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

Intestinal ischemia contributes to shock-induced multiple organ failure. Our recent evidence suggests that pancreatic proteases may be involved in the formation of inflammatory activators within an ischemic intestine. These inflammatory mediators are released early into the circulation and may contribute to the severe systemic inflammatory response syndrome (SIRS) during shock. We examined the impact of intra-intestinal pancreatic protease inhibition on acute intestinal ischemia-induced hypotension, the formation of activating factors for cardiovascular cells, as well as cremaster muscle cell death and intestinal injury by intravital microscopy. Male Wistar rats were divided into four groups: (1) a sham group; and experimental groups with 100 min of superior mesenteric artery occlusion (2) without (SMAO group), and (3) with intestinal lavage using Krebs-Henseleit solution (LAV group), or (4) lavage using the protease inhibitor gabexate mesilate in Krebs-Henseleit solution (FOY group, 0.37 mM). Intestinal ischemia and reperfusion-induced hypotension upon reperfusion was accompanied by a significant increase in the level of neutrophil-activating factors in the intestine and plasma. During reperfusion, a significant increase in leukocyte-endothelium interactions in postcapillary venules and parenchymal cell death were observed in the cremaster muscle in LAV and SMAO animals suggesting peripheral neutrophil cell activation. Intra-intestinal pancreatic protease inhibition resulted in a stable blood pressure throughout the experiment. Cell activation, leukocyte-endothelial interactions and cell death in the cremaster muscle were almost completely abolished in the FOY group. In addition, ischemia-induced intestinal mucosal injury was attenuated with intestinal pancreatic protease inhibition. These results indicate that intestinal pancreatic protease inhibition significantly attenuates intestinal ischemia-induced shock by reducing SIRS and gut injury.
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PMID:Pancreatic protease inhibition during shock attenuates cell activation and peripheral inflammation. 1218 22

Bowel ischemia may be caused by many conditions and manifest with typical or atypical and specific or nonspecific clinical, laboratory, and radiologic findings. It may mimic various intestinal diseases and be confused with certain nonischemic conditions clinically and at computed tomography (CT). Bowel ischemia severity ranges from mild (generally transient superficial changes of intestinal mucosa) to more dangerous and potentially life-threatening transmural bowel wall necrosis. Causes of critically reduced blood flow to the bowel are diverse, ranging from occlusions of mesenteric arteries or veins to complicated bowel obstruction and overdistention. CT can demonstrate changes in ischemic bowel segments accurately, is often helpful in determining the primary cause of ischemia, and can demonstrate important coexistent findings or complications. Unfortunately, common CT findings in bowel ischemia are not specific, and specific findings are rather uncommon. Therefore, it often is a combination of nonspecific clinical, laboratory, and radiologic findings-especially detailed knowledge about the pathogenesis of acute bowel ischemia in different conditions-that helps most in correct interpretation of CT findings. To improve understanding of this complex heterogeneous entity, this article provides an overview of the anatomy and physiology of mesenteric perfusion and discussions of causes and pathogenesis of acute bowel ischemia, CT findings in various types of acute bowel ischemia, and potential pitfalls of CT.
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PMID:CT of acute bowel ischemia. 1260 Dec 5

Nonspecific investigations resulting in treatment delays contribute to the 30 per cent mortality associated with acute mesenteric ischemia (AMI). As preliminary studies indicate that alpha-glutathione S-transferase (alpha-GST) is elevated in AMI we compare the ability of alpha-GST against conventional biochemical tests to predict AMI. There were 58 patients prospectively evaluated for AMI. Samples for alpha-GST (Biotrin International, Dublin, Ireland), lactate, pH, amylase, base excess, and white blood cell count (WBC) were evaluated. Intestinal ischemia was confirmed by colonoscopy, angiography, or laparotomy. Ischemia was present in 35 (60%) patients: small bowel (n = 14), colonic (n = 17), and global (n = 4). Four patients without autopsy were excluded. Alpha-GST was elevated in those with AMI [22.2 (7-126) ng/mL vs 2.2 (1-3) (P = 0.001)]. Alpha-GST was more accurate at predicting intestinal ischemia (74%) than conventional tests (47-69% accuracy). Accuracy was increased to 80 per cent by combination with lactate or WBC, which increased sensitivity to 97 to 100 per cent. Alpha-GST monitoring is a useful tool for the diagnosis of intestinal ischemia. A normal alpha-GST and WBC may exclude the presence of AMI.
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PMID:Prospective assessment of the predictive value of alpha-glutathione S-transferase for intestinal ischemia. 1271 91

