Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Intestinal ischemia is a common clinical event and reperfusion results in further tissue damage exceeding that of ischemia alone. The present study was designed to test this and to assess the role of pentoxifylline, (administered intravenously as a bolus dose of 25 mg/kg in 1 ml normal saline, followed by continuous infusion of 0.2 mg/kg/minute for 95 minutes), in ischemia-reperfusion injury of the rat intestine. Intestinal ischemia was produced by occlusion of the superior mesenteric artery (SMA) with interruption of the collateral flow for 30 minutes. Reperfusion was established by declamping the (SMA) for 1 hour and evaluation of the mucosal damage was determined using a grading scale from 0 to 5, with estimation of mean mucosal thickness, villous height and crypt depth. The grade of mucosal damage, mucosal thickness, villous height and crypt depth were 2.2, 407 microns, 210 microns, and 196 microns respectively in the ischemia group, and 3.6, 327 microns, 156 microns, and 171 microns respectively in the ischemia reperfusion group, while these values in ischemia reperfusion with administration of pentoxifylline group were 2.5, 505 microns, 294 microns, and 200 microns respectively. The severity of the tissue injury increased considerably after reperfusion of the ischemic intestine and pentoxifylline was effective in attenuating the reperfusion injury significantly.
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PMID:Effect of pentoxifylline on the ischemia-reperfusion injury of the intestine. 853 Feb 33

The epithelial damage and the accumulation of the leucocytes within intestinal wall layers after ischemia and reperfusion was investigated in a pig model. Superior mesenteric artery (SMA) was occluded for 1 h (group 2, n = 9), 2 h (group 3, n = 6) and 3 h (group 4, n = 7) with a consecutive 2 h reperfusion period. The histological evaluation was performed on hematoxylin-eosine and Naphtol AS-D chloracetate stained preparations. The intensity of reperfusion shock depended on the duration of the intestinal ischemia. After 1 h SMA occlusion systolic blood pressure stabilized at a lower level with a normalization of the serum lactate level and the intestinal intramural pHi within the reperfusion period. After 2 h SMA occlusion the decrease of the systolic blood pressure was intensified (54-69 mm Hg) with a persistent elevated serum lactate concentration and a delayed increase of the ischemic pHi values. Reperfusion after 3 h SMA occlusion caused an irreversible shock. The epithelial damage also depended on the duration of the SMA occlusion. There were no significant changes of the leucocytic accumulation within the submucosa. But a significant increase of the number of the leucocytes was seen within the inner and the outer layer of the muscularis after 1 h SMA occlusion (106+/-5/mm2 resp. 280/mm2; p<0.05). This increase was less pronounced after 2 h (92+/-5/mm2*resp. 189+/-4/mm2; *p<0.05) and 3 h of SMA occlusion (84+/-5/mm2 resp. 185+/-23/mm2). Intestinal ischemia and reperfusion caused no changes of the leucocytic accumulation within the submucosa but a significantly increased accumulation within the muscularis after 1 h SMA occlusion, which was not seen after a more elongated occlusion period. A reperfusion shock without normalization of the serum lactate level and the intramural pHi suggesting intestinal perfusion disturbances may also lead to a depression of the leucocytic accumulation within the muscularis.
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PMID:[Reperfusion shock after occlusion of the superior mesenteric artery and accumulation of leukocytes within the wall of the small intestine]. 864 31

Intestinal ischemia-reperfusion (I/R) causes local and distant tissue injury via neutrophil (PMN) activation and adhesion. Endothelial cell adhesion molecules (E-selectin, ICAM-1) mediate the adhesion and transmigration of PMN in the microcirculation. Expression of these receptors is influenced by cytokines. To determine the physiologic concentrations of two specific cytokines involved in I/R, tumor necrosis factor (TNF) and interleukin-1 (IL-1), human intestinal segments were exposed to 30 min of ischemia followed by reperfusion. Venous effluent samples were obtained; enzyme immunoassays measured maximum concentrations of TNF (30.5 +/ 1.0 pg/ml) and IL-1 (59.0 +/- 6.0 pg/ml). Cultured human endothelial cells were then exposed to physiologic concentrations of human recombinant TNF (10 pg/ml) and IL-1 (10 pg/ml), individually and in combination. Flow cytometric analysis of receptor expression demonstrated upregulation of E-selectin as early as 2 hr (P < 0.05) with maximum effects at 4 hr. At 4 hr, E-selectin expression (% shift from baseline) was greater with TNF and IL-1 combined (50.9 +/- 2.9, P < 0.01) than with either cytokine alone (TNF 34.6 +/- 4.0; IL-1 23.5 +/- 4.0, P < 0.01). ICAM-1 receptor expression began at 4 hr with maximum effects at 24 hr. ICAM-1 expression after TNF and IL-1 exposure (15.4 +/- 1.3, P < 0.001) was also greater than TNF (10.9 +/- 0.3, P < 0.01) or IL-1 (3.1 +/- 1.5) alone. TNF and IL-1 are present in venous effluent in concentrations capable of increasing PMN adhesion in the microcirculation. These findings support a role for these cytokines in local and distant organ injury from I/R. Since combined effects are greater than either cytokine alone, antagonism of both TNF and IL-1 may be required for a therapeutic benefit in clinical applications.
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PMID:Physiologic concentrations of TNFalpha and IL-1beta released from reperfused human intestine upregulate E-selectin and ICAM-1. 866 Dec 21

