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

The hypothesis that a significant reduction in colonic mucosal perfusion, and hence ischemic injury, precedes the development of mucosal ulceration and inflammation is tested in this report. The microcirculatory changes in the rat colonic mucosa within 1 hr of topical exposure to 10% acetic acid were assessed. Colonic mucosal blood flow signals measured by laser Doppler flowmetry were significantly reduced to 61 +/- 8, 52 +/- 10, and 37 +/- 13% (mean +/- SEM) of baseline values at 1 min, 4 min, and 10 min after the colonic mucosa was exposed to 10% acetic acid, respectively, but not in controls exposed to saline. After the start of application of 10% acetic acid (for 4 min), in vivo microscopy studies demonstrated that colonic mucosal ischemia (stasis of the red blood cells in the mucosal capillaries) occurred at 9 +/- 5 min (mean +/- SEM). Evidence of endothelial cell death (failure to exclude a fluorescent dye, propidium iodide, by endothelial cells) developed at 25 +/- 10 min (mean +/- SEM). These findings indicate that within minutes after contact of the colonic mucosa with 10% acetic acid, colonic mucosal ischemia develops, followed shortly by death of endothelial cells. The data do not establish a cause-and-effect relationship between the reductions in mucosal blood flow and loss of endothelial cell viability in response to acetic acid. Nevertheless, because these events occur at such an early time point, they may play a pathogenetic role in the development of the subsequent inflammatory and ulcerative changes in this animal model of colitis. Further studies to define the potential causal relationships between these parameters are warranted.
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PMID:Mucosal vascular stasis precedes loss of viability of endothelial cells in rat acetic acid colitis. 203 12

Extraction and clearance kinetics of [1-11C]acetate were examined in 65 experiments in 30 open-chest dogs. Twenty-nine studies were performed at control, 13 during ischemia, eight after reperfusion, 13 during dipyridamole-induced hyperemia, and two during alteration of cardiac workload. [1-11C]Acetate was injected directly into the left anterior descending coronary artery, and myocardial tissue-time activity curves were recorded with a gamma probe. The single-pass extraction fraction averaged 64.2 +/- 9.7% in control, 65.3 +/- 9.1% in ischemia, 70.0 +/- 4.4% in reperfusion, and 46.5 +/- 7.4% in dipyridamole-induced hyperemia groups. 11C clearance was biexponential in all cases. The rate constant k1 for the first rapid clearance phase correlated closely with myocardial oxygen consumption (r = 0.94) in control, ischemia, reperfusion, and dipyridamole-induced hyperemia groups. Monoexponential fitting of only the first linear part of the clearance curve yielded the rate constant kmono, which also correlated with myocardial oxygen consumption (r = 0.96). Arterial lactate concentrations and the amount of free fatty acid oxygen equivalents consumed by the myocardium were shown to have a small but statistically significant impact on the relation between [1-11C]acetate clearance rate constants and myocardial oxygen consumption. The fraction of 14CO2 activity contributing to overall 14C activity leaving the myocardium after simultaneous injection of [1-14C]acetate (n = 24) was relatively high in all cases (97.4 +/- 2.5% in control, 89 +/- 2.6% in ischemia, 94.1 +/- 3.5% in reperfusion, and greater than 99% in dipyridamole groups), indicating that externally measured 11C clearance corresponds to CO2 production and thus to tricarboxylic acid cycle activity. In conclusion, the results validate the use of [1-11C]acetate as a tracer of oxidative myocardial metabolism for use with positron emission tomography.
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PMID:Validation of [1-11C]acetate as a tracer for noninvasive assessment of oxidative metabolism with positron emission tomography in normal, ischemic, postischemic, and hyperemic canine myocardium. 211 37

