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)

Mesenteric ischemia stimulates both A delta- and C-fiber afferents to reflexly activate the cardiovascular system. Leukotriene B4 (LTB4) concentration is increased in intestinal mucosa following prolonged ischemia (3 h) followed by reperfusion. Because LTB4 sensitizes afferent nerve endings in the skin, we determined whether LTB4 is produced during brief mesenteric ischemia and thus would be present to sensitize afferent nerve endings in the abdominal visceral region. Cannulas were placed in the portal vein and in a mesenteric lymphatic vessel distal to the lymph node. Mesenteric lymph and portal venous immunoreactive LTB4 (iLTB4) and immunoreactive thromboxane B2 (iTxB2) concentrations were measured before, during, and after 5-7 min of ischemia induced by occlusion of the descending thoracic aorta in cats. Simultaneously, lymph and plasma lactate concentrations were measured. During arterial occlusion, femoral arterial pressure dropped to less than 30 mmHg, and portal venous and mesenteric lymph lactate concentrations were increased significantly (3.3 +/- 0.6 to 6.3 +/- 1.0 mM and 5.2 +/- 0.9 to 7.2 +/- 1.1 mM, respectively, P less than 0.05). During ischemia, iLTB4 concentration increased in lymph from 261 +/- 70 to 424 +/- 102 pg/0.1 ml (P less than 0.05) but did not increase in portal venous blood (135 +/- 26 vs. 168 +/- 44 pg/0.1 ml, control vs. ischemia). iTxB2 concentration was not increased during ischemia in either portal venous blood or lymph (12 +/- 4 to 24 +/- 9 pg/0.1 ml and 19 +/- 7 to 24 +/- 11 pg/0.1 ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased concentration of leukotriene B4 but not thromboxane B2 in intestinal lymph of cats during brief ischemia. 131 30

Mesenteric ischemia reflexly activates the cardiovascular system. In addition, mesenteric ischemia and reperfusion generate reactive oxygen species. However, the ability of these short-lived reactive oxygen species to generate cardiovascular reflexes is unknown. We therefore investigated cardiovascular reflexes induced by serosal application of hydrogen peroxide (H2O2) to the gallbladder, stomach, or duodenum in anesthetized cats. Serosal application of hydrogen peroxide (44 mumols) to the gallbladder (n = 14) significantly (p less than 0.05) increased mean arterial blood pressure (MAP) by 37 +/- 6 mm Hg, left ventricular dP/dt by 1,893 +/- 416 mm Hg/sec, heart rate by 6 +/- 1 beats per minute, and systemic vascular resistance from 0.34 +/- 0.01 to 0.42 +/- 0.04 peripheral resistance units. The cardiovascular effects were dose-dependent over a range of 0.4 pmol to 132 mumols H2O2. Celiac and superior mesenteric ganglionectomy abolished H2O2-induced cardiovascular effects. Dimethylthiourea (10 mg/kg), a reactive oxygen species scavenger, significantly (p less than 0.05) attenuated 44 mumols H2O2-induced increases in MAP from 36 +/- 3 to 2 +/- 2 mm Hg. Deferoxamine (10 mg/kg) also significantly attenuated 44 mumols H2O2-induced increases in MAP from 40 +/- 7 to 19 +/- 10 mm Hg, but iron-loaded deferoxamine did not. Aspirin (50 mg/kg) did not attenuate H2O2-induced excitation of the cardiovascular system. These data suggest that H2O2 activates abdominal visceral afferents to reflexly stimulate the cardiovascular system by a mechanism involving hydroxyl radicals. Thus, reactive oxygen species could modulate systemic vascular tone by stimulating abdominal visceral afferents during mesenteric ischemia and reperfusion.
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PMID:Hydrogen peroxide-induced cardiovascular reflexes. Role of hydroxyl radicals. 162 88

Mesenteric ischemia is a devastating disease. Without early diagnosis and intervention, the process proceeds to intestinal gangrene with its associated high morbidity and mortality rates. Although newer operative techniques and better intensive care unit management may improve patient outcome, it is only by obtaining an earlier diagnosis that greater patient survival rates will be possible. In an attempt to improve diagnostic accuracy, many modalities have been explored. These include serum biochemical markers, peritoneal fluid analysis, tonometry, radionuclide imaging, laparoscopy, and endoscopic techniques. At present, no single test has enabled the clinician to improve the patient's outcome. We are hopeful that the newer techniques, including radionuclide-labeled antibodies, tonometry, and reflectance spectrophotometry, may in the future be of assistance in improving the results for patients sustaining intestinal ischemia.
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PMID:Diagnostic tests for intestinal ischemia. 173 91

