) infection. A 42-year-old kidney transplant recipient experienced on postoperative day 10 a dehiscence of the ureterovesical anastomosis, associated with a 7-cm longitudinal tear graft on the lower pole of the kidney and an ureteral ischemia. A graft biopsy demonstrated a mild acute rejection for which the patient received an unsuccessful administration of steroids, with progression of the rejection, so that 1 mg/kg/day antithymocyte globulin was administered. Two days later the patient presented with fever (39.5 degrees C), diffuse abdominal pain with tenderness and bloody diarrhea, and diagnosis of CMV colitis was achieved; rectal samples were taken for histologic examination, and Clostridium difficile toxin was isolated. A subtotal colectomy with Hartmann's procedure was performed, but the patient died 13 days later of a multiple organ failure. The risk of lethal CMV colitis is increased in patients being treated with anti-rejection therapy for severe acute rejection; the occurrence of simultaneous infection, such as pseudomembranous colitis, usually characterized by a favorable prognosis, increases the mortality rate in these patients.
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PMID:Cytomegalovirus and Clostridium difficile ischemic colitis in a renal transplant recipient: a lethal complication of anti-rejection therapy? 1785 Dec 90

In this study, the involvement of 5-HT2A receptors on mesenteric ischemia-reperfusion injury was examined in mice. Intestinal ischemia produced by 45 min occlusion of superior mesenteric artery was followed by 24h reperfusion (I/R). The 5-HT2A selective antagonist, ketanserin (0.5 mgkg(-1)) or the 5-HT2A agonist DOI (0.25 mgkg(-1)) was intravenously administered before ischemia and 8h after the beginning of reperfusion. The effects were compared with those obtained in sham operated animals (S). Ketanserin prevented the upper gastrointestinal transit delay induced by I/R (P<0.01), protected intestine from leukocyte recruitment as indicated by jejunal myeloperoxidase activity (P<0.05) and reverted Evans Blue extravasation elicited by I/R in lung, colon and jejunum (P<0.05). On the other hand, 5-HT2A activation by DOI mimicked the effects of I/R in S mice prolonging small intestine transit (P<0.05) and enhancing neutrophil accumulation in jejunal tissues (P<0.05). Furthermore, the reduction of ADP-induced platelet aggregation in plasma of I/R mice was prevented by ketanserin treatment. All together, these findings support the critical involvement of 5-HT2A receptor subtype in mediating the damage induced by mesenteric I/R in mice.
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PMID:Evidence for the involvement of 5-HT2A receptors in mild mesenteric ischemia/reperfusion dysfunctions in mice. 1802 56


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