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

Intestinal ischemia induces a spectrum of injury from relatively subtle changes in mucosal capillary permeability to gross transmural infarction depending on severity and duration. There is basically two events that can induce intestinal tissue injury in ischemic states, namely hypoxia during the ischemic period and generation of oxygen free radicals following ischemia at reperfusion. In this paper we review data indicating that there is a continuum of injury from the least to the most severe, and by approaching the problem from this perspective we have, in addition, tentatively defined the roles of the two mechanisms in the development of various degrees of intestinal ischemic tissue injury.
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PMID:On the pathophysiology of intestinal ischemic injury. Clinical review. 331 Apr 86

Bowel ischemia and infarction are diseases primarily of, but not confined to, the elderly. Insidiously developing bowel ischemia may mimic more common gastrointestinal disturbances, such as peptic ulcer disease or malignancy, and go undiagnosed for long periods. Bowel infarction is a catastrophic event: Mortality rates approach 90%. Chronic intestinal ischemia may precede infarction, or infarction may occur with no warning. Laboratory and radiologic studies have minimal value in diagnosis of these disorders. A high index of suspicion must be maintained in patients complaining of abdominal pain if these diagnoses are to be made promptly.
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PMID:Bowel ischemia and infarction. Chronic and acute causes of abdominal pain. 368 21

Intestinal ischemia should be suspected in any patient following aortic surgery who has pain out of keeping with the operation, postoperative diarrhea (with or without bleeding) or an unexplained metabolic acidosis. Ten such cases of intestinal ischemia were identified during a 10-year period at the Toronto General and Toronto Western hospitals. Six occurred following repair of a ruptured abdominal aneurysm, one followed elective aneurysmectomy and three followed elective bypass for occlusive disease. The overall mortality was 70%. Transmural bowel infarction was found in six patients (all died), while four patients had partial-thickness injury (one died, three had late strictures). Potentially preventable factors in each patient, either single or multiple, were identified and are discussed. Emphasis on early diagnosis is stressed, because once transmural necrosis has occurred the prognosis is poor.
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PMID:Incentive breathing devices and chest physiopathy: a controlled therapy. 697 22

This study was carried out to determine if an RE depressing substance is present following intestinal ischemia or thermal injury. Intestinal ischemia consisted of occluding the celiac and mesenteric arteries for 3 hr, and thermal injury was a 30% body-surface-area scald (30 sec in 90 degrees C water) in dogs anesthetized with sodium pentobarbital. Immediately following release of the arterial occlusions or 3 hr after thermal injury, portal vein blood was collected and plasma extracts prepared. RE depressing substance activity was assayed by measuring the colloidal carbon clearance rate in rats following the IV injection of the plasma extracts or saline. Plasma extracts from control animals never had detectable RE depressing substance activity. Following intestinal ischemia RE depressing activity was consistently detected in 6 assays on plasma extracts from 12 animals. Thermal injury was associated with the presence of RE depressing activity in each of the 4 animals studied. Neither intestinal ischemia or thermal injury was associated with a significant decrease in mean arterial blood pressure. These results indicate that RE depressing substance may contribute to the RES depression and impaired host-defense seen following intestinal ischemia and thermal injury.
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PMID:Presence of a reticuloendothelial depressing substance in portal vein blood following intestinal ischemia and thermal injury. 730 32

Intestinal ischemia should be suspected in any patient following aortic surgery who has pain out of keeping with the operation, postoperative diarrhea (with or without bleeding) or an unexplained metabolic acidosis. Ten such cases of intestinal ischemia were identified during a 10-year period at the Toronto General and Toronto Western hospitals. Six occurred following repair of a ruptured abdominal aneurysm, one followed elective aneurysmectomy and three followed elective bypass for occlusive disease. The overall mortality was 70%. Transmural bowel infarction was found in six patients (all died), while four patients had partial-thickness injury (one died, three had late strictures). Potentially preventable factors in each patient, either single or multiple, were identified and are discussed. Emphasis on ealy diagnosis is stressed, because once transmural necrosis had occurred the prognosis is poor.
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PMID:Prevention of severe intestinal ischemia following reconstruction of the abdominal aorta. 732 30

Hemorrhagic mucosal lesions are produced during intestinal ischemia and after reperfusion due at least in part to the accumulation and activation of polymorphonuclear leukocytes in the tissue. It has been shown in vitro that adenosine is instrumental in attenuating this pathophysiological process. Acadesine [5-amino-4-imidazolecarboxamide (AICA) riboside], a purine nucleoside analogue, increases the availability of adenosine in the tissue. The aim of the study was therefore to assess the influence of acadesine treatment on neutrophil accumulation, purine metabolism, and mucosal damage after intestinal ischemia and reperfusion. Intestinal ischemia was induced in cats by partial occlusion of the superior mesenteric artery for 2 h. Samples of the small intestine were exercised before and at the end of the hypotensive period as well as 10 and 60 min after reperfusion. Conjugated dienes, myeloperoxidase, and reduced and oxidized glutathione, as well as the purine metabolites, were determined in the tissue samples. The tissue was also examined histologically. Six cats received saline, and six cats were treated initially before ischemia with acadesine (2.5 mg/kg body wt i.v.) over 5 min as a bolus. Thereafter, acadesine (0.5 mg.kg-1.min- i.v.) was given continuously during ischemia and 30 min after reperfusion. Acadesine treatment significantly attenuated the mucosal lesions seen during reperfusion. This improvement was due at least in part to the inhibition of neutrophil accumulation, as judged by low myeloperoxidase levels. The prevention of neutrophil activation resulted most likely from increased adenosine concentrations in the intestinal tissue in the early reperfusion period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of acadesine treatment on postischemic damage to small intestine. 750 74