Mesenteric ischemia associated with carcinoid tumors often presents with nonspecific abdominal pain and is usually due to mesenteric branch artery occlusion caused by elastic vascular sclerosis. Mesenteric ischemia was defined by the operative findings of cyanosis or infarction. Eleven patients with intraabdominal metastatic carcinoid tumor were evaluated by angiography. Angiographic narrowing and occlusion of multiple peripheral jejunal and ileal intramesenteric branch arteries was present in 3 patients with mesenteric ischemia, but also occurred in 5 of 8 patients without mesenteric ischemia. Other angiographic abnormalities included staining of the primary tumor (5) or metastases (6), tenting of small mesenteric vessels (5), and occlusion of draining mesenteric veins (2). We conclude that in patients with midgut carcinoid tumors, angiographic narrowing and occlusion of peripheral mesenteric arteries most likely represents elastic vascular sclerosis, is indicative of mesenteric invasion of tumor, but correlates poorly with the presence of ischemia in the subtended bowel. Alternatively, a normal selective arteriogram should exclude mesenteric ischemia as the cause of abnormal pain.
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PMID:Limitations of angiography for mesenteric ischemia caused by midgut carcinoid tumors. 250 47

Mesenteric ischemia is a catastrophic event, which has a mortality due to florid sepsis that approaches 100%. The demography of the bacterial changes has not been documented. After 72 hr of colonic ischemia in the dog, the total number of anaerobic organisms increased while the number of aerobic organisms decreased. After 24 hr of ischemia, anaerobic bacteria appeared only in the portal vein and persisted. Cultures of peritoneal fluid and aortic blood became positive for the same anaerobic organisms after 48 hr. Acute colonic ischemia promotes a relative overgrowth of intraluminal anaerobic bacteria, which progressively invade the portal vein and later the systemic circulation.
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PMID:The role of gastrointestinal microflora in the pathogenesis of complications of mesenteric ischemia. 671 33

Mesenteric ischemia follows a critical reduction in blood flow to the intestine. Absence of a practical diagnostic test results in delayed diagnosis and inability to evaluate changes in blood flow due to vasodilator therapy. We recorded the disappearance of radioxenon (133Xe) from ischemic bowel to quantitate the decreased perfusion and to assess changes in submucosal blood flow after intra-arterial papaverine. The ischemic colon, its only blood supply from collaterals, was formed into a Thirty-Vella loop. An infusion catheter placed at the origin of the superior mesenteric artery (SMA) was used to deliver saline or papaverine (0.1 mg./kg./min). Eleven control dogs received N.S. only. In nine dogs papaverine infusion was started immediately and in another 12 dogs two hours after the production of ischemia. Submucosal blood flow was determined by the per cent washout at two minutes of an 0.05 ml. injection of 133Xe dissolved in N.S., made into the submucosal space of the colostomy.
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PMID:Radioxenon washout for evaluation of vasodilator therapy in mesenteric ischemia. 741 36

Among the vascular disorders of the small intestine, two major categories are mesenteric ischemia and occult gastrointestinal bleeding secondary to a mucosal or muscular lesion. Mesenteric ischemia remains a clinical entity with a high mortality. Recent advances in the understanding of the pathogenesis of mesenteric ischemia have focused on the role of the neutrophil in modulating reperfusion injury. The advent of duplex scanning has provided a noninvasive method to detect hemodynamically significant stenoses in the mesenteric vessels. Effective small bowel endoscopy remains a critical requirement for endoluminal intestinal enteroscopy, and its application has proved of increasing advantage in the localization of small intestinal lesions that may be the source of occult gastrointestinal bleeding.
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PMID:Gastrointestinal vascular and ischemic syndromes. 758 76