23Na nuclear magnetic resonance (NMR) spectroscopy was utilized to measure intracellular Na+ in perfused ferret hearts exposed to the shift reagent dysprosium triethylenetramine-hexa-acetic acid [Dy(TTHA)3-]. The intracellular Na+ signal was small under normal perfusion conditions; resolution was enhanced by using a Jump-Return NMR pulse protocol. During 20 min of total global ischemia at 30 degrees C, intracellular Na+ concentration ([Na+]i) increased steadily to a peak value fivefold greater than control. [Na+]i declined monotonically back to control levels within 9 min of reperfusion. In contrast, the mean contractile pressure only recovered to 54% of control levels. Thus major alterations in Na+ homeostasis occur during severe ischemia. [Na+] recovers rapidly during reperfusion and is therefore dissociated from the lingering postischemic depression of contractile function known as "stunning."
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PMID:23Na-NMR measurements of intracellular sodium in intact perfused ferret hearts during ischemia and reperfusion. 226 Jul 1

We have studied changes of cerebral monoamine metabolism and water content, during recirculation following global transient ischemia (20 min) using the four-vessel occlusion model in rats. Levels of monoamines and their metabolites were determined in cortex, striatum, hippocampus, and hypothalamus. Water content was evaluated by weight and by the analysis of T1 and T2 relaxation times in 1H-nuclear magnetic resonance. Norepinephine levels decreased; 3,4-dihydroxyphenylethylamine, 3,4-dihydroxyphenylacetic acid, and 5-hydroxytryptamine levels oscillated and levels of the end products homovanillic acid and 5-hydroxyindole-3-acetic acid increased. The regional changes were qualitatively similar but quantitatively different, and were greatest in the hippocampus, illustrating the concept of neuronal selective vulnerability. The changes suggest an initial monoamine depletion and catabolism due to massive release from stores followed by autoregulatory processes. The water content increased moderately, with a maximum at 1 h. The variations of T1 were similar, positively correlated with water content and more pronounced in the cortex than in the white matter. T2 was markedly altered over the entire 24-h period. Those latter parameters are positively correlated with 5-hydroxytryptamine concentration in the hypothalamus consistent with a relationship between 5-hydroxytryptamine and cerebral edema.
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PMID:Aminergic neurotransmitter and water content changes in rats after transient forebrain ischemia. 243 56

We devised the present experiments to assess the effects of ischemia on the production of dopamine in the caudate nucleus of spontaneously hypertensive stroke-resistant rats. Ringer's solution was continuously perfused at a rate of 10 microliters/min through 0.2-mm-diameter dialysis tubing implanted in the rat's caudate nucleus. After bilateral occlusion of the common carotid artery, perfusate was collected at 20-minute intervals for 120 minutes and was analyzed for monoamines and their metabolites using high-performance liquid chromatography and an electrochemical detection system. The extracellular concentration of dopamine increased abruptly approximately 3 minutes after the ischemic insult, reached a maximum at between 20 and 40 minutes after the insult, and subsequently decreased. During the 120 minutes, 3,4-dihydroxyphenylacetic acid and 5-hydroxyindole-3-acetic acid concentrations decreased significantly, whereas 5-hydroxytryptamine was not detected. Our results indicate that during cerebral ischemia a large increase in extracellular dopamine concentration in the caudate nucleus occurs, probably as a result of energy failure of the cell membranes. This leakage of dopamine may be a causal factor in the neuronal damage associated with cerebral ischemia.
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PMID:Striatal dopamine in acute cerebral ischemia of stroke-resistant rats. 246 90

Changes in cerebral monoamine metabolism were investigated in gerbils following a 5-min ischemia. During ischemia, monoamines were not changed, and 3-methoxy tyramine increased remarkably. After re-circulation, noradrenaline and serotonin decreased, and 5-hydroxyindole-3-acetic acid increased. Dopamine was not significantly changed, but its metabolites were elevated. At 1, 3 and 7 days after the ischemia, monoamine metabolism did not change. We discussed the possibility that these monoamine metabolism changes in the early period of reflow might be related to the delayed neuronal damage.
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PMID:Changes in monoamine contents in the brains of Mongolian gerbils following a 5-min occlusion of the bilateral carotid arteries. 247 87