Intestinal ischemia/reperfusion (IIR) is a critical and triggering event in the development of distal organ dysfunction, frequently involving the lungs. Respiratory failure is a common cause of death and complications after intestinal I/R. Stress protein heme oxygenase-1 (HO-1) confers the protection against a variety of oxidant-induced cell and tissue injuries. The aim of this study was to investigate the hypothesis that the induced HO-1 expression by pharmacological preconditioning with anticancer drug doxorubicin (Dox) could protect the lung injury induced by intestinal I/R. Intravenous administration of Dox induced HO-1 expression in the lungs and high levels of the expression were sustained at least to 48 h after the injection. Therefore, as pharmacological preconditioning, a low dose of Dox was injected intravenously into rats at 48 h before the start of intestinal ischemia. Rats underwent intestinal I/R by superior mesenteric artery occlusion for 120 min followed by 120 min of reperfusion. Preconditioning with Dox significantly ameliorated the lung injury induced by the intestinal I/R. Administration of a specific inhibitor of HO activity reduced the efficacy of the preconditioning. Our results suggest that this improvement may be mediated at least in part by the HO-1 induction. These findings may offer interesting perspectives for patient management In Intestinal surgical operation and intestine transplantation.
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PMID:Pharmacological preconditioning protects lung injury induced by intestinal ischemia/reperfusion in rat. 1274 91

It is suggested that gastrointestinal mucosal blood flow depends on a balanced release of vasoactive substances from the endothelium. The present study investigated the effects of molsidomine on the small intestine after ischemia-reperfusion (I/R) injury in four groups of 10 rats each composed: (1) SO, sham operation; (2) untreated I/R; (3) ML, I/R plus molsidomine pretreatment; (4) L-NAME, I/R plus N-omega-nitro-L-arginine methyl ester pretreatment. Intestinal ischemia for 45 min and reperfusion for 60 min were applied. Ileum specimens were obtained to determine the tissue level of malondialdehyde (MDA) and histologic changes. Mean MDA levels in the SO, untreated I/R, ML, and L-NAME groups were 95.60 +/- 2.59, 136.90 +/- 4.35, 121.10 +/- 3.38, and 137.40 +/- 4.42 nmol/g wet tissue, respectively. Although the MDA level in the ML group was higher than in the SO group ( P < 0.0001), it was significantly lower compared to the untreated I/R and L-NAME groups ( P < 0.0001, P < 0.0001). Mucosal injury scores (MIS) in groups 1-4 were 0.2 +/- 0.42, 3.9 +/- 0.73, 1.5 +/- 0.70, and 4.1 +/- 0.56, respectively. In group 3 the MIS was significantly lower than in groups 2 and 4 ( P < 0.0001, P < 0.0001). Molsidomine plays a role in attenuating reperfusion injury of the small intestine by depression of tissue MDA levels and MIS and regulates post-ischemic intestinal perfusion while restoring the intestinal microcirculatory blood flow and histologic injury.
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PMID:The nitric oxide donor molsidomine prevents ischemia/reperfusion injury of the adult rat small intestine. 1278 56

Bacterial translocation is believed to occur during cardiopulmonary bypass (CPB) because serum endotoxin concentrations rise. Intestinal ischemia during CPB, however, has never been proven directly. The condition of the intestinal mucosa during CPB was studied by measuring serum diamine oxidase (DAO) activity, an index of intestinal ischemia. Serum DAO activity, blood lactate concentration, and the arterial ketone body ratio (AKBR) were measured intraoperatively in four successive patients who underwent aortic arch replacement by the open distal anastomosis method. DAO activity rose after restoration of blood flow to the lower half of the body, and continued to rise throughout CPB. The lactate concentration also rose, mirroring the change in DAO activity, and returned to nearly normal 12 h after the operation. The AKBR decreased during CPB, with a mean minimum vale of 0.16-0.07 immediately after the restoration of blood flow to the lower half of the body. The parallel rise in DAO activity and serum lactate concentration once blood flow to the lower half of the body was restored implies that ischemic injury to the mucosa of the small intestine occurs during CPB. The continued rise in these parameters throughout CPB is consistent with ongoing injury due to splanchnic hypoperfusion, as reflected in the decrease in the AKBR during the same period.
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PMID:Ischemia of the intestinal mucosa during cardiopulmonary bypass. 1462 95

