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)

Three patients with carcinoid tumors of the ileum are presented; two had severe intestinal ischemia, one with infarction of the small intestine. In all three cases, histopathological examination revealed elastic vascular sclerosis (EVS) in the mesenteric blood vessels. Intestinal ischemia in the presence of a carcinoid tumor is probably due to a combination of tumoral secretion products, vascular changes, mesenterial retraction and nodal involvement. Selective superior mesenteric artery arteriography is diagnostic. All the reported carcinoid tumors with ischemic manifestations are ileal and invaded the mesentery or had positive nodes or metastases; two-thirds had EVS, and one-third mesenterial vascular luminal narrowing. Intestinal ischemia may be the underlying cause of vague symptoms in patients with a carcinoid tumor. This tumor may be small and must be looked for during laparotomy, mild intestinal ischemia or mesenterial thickening are important signs. Early resection can prevent intestinal complications. An aggressive attitude, including debulking of metastases, is justifiable.
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PMID:Ileal carcinoid tumors and intestinal ischemia. 785 61

Intestinal ischemia-reperfusion (I/R) provokes polymorphonuclear neutrophil (PMN)-mediated lung injury via a process characterized by circulating PMN priming, pulmonary PMN sequestration, and increased microvascular leak in the lung. We found in rats subjected to intestinal I/R (ischemia 45 min and reperfusion 6 h) that 1) intestinal phospholipase A2 (PLA2) was activated during ischemia, 2) circulating PMN priming (assessed by superoxide production with N-formyl-Met-Leu-Phe) occurred after 1 h reperfusion, and 3) exaggerated 125I-labeled albumin lung leak occurred after 2 h reperfusion, compared with sham-treated animals (P < 0.05). Treatment with a PLA2 inhibitor, quinacrine, within 15 min of reperfusion reversed the exaggerated gut PLA2 activity and abrogated subsequent PMN priming and lung leak (P < 0.05). However, when quinacrine was administered after 2 h of reperfusion, circulating PMN priming and lung leak continued to evolve despite suppression of intestinal PLA2 activity. We conclude that intestinal PLA2 activation may be a prerequisite for the sequelae of circulating PMN priming and pulmonary microvascular leak observed after intestinal I/R.
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PMID:Gut phospholipase A2 mediates neutrophil priming and lung injury after mesenteric ischemia-reperfusion. 790 Aug

In a model of intestinal ischemia-reperfusion resulting in hypotension, mucosal lesions in the small intestine and mortality, the effects of a combination of superoxide dismutase (SOD) and catalase (cat) or a PAF receptor antagonist were tested. Intestinal ischemia was induced in rats and continued for 60 min. After this, the intestine was reperfused. A PAF receptor antagonist, BN 52021, was given 50 min before ischemia in one group, and SOD + cat was given 10 min before reperfusion in one group. One group received normal saline and one group were controls. Blood pressure, mucosal lesions, plasma volume, and endotoxin in plasma were determined up to 3 hr after reperfusion. Mortality was determined over 4 days. Endogenous endotoxin was not found in any of the groups, but the first types of SOD and cat used were contaminated with endotoxin, resulting in exogenous endotoxemia in animals which received those substances. Later endotoxin-free enzymes were used. Neither SOD + cat nor PAF antagonist had any effect on the hypotension or mucosal lesions. Plasma volume remained at the level of the control group after administration of either regimen. Mortality decreased in the group that received SOD + cat. The effects of SOD + cat indicate that free radicals were released in this model at reperfusion, and the effects of the PAF receptor antagonist indicate that PAF participates in membrane damage, but is an intermediary mechanism in the shock model used. The clearance of infused endotoxin from plasma was less effective in the shocked animals, possibly due to a shock effect on reticuloendothelial system (RES).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of antioxidants and PAF receptor antagonist in intestinal shock in the rat. 801 65