This study examines the hypothesis that pentoxifylline protects renal PGE2 synthesis during mesenteric ischemia/reperfusion injury. Anesthetized Sprague-Dawley rats (300 g) were subjected to sham or superior mesenteric artery occlusion for 20 min followed by 30 min of reperfusion. The ischemia/reperfusion groups received either enteral allopurinol (10 mg/kg) daily for 5 d prior to ischemia, pentoxifylline (50 mg/kg) 10 min prior to ischemia or carrier. The kidney was removed and perfused in vitro with oxygenated Krebs buffer and the effluent was assayed for release of 6-keto-PGF1 alpha, PGE2 and thromboxane B2 (TXB2) by enzyme immunoassay. Mesenteric ischemia/reperfusion decreased renal PGE2 release by 50% (compared to sham) but did not alter release of TXB2 or 6-keto-PGF1 alpha. Pentoxifylline pretreatment (not allopurinol) preserved renal PGE2 release at the sham level. These data showed pentoxifylline exerted a protective effect against severe mesenteric ischemia/reperfusion injury by maintaining release of renal PGE2, a potent endogenous renal vasodilator.
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PMID:Acute mesenteric ischemia/reperfusion down regulates renal PGE2 synthesis. 770 19

Mesenteric ischemia of short duration (5-10 min) can stimulate A delta- and C-fiber afferent nerve endings in the viscera to reflexly activate the cardiovascular system. The mechanism of activation of abdominal visceral afferents is probably multifactorial and may involve prostaglandins (PGs), which have been shown to directly stimulate and/or sensitive visceral afferents when administered exogenously. We hypothesized that brief visceral ischemia is accompanied by release of PGI2 and PGE2 into the interstitium, where these cyclooxygenase products could stimulate or sensitize visceral afferent nerve endings. Accordingly, we measured immunoreactive PGE2 (iPGE2) and 6-keto-PGF1 alpha (i6-keto-PGF1 alpha), the stable metabolite of PGI2, in lymph draining the ischemic viscera as well as in portal venous blood. An intestinal lymph duct distal to the lymph node was cannulated in pentobarbital sodium-anesthetized cats. Lymph and plasma iPGE2 and i6-keto-PGF1 alpha concentrations were measured by radioimmunoassay before, during, and immediately after a 5- to 10-min occlusion of the descending aorta. The i6-keto-PGF1 alpha concentration increased significantly (P < 0.001) in portal venous plasma (61 +/- 12 to 107 +/- 18 pg/0.1 ml; n = 14) but not in lymph (148 +/- 30 to 159 +/- 24 pg/0.1 ml; n = 16). In contrast, iPGE2 concentration was significantly (P < 0.01) elevated in both venous plasma (156 +/- 16 to 207 +/- 26 pg/0.1 ml; n = 19) and lymph (520 +/- 48 to 590 +/- 52 pg/0.1 ml; n = 20).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brief mesenteric ischemia increases PGE2, but not PGI2, in intestinal lymph of cats. 820 52

Hypoplastic left heart syndrome (HLHS) has been widely viewed as a uniformly fatal form of congenital heart disease. Between January 1984 and December 1990, 387 patients with the diagnosis of HLHS were treated at this institution. Mesenteric ischemia was clinically diagnosed in 31 patients (8% incidence) and confirmed by pathology or surgery in 25 of those patients. The mean age at the time of onset was 17.5 +/- 5.4 weeks and only 13% were premature newborns. In 80% of the patients a low perfusion state and significant hypotension were documented within 48 hours prior to the diagnosis of bowel ischemia. Nine patients (29%) required operative intervention (bowel resection 4, diffuse ischemia 3, and simple drainage 2). Overall, at operation or at autopsy, nine patients (29%) had diffuse gastrointestinal ischemia. Of 31 patients with mesenteric ischemia, 26 children (84%) died shortly after onset of the gastrointestinal symptoms regardless of means of management. Five patients (10%) initially improved with aggressive medical and/or surgical management; however, 4 subsequently died secondary to complications of their primary cardiac disease. Therefore, the overall mortality of patients with mesenteric ischemia was 97%. Previous reports have estimated that up to 7% of full-term newborns with symptomatic congenital heart disease may develop necrotizing enterocolitis (NEC). Our unique group of patients with HLHS is comprised mostly of full-term infants who developed onset of mesenteric ischemia at a mean age of 4 months associated with an underlying low perfusion state. This mesenteric ischemia has been erroneously identified as NEC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mesenteric ischemia in hypoplastic left heart syndrome. 848 77


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