Both burn injury and intestinal ischemia have been proven to induce bacterial translocation from the gut. It is still unknown, however, whether the bacteria induces immune response in these different models. To assess this, we measured in vitro IgM synthesis to peptidoglycan polysaccharide (PGPS), a ubiquitous gut bacterial antigen, after burn injury or gut ischemia-reperfusion in a mouse model. Eighty-five BALB/c mice were divided into four groups. Gut ischemia was produced by placing a vessel loop around the superior mesenteric artery at celiotomy (group Isc; n = 31). After 45 minutes, the abdomen was reopened, and the vessel loop removed. All animals had visible gut ischemia. Control mice (group Isc-C; n = 15) underwent two sham operations. Burn injury was 25% body surface area full-thickness to the dorsum (group B; n = 27). Another control group (B-C; n = 12) was also used. Animals were euthanized 24 hours after recirculation or 5 days after the burn injury. All spleens were removed, and cell suspensions prepared. Cells were cultured in 2.5 micrograms/ml lipopolysaccharide for 5 days, and anti-PGPS IgM level in the supernatant was measured by an enzyme-linked immunosorbent assay. Intestinal ischemia produced a significant rise in in vitro anti-PGPS IgM synthesis per 10(5) lymphocytes, which is the principal immunoglobulin response to infection. However, anti-PGPS IgM in mice after burn injury was significantly decreased. This decreased IgM synthesis after burn injury compared to gut ischemia may represent continued immune impairment from the burn wound, and may account for organ dysfunction related to bacterial translocation after burn injury.
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PMID:Differences in IgM synthesis to gut bacterial peptidoglycan polysaccharide after burn injury and gut ischemia. 873 68

A segmental necrosis of the ascending colon sometimes affecting the terminal ileum was observed 13 times in 12 end-stage renal disease patients over a 5400 patient-years observation period. In all but three cases the patient was operated within 24 h of onset of the abdominal pain. Three patients had a bowel perforation; nine had a limited intestinal necrosis. All underwent a partial resection or colectomy. Two died within 1 month. In all cases the mucosa was necrotic, the submucosa small vessels were congested and the mesenteric vessels were normal. Ischaemic bowel disease has been previously reported in uraemic patients, but our cases do not fit with the usual reported features of this complication. The absence of typical mesenteric infarction, vascular thrombosis, stenosis or major atherosclerotic lesions is surprising. The ascending colon topography of the lesions is very unusual. Ischaemia, constipation and other factors may play a role.
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PMID:Segmental necrosis of ascending colon in haemodialysis patients. 891 53

Superoxide dismutase (SOD) scavenges oxygen radicals that are implicated in the pathogenesis of intestinal ischemia-reperfusion injury. The effect of intestinal ischemia and reperfusion was investigated in transgenic mice overexpressing human Cu-Zn SOD. Ischemia was induced by occluding the superior mesenteric artery. Myeloperoxidase activity was determined as an index of neutrophil infiltration, and malondialdehyde levels were measured as an indicator of lipid peroxidation. Forty-five minutes of intestinal ischemia followed by 4 h of reperfusion caused an increase in intestinal levels of malondialdehyde in both nontransgenic and transgenic mice, but the concentration of malondialdehyde was significantly greater in nontransgenic mice. Intestinal ischemia-reperfusion also caused an increase in intestinal and pulmonary myeloperoxidase activity in nontransgenic and transgenic mice, but the transgenic mice had significantly lower levels of myeloperoxidase activity than nontransgenic mice. Transgenic mice had higher levels of intestinal SOD activity than nontransgenic mice. There were no significant differences in the catalase or glutathione peroxidase activities. In conclusion, our study demonstrates that the overexpression of SOD protects tissues from neutrophil infiltration and lipid peroxidation during intestinal ischemia-reperfusion.
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PMID:Intestinal ischemia and reperfusion injury in transgenic mice overexpressing copper-zinc superoxide dismutase. 935 55