Intestinal ischemia/reperfusion (I/R) injury affects patients of different ages, especially premature babies and the elderly. The outcome after intestinal I/R is often dismal, which may be attributed to loss of the barrier and immune functions of the intestines, as well as development of secondary injury in remote organs. The available treatment for advanced gut ischemia mandates extensive resection, which may cause growth retardation in infants and nutritional problems in the elderly. Throughout the past decade we have been investigating the potential therapeutic role of heparin-binding epidermal growth factor-like factor (HB-EGF) in intestinal I/R. The mitogenic and chemoattractant functions of HB-EGF formed the initial rationale for our investigations. In addition, HB-EGF is a potent antiapoptotic protein that enables cells and tissues exposed to different apoptotic stimuli to survive hypoxic, oxidative, and nutritional stresses. HB-EGF is known to have a vital role in wound healing and postischemic regeneration in different organs. In the current review, we summarize the results of our findings of the beneficial effects of HB-EGF in intestinal I/R, supported by additional evidence from the literature and an explanation of different possible mechanisms of its actions. Collectively, the data strongly suggest a potential therapeutic role for the use of HB-EGF to treat intestinal ischemic diseases such as I/R and necrotizing enterocolitis.
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PMID:Heparin-binding epidermal growth factor-like growth factor and intestinal ischemia-reperfusion injury. 1476 65

Intestinal ischemia-reperfusion is a common pathway for many diseases in infants, children, and adults, and this may lead to multiple organ dysfunction syndrome and death. While several studies have investigated reperfusion injury in cardiac, cerebral, and hepatic disease, limited work has been published on intestinal ischemia-reperfusion and its multiorgan effects. The authors have developed models of intestinal ischemia-reperfusion in rats and have demonstrated that intestinal reperfusion causes liver energy failure at normothermia. This is followed by 100% mortality within 4 hours of reperfusion. Moderate hypothermia (32 degrees C to 33 degrees C) induced throughout ischemia and reperfusion prevents liver energy failure, intestinal damage, and neutrophil infiltration in the lungs. Moderate hypothermia in this model of intestinal ischemia and reperfusion prevents mortality. Further studies are needed to establish whether therapeutic hypothermia is a useful intervention in the treatment of infants and children with intestinal injuries caused by ischemia and reperfusion.
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PMID:Intestinal ischemia reperfusion injury and multisystem organ failure. 1476 66

Ischemic bowel disease includes acute and chronic mesenteric ischemia, and colon ischemia. Cross-sectional imaging, and more particularly computed tomography, has an increasing role in the detection of acute and chronic mesenteric ischemia. Vascular obstructions or stenoses and changes in the bowel wall can be observed. Functional information can be added with MRI by using sequences that are sensitive to oxygen saturation in the superior mesenteric vein. Arteriography remains the reference examination in patients with acute mesenteric ischemia.
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PMID:[Imaging of intestinal ischemia]. 1518 99

Free radical (FR) formation in the rat intestinal lumen was measured using the spin-trapping technique and electron paramagnetic resonance spectroscopy. Intestinal ischemia was produced by occluding the celiac and the superior mesenteric arteries for 30 min followed by reperfusion. The lumen was filled with a solution of PBN (N-tert-butyl-alpha-phenyl-nitrone) and the intestine was squeezed to enhance the interaction between the PBN solution and the intestinal mucosal cells. Free radicals were produced upon reperfusion, with peaks at 5 and 90 min. Post-ischemic treatment with superoxide dismutase (20 mg.kg(-1)) inhibited the increase of FR production during the second peak by 36%. In a single study in a group of leucocytopenic rats (WBC < 1500/mm(3)), the increase of FR production during the second peak was decreased by 80%. However, these treatments did not inhibit the FR production during the first peak in either group. In contrast, pretreatment with allopurinol (40 and 100 mg.kg(-1) injection at 24 and 3 hours before ischemia, respectively) inhibited the FR production during the first peak by 76%, but did not inhibit during the second peak. The changes in lipid peroxidation in the intestinal mucosa, specific gravity of the intestine and in the hematocrit were correlated to the FR production in the second peak. These results suggest that a major cause of tissue injury after reperfusion in the ischemic intestine may largely be produced by neutrophils.
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PMID:Free radical formation during splanchnic artery occlusion shock. 1527 14


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