Intestinal ischemia/reperfusion injury (I/R) results from reactive oxygen metabolites generated by the xanthine oxidase system and activated neutrophils (PMN). In animal models, removing PMN from initial reperfusate has consistently decreased tissue injury. This experiment was designed to test this potential clinical treatment in human bowel subjected to I/R. The extent of reperfusion injury was assessed by measuring the activity of mucosal alkaline phosphatase (A phi), which is a specific marker of reperfusion injury. Human small intestine (n = 13) obtained at the time of organ harvest for transplantation was perfused for 60 min on an ex vivo perfusion circuit. Reperfusate consisted of autologous blood passed through a leukocyte filter (n = 6) or unfiltered blood (n = 7). Control intestine was sampled at harvest, after transport to the lab on ice (cold ischemia), and after 60 min warm ischemia. Mucosa was homogenized and assayed for A phi activity by cleavage of p-nitrophenyl phosphate. A phi activity (nmole/mg/min) was not decreased after either cold (774 +/- 37) or warm (753 +/- 40) ischemia compared to freshly harvested bowel (770 +/- 51). Both reperfused segments showed a significant decrease in A phi activity compared to controls (P < 0.05); however, reperfusion with leukocyte-filtered blood attenuated the decrease in enzyme activity compared to unfiltered blood (327 +/- 30 vs 506 +/- 25, P < 0.05), constituting an apparent reduction in injury of 35%. The observation that the severity of reperfusion injury was decreased by removal of PMN from the reperfusate demonstrates the efficacy of this strategy in human intestine for the first time.
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PMID:Neutrophil depletion attenuates human intestinal reperfusion injury. 804 Nov 37

Intestinal ischemia/reperfusion (I/R) causes formation of reactive oxygen intermediates (ROI) which lead to mucosal cell injury. Glutathione (GSH), an ROI scavenger, protects tissues from ROI-mediated cell injury. Since GSH biosynthesis is partially dependent on glutamine (Gln) levels, we tested the hypothesis that intravenous Gln infusion will assist in maintaining mucosal cell GSH levels and decrease membrane lipid peroxidation during intestinal I/R. The external jugular vein of male Sprague-Dawley rats was cannulated and infused with normal saline (NS) at 2 cc/hr. After 3 days, matched pairs of rats received either NS alone or NS+ 3% Gln for an additional 24 hr. Next, mucosal GSH levels were measured after a sham I/R in 6 rats and after either 30 or 60 min of ischemia/60 min of reperfusion in a group of 8 and 12 rats, respectively. Finally, conjugated diene (CD), a byproduct of membrane lipid peroxidation, was measured following 60 min of ischemia/60 min of reperfusion in a separate group of 12 rats. Control rats had the highest GSH levels and there was no difference between NS vs NS + 3% Gln rats (2.50 +/- 0.48 vs 2.50 +/- 0.43, P = NS). With 30 and 60 min of ischemia/60 min of reperfusion, GSH levels were significantly lower in NS-infused rats compared to those in NS + 3% Gln-infused rats (30 min: 1.54 +/- 0.14 vs 1.80 +/- 0.16, P < 0.05; 60 min: 1.27 +/- 0.15 vs 1.52 +/- 0.20, P < 0.04). In addition, CD levels were lower in NS + 3% Gln-infused rats compared to those in NS alone-infused rats (5.58 +/- 0.87 vs 7.94 +/- 0.55, P < 0.04). In conclusion, Gln supplementation partially maintains gut GSH levels during bowel I/R, which in turn lessens I/R-induced cell membrane lipid peroxidation.
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PMID:Glutamine preserves gut glutathione levels during intestinal ischemia/reperfusion. 815 29