Ischemic bowel disease is a rare disorder whose incidence is increasing as the mean age of the population increases. Diagnosis by clinical, laboratory and radiologic means is often difficult, and delay in definitive therapy results in substantial morbidity and mortality. A series of 26 consecutive patients, with proved acute superior mesenteric ischemia, was retrospectively reviewed: the authors report the diagnostic methods performed preoperatively, the site and the cause of infarction and the time passed between the first radiograph ans surgery. Plain abdominal radiographs were performed in 25 of 26 patients, screening abdominal US in 23 cases and CT in 19 cases. All radiological examinations were retrospectively reviewed by three authors, independently, to recognize the different signs of infarction. On plain abdominal films, the findings warranting a presumptive diagnosis of bowel infarction were air-fluid levels (84% of cases), dilated bowel loops (48%), thickened and unchanging loops (20%), gastric distension and gasless abdomen (12%), small bowel pseudo-obstruction (8%). Screening abdominal US demonstrated intraperitoneal free fluid (26%) and dilated bowel loops (22%). Abdominal CT showed air-fluid levels (79%), dilated loops and free intraperitoneal fluid (47%), intramural gas and thickened bowel loops (36.8%), engorgement of the mesenteric vessels (31%), mesenteric-portal gas, mesenteric thrombus and marked reduction in the volume of gas in the small bowel (10.5%) and paper-thin bowel loops (5%). The authors conclude that air-fluid levels, dilated loops and intraperitoneal free fluid are the most frequent findings, even though they are not specific. While abdominal plain film and screening ultrasonography can be negative, CT detects at least one abnormal finding and at least three abnormal findings in 73% of cases.
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PMID:[Twenty-six consecutive patients with acute superior mesenteric infarction. Comparison of conventional radiology, ultrasonography, and computerized tomography]. 941 16

Intestinal ischemia and reperfusion elicits changes in leukocyte counts and increased production of reactive oxygen species (ROS). The purpose of this study was to investigate whether these changes were followed by and/or connected with changes in the extracellular antioxidative capacity in a rat superior mesenteric artery (SMA) occlusion/reperfusion model. The SMA was occluded for 45 min and then allowed to be reperfused. Changes of leukocyte, polymorphonuclear (PMN), and lymphocyte counts, chemiluminescence (CL) of whole blood samples as a marker of ROS production, and the total antioxidative capacity of the serum were quantified at the end of ischemia and in 1 h intervals during the postischemic period up to 4 h. The myeloperoxidase (MPO) activity in the serum and intestinal tissue samples was also determined. The MPO activity in the intestinal tissue samples was significantly elevated at the end of ischemia, and this elevation lasted for the whole postischemic period. The oxidative challenge to the body induced a fast mobilization of extracellular antioxidative mechanisms already at the end of ischemia, which was followed by a significant increase in PMN counts and whole blood CL starting at the 2nd hour after reperfusion. The increased CL activity of whole blood was attributed to the increase of the circulating PMNs. No significant changes were observed in leukocyte and lymphocyte counts. It is concluded that compensatory mechanisms of the oxidative-antioxidative balance of the body react very quickly if challenged.
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PMID:Leukocyte mobilization, chemiluminescence response, and antioxidative capacity of the blood in intestinal ischemia and reperfusion. 941 64

Intestinal ischemia may evoke an inflammatory response and eventually multiple organ failure. We investigated whether intestinal ischemic injury induces systemic lipid peroxidation and changes in the plasma antioxidant capacity in a pig model. Together with cardiovascular parameters, arterial and portal venous blood of 7 pigs were measured for thiobarbituric acid-reactive material diene conjugates, fluorescent chromolipids and plasma antioxidant capacity during graded occlusion of superior mesenteric artery and reperfusion. Plasma levels of lipid peroxidation products did not change significantly during graded ischemia and reperfusion. Portal venous plasma antioxidant capacity increased slightly during reperfusion (from 96.16 +/- to 3.91 to 142.49 +/- 12.01 mumol/l, p < 0.05). Although elevated levels of free radical reaction products have been found in ischemia-reperfusion, we found no evidence of systemic lipid peroxidation in our intestinal ischemia model.
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PMID:Lipid peroxidation products and antioxidant capacity in portal venous and systemic arterial plasma during gradual intestinal ischemia and reperfusion in pigs. 956 42

Multiple organ failure is with an incidence of 10-25% and a mortality of 50-70% the most severe complication after severe trauma. Intestinal ischemia and a corresponding impaired gut barrier function is thought to have a high impact on the development of multiple organ failure after severe trauma. Under normal conditions the intestinal wall is a sufficient barrier against bacteria and their products. Gut ischemia is followed by mucosal lesions, the intestinal permeability is increased. Translocating bacteria and bacterial products (endotoxin, peptidoglykan) can lead to a local and/or systemic immun-inflammatory response, which is made responsible for the development of multiple organ failure. Tonometry as a possibility of monitoring intestinal ischemia as well as a tool to estimate the prognosis of multiple trauma patients is still discussed controversially. Dopexamin, which directly influences intestinal ischemia (goal directed therapy) might be a successful treatment option, however until now no clinical study about beneficial effects of dopexamine in severely injured patients is available. Selective gut decontamination showed no clinical benefits in multiple trauma patients. Early enteral nutrition especially with immunomodulating ingredients ("immunonutrition") decreases posttraumatic complications as well as the incidence of MOF. However a reduction of mortality could not be described in severely injured patients so far.
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PMID:[The intestine as the central organ in the development of multiple organ failure after severe trauma--pathophysiology and therapeutic approaches]. 958 78


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