Intestinal ischemia is characterized by rapid early inhibition of absorptive function and the appearance of net secretion, although why active secretion persists in the setting of a mucosal energy deficit is unknown. The cryptlike epithelial line T84, a well-characterized model of intestinal Cl- secretion, develops a prominent increase in short-circuit current (Isc, indicative of active Cl- transport) in response to "hypoxia" induced by metabolic inhibitors. The increased Isc is associated with the initial decrease in monolayer ATP content. The Isc is transient and disappears with progressive energy depletion, although graded degrees of ATP depletion induce a more sustained Isc response. Chromatographic analysis and secretory bioassays show that the Isc response to metabolic inhibitors is related to the endogenous release of adenosine into the extracellular space in quantities sufficient to interact locally with stimulatory adenosine receptors. Unlike its classical role as a metabolic feedback inhibitor, adenosine appears to function as an autocrine "feed-forward" activator of active intestinal Cl- secretion. These studies suggest a novel role for adenosine in the conversion of the gut from an absorptive to a secretory organ during ischemic stress, thus contributing to the initial diarrheal manifestation of intestinal ischemia.
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PMID:Activation of Cl secretion during chemical hypoxia by endogenous release of adenosine in intestinal epithelial monolayers. 761 80

The significance of the reperfusion period in the pathophysiology of complete occlusion of the intestinal circulation is controversial. Our study was designed to evaluate the exact magnitude of reperfusion-induced intestinal mucosal damage in a standardized rat model of complete segmental arterial ischemia as a function of the occlusion time. Intestinal ischemia was maintained for 15, 30, or 60 min, or ischemia was followed by a 30-min reperfusion period. Intraarterial India ink perfusion was applied to visualize the mucosal vascularity changes induced by ischemia or ischemia-reperfusion. The height of the distributing arterioles of the villi and the average mucosal thickness were recorded by an image analysis system, and the degree of mucosal damage was established on a semiquantitative 0 to 5 grade scale. Ischemia induced erythrocyte obstructions at the villus tip, a progressive decrease in carbon-filled arteriole height, and a concomitant 7, 23, or 35% reduction of the mucosal thickness. The percentage decrease in perfused arteriole height/percentage mucosal thickness reduction ratio was 2.2, 1.5, or 1 during the 15-, 30-, or 60-min ischemia, respectively. Extravasation of the carbon tracer was observed in the 60-min ischemia group. During reperfusion, the mucosal layer was reduced by 27, 38, or 57%, respectively, compared with the baseline values. The arteriole height reduction/mucosal thickness reduction ratio was 1:1 in all ischemic-reperfused groups. The degree of mucosal damage was significantly increased during reperfusion after the 15-min ischemia. Microvessel obstruction is initiated at the villus tip following the onset of arterial occlusion, with subsequent destruction of the surrounding tissues during reperfusion. The reperfusion component of the net mucosal damage may be very significant in early forms of complete occlusion of the mesenteric circulation.
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PMID:Ischemic time-dependent microvascular changes and reperfusion injury in the rat small intestine. 763 47

An inverse correlation between postischemic gastrointestinal motility and the length of intestinal ischemia was found in an animal model. Intestinal ischemia was caused without concurrent laparotomy and for a predetermined time period (ischemia time) by pulling on an external nylon thread that was threaded through a double-lumen catheter. This catheter was passed into the abdominal cavity to encircle the superior mesenteric artery. Gastrointestinal motility was determined by the introduction of a color-marked meal into the animal's stomach and the measurement of the proportionate length of the small bowel filled with it (transit index). This simple and reliable animal model can also be used for the evaluation of techniques and pharmacological manipulations aimed at modulation of the effects of intestinal ischemia on intestinal motility and its consequences.
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PMID:Postischemic intestinal motility in rat is inversely correlated to length of ischemia. An in vivo animal model. 772 59

It is well recognized that reperfusion causes tissue damage in excess of that produced by ischemia alone. The present study was designed to test this and to evaluate the role of the calcium antagonist, diltiazem (400 micrograms/kg body weight administered intravenously over 95 min), in ischemia-reperfusion injury of the intestine. Intestinal ischemia was produced by occlusion of the superior mesenteric artery (SMA) with interruption of the collateral flow for 30 min. Reperfusion was established by declamping the SMA for 1 h, and mucosal injury was assessed using a grading scale from 0 to 5. The severity of mucosal damage increased significantly after 1 h of reperfusion, from a mean grade of 2.1 in the ischemia group to 3.8 in the ischemia-reperfusion group (p < 0.01). Diltiazem was effective in the amelioration of histologic changes of reperfusion injury and reduced the degree of mucosal injury from a mean grade of 3.8 in the ischemia-reperfusion group to 2.5 in the diltiazem group (p < 0.05). This study strongly suggests that calcium ions are involved in the pathogenesis of ischemia-reperfusion injury and that diltiazem attenuates this injury by preventing the intracellular calcium influx that occurs during reperfusion.
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PMID:Role of diltiazem in ischemia-reperfusion injury of the intestine. 785 59


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