This study was designed to characterize the role of arachidonate 5-lipoxygenase metabolism during experimental intestinal ischemia-reperfusion (I/R) injury. Canines were subjected to 3 hr of intestinal ischemia followed by 1 hr of normobaric reperfusion. Intestinal ischemia followed by 1 hr of normobaric reperfusion. Intestinal mucosal leukotriene B4 and leukotriene C4 synthesis tripled after ischemia and ischemia-reperfusion, relative to non-ischemic intestinal mucosa. The flux of fluid and protein from the capillary to the lumen also increased 3-fold after I/R. The selective 5-lipoxygenase synthesis inhibitor A-64077 (Ziluten, 5 mg/kg, p.o.) abolished I/R-induced leukotriene synthesis and reduced transluminal protein flux (50%) but did not influence the lumenal accumulation of fluid after I/R. In animals treated with the leukotriene synthesis inhibitor, intestinal vascular resistance significantly declined during the imposed ischemia period and after 60 min of reperfusion. Mucosal myeloperoxidase activity, a biochemical marker for tissue neutrophils, rose significantly after I/R, and these increases were prevented with the 5-lipoxygenase synthesis inhibitor. In other experiments, the lipoxygenase inhibitor nondihydroguaretic acid produced similar results to those of A64077. In an attempt to determine the source of mucosal leukotrienes during intestinal I/R, we imposed in vitro ischemia and reperfusion on normal mucosal tissue in a blood-free environment. Mucosal tissue was incubated in Krebs buffer under oxygen for 3 hr to simulate the control condition, under nitrogen for 3 hr to simulate ischemia and under nitrogen for 2 hr followed by oxygen for 1 hr to simulate I/R.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of the arachidonate 5-lipoxygenase synthesis inhibitor A-64077 in intestinal ischemia-reperfusion injury. 816 54

Between 1978 and 1991, 116 of 19,246 patients (0.6%) undergoing cardiac surgery developed abdominal complications (renal/hepatic failure excluded) within 30 days of their cardiac operation. Comparison with a randomly selected control group of 217 patients operated upon over the same period of time was also undertaken. Compared to the control group, the study patients were older (mean age, 63.3 +/- 12.5 years vs 57.5 +/- 21.5 years; P = 0.03), more likely to have a history of alcohol abuse (10% vs 4%; P = 0.03), and more likely to have a previous history of gastrointestinal problems (43% vs 17%; P = 0.0001). There was also a trend towards a greater number of patients having valvular surgery, particularly reoperative surgery, in the study group. Postoperatively, patients with marked low cardiac output, requiring the intra-aortic balloon pump, were more likely to develop abdominal complications. These complications included complicated peptic ulcer disease in 54 (47%), intestinal obstruction and/or perforation in 19 (16%), biliary tract disease in 13 (11%), mesenteric ischemia in 13 (11%), acute pancreatitis in 3 (3%), and miscellaneous complications in the remaining 14 (12%). Forty-three patients were treated medically and 73 patients required operative intervention. The surgical procedures performed were truncal vagotomy and drainage (12), oversewing of a perforation or a bleeding vessel (6), gastrectomy (2), intestinal resection (14), laparotomy only (14), cholecystectomy (14), and other (11). Mortality was 26% (30/116) with the mortality for medical and surgical treatment being 16% vs 32%, respectively (P = 0.112). Intestinal ischemia had the highest mortality, with a rate of 85% (11/13). Despite intensive monitoring and care of cardiac surgical patients, abdominal complications do occur, although rarely. Risk factors include older age, a positive history of gastrointestinal disease, reoperative valve surgery, and severe postoperative low cardiac output.
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PMID:Abdominal complications following cardiac surgery. 820 26

Intestinal ischemia is associated with changes of the basic electric rhythm (BER) of the small intestine. We hypothesized that these changes can be measured noninvasively using a superconducting quantum interference device (SQUID). After general anesthesia, a laparotomy was performed on 10 animals and the jejunum was placed in a nonmagnetic recording chamber containing Krebs' solution at 38 degrees C. Five animals had electrodes placed while five others were placed under the SQUID. Injection of thrombin into the mesenteric artery decreased blood flow (measured with a laser doppler flow-meter) 95% within 5 minutes. SQUID measurements showed significant decreases (P < 0.01 for all changes) in the frequency (15.5 +/- 0.3 to 8.9 +/- 0.2 cycles/min) and the propagation velocity of slow waves (3.5 +/- 0.2 to 1.9 +/- 0.3 sec). The changes in intestinal biomagnetic activity after ischemia were similar to the changes in electrical activity. The SQUID magnetometer is a reliable noncontact device that can detect early intestinal ischemia in animal models. We have recently recorded human small bowel biomagnetic activity using a SQUID magnetometer and believe further technical developments will permit the noninvasive diagnosis of mesenteric ischemia.
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PMID:Diagnosing intestinal ischemia using a noncontact superconducting quantum interference device. 820 33

Intestinal ischemia-reperfusion is a common clinical event associated with both clinical and experimental distant organ injury. In particular, the pulmonary microvasculature appears to be susceptible to injury resulting from systemic inflammatory mediator activation. This study was designed to evaluate the hypothesis that noncellular humoral factors associated with intestinal ischemia-reperfusion result in pulmonary endothelial cell adenosine triphosphate (ATP) depletion. Male Sprague-Dawley rats had intestinal ischemia induced by microvascular clip occlusion of the superior mesenteric artery (SMA) for 120 minutes. Reperfusion resulted from superior mesenteric artery clip removal. After reperfusion for 0, 15, or 30 minutes, plasma samples were obtained from the portal vein. Monolayers of cultured rat pulmonary artery endothelial cells then were incubated with the plasma samples. Adenosine triphosphate levels were determined using a luciferin-luciferase assay. A 51Cr-release assay using labeled endothelial cells was performed under identical conditions to assess cytotoxicity. Potential mechanisms of ATP depletion were evaluated by analysis of cellular energy charge and assessment of microfilament architecture. Endothelial cell ATP levels decreased from 2.23 +/- 0.16 x 10(-11) moles/microgram DNA in sham preparations to 1.23 +/- 0.09 x 10(-11) moles/microgram DNA (p < 0.001) after 4 hours in plasma from animals undergoing 120 minutes of intestinal ischemia. For plasma obtained after 15 minutes of reperfusion, the decrease in cellular ATP concentration persisted (1.23 +/- 0.27 x 10(-11) moles/microgram DNA, p < 0.001 vs. sham). After 30 minutes' reperfusion, cellular ATP levels increased only slightly after the 4-hour incubation (1.39 +/- 0.26 x 10(-11) moles/microgram DNA, p < 0.005 vs. sham). No significant cytotoxic injury occurred in any group when compared with controls. Cellular energy charge was unchanged, and microfilament architecture was preserved. These data confirm the hypothesis that humoral factors, independent of the neutrophil, result in endothelial cell ATP depletion without metabolic inhibition or cell death. Depletion of energy stores by noncellular humoral factors may represent an early event that predisposes the cell to more severe injury by other mediators of the endogenous inflammatory response.
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PMID:Intestinal ischemia-reperfusion injury causes pulmonary endothelial cell ATP depletion. 842

Intestinal ischemia is considered a major factor in the development of necrotizing enterocolitis (NEC). Despite this, the majority of affected infants lack documentation of clinical events associated with obvious gut hypoperfusion. Recent evidence in adults suggests that endotoxin may impair flow in the microcirculation through alterations in erythrocyte deformability. As the gut serves as a semipermeable reservoir of endotoxin in the stressed neonate, such localized activity may result in intestinal ischemia at the microcirculatory level through alterations in the red cell membrane. This study evaluates the role of endotoxin on neonatal erythrocyte membrane viscosity. Paired anticoagulated whole blood specimens were obtained from the umbilical cord of 10 neonates at delivery. Samples were incubated with either 2 micrograms/mL of E coli endotoxin (LPS) or an equal volume of saline (control). Following incubation, erythrocytes were isolated, washed, and incorporated with the fluorescent membrane probe TMA-DPH. Membrane viscosity was assessed by spectroscopic analysis of the fluorescent emissions induced by excitation of the probe at 365 nm. Results were calculated as anisotropy and analyzed for differences by ANOVA. Endotoxin resulted in a significant increase in red cell membrane viscosity as compared to control (LPS 291.2 +/- 5.1 v Control 271.7 +/- 3.3, P < .01). As the effects of endotoxin are known to be primarily the result of white blood cell (WBC) activation, this study was repeated in an additional 10 neonates in whom WBCs were removed prior to endotoxin/saline incubation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of endotoxin on the neonatal erythrocyte. 846 42


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