During the period of recirculation following transient global ischemia, an initial hyperemia is succeeded by a secondary decrease in cerebral blood flow, termed "delayed postischemic hypoperfusion." It has been suggested that this phenomenon can lead to additional brain damage after the initial ischemic insult. One proposed mechanism of delayed postischemic hypoperfusion is increased cerebrovascular smooth muscle tone. Release of vasoactive amines, formation of vasoactive products of arachidonic acid metabolism, and disturbance of calcium ion homeostasis in cerebrovascular smooth muscle may contribute to postischemic vasoconstriction. In this study, monoamine metabolism following transient global ischemia was investigate. Mongolian gerbils subjected to 15 minutes of temporal bilateral common carotid artery occlusion and up to 6 hours of recirculation were employed as a model of transient global ischemia. In this model, secondary energy failure reportedly occurs after 6 hours of recirculation. Regional cerebral concentrations of monoamines and their metabolites were determined by high-performance liquid chromatography with electrochemical detection. After 4 to 6 hours of recirculation, accumulation of vasoactive amine, 5-hydroxytryptamine, its major metabolite, 5-hydroxyindole acetic acid, and its precursor amino acid, tryptophan were detected. This finding strongly suggests a postischemic increase in both synthesis and release of this amine, which may explain postischemic vasoconstriction. Moreover, increased dopamine synthesis and release after 1 hour of recirculation was suggested. As dopamine release is reported to increase cerebral glucose utilization, its elevation may contribute to an increase in cerebral energy demand after ischemia. Thus, the brain becomes relatively ischemic and secondary ischemic cell damage occurs.
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PMID:[Monoamine metabolism after transient global ischemia. Mechanism of delayed postischemic hypoperfusion]. 248 87

Free oxygen radicals (F.O.R.) belong to a very aggressive chemical species derived from molecular oxygen. Their role in inflammation is well established and Polymorphonuclear neutrophils (PMNS) make use of them as antibacterial weapons. Their role has been experimentally demonstrated in numerous ischemia-reperfusion models. Free radical scavengers such as the superoxide dismutase, allopurinol or desferrioxamine can prevent the occurrence of lesions. The essential role of PMNS in these models is demonstrated by the fact that previous depletion of the animal in PMNS also prevents such lesions. Histologically, in these ischemia-reperfusion models, PMNS infiltration may be quantified by assay of myeloperoxidase. In experimental models of inflammatory colitis (acetic acid, bacterial polysaccharides) intestinal wall infiltration by PMNS is a fundamental phenomenon and is also a characteristic of Crohn's disease and exacerbations of Ulcerative Colitis. Thus, it is probable in both disorders that F.O.R. play an important role since steroids inhibit their secretion by PMNS and 5-aminosalicylic acid has been shown to be a F.O.R. scavenger.
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PMID:[Oxygen free radicals and inflammatory diseases of intestines]. 254 36

The effects of total brain ischemia (decapitation) on striatal extracellular levels of dopamine (DA) dihydroxyphenyl acetic acid (DOPAC) and ascorbic acid (AA) in chloral hydrate anesthetized rats were monitored at 1-min intervals by differential normal pulse voltammetry (DNPV) with numerical deconvolution of the catechol peak. Changes in pH were assessed by the shift of AA oxidation potential and incorporated into the computational procedure. The AA peak showed a sharp, short-lived (less than 15 min) postdecapitation rise, followed by a slower secondary increase. The DA signal increased 100-fold in the first 20 min followed by a slow decline. DOPAC levels fell 80% within 15 min after death. The post-mortem changes in extracellular DA and DOPAC were verified by a similar experiment using microdialysis. These observations probably reflect massive release and impaired uptake of DA combined with reduced monoamine oxidase activity. Changes in membrane permeability to DOPAC as a consequence of a post-mortem drop in pH may also contribute to the decline in extracellular DOPAC levels.
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PMID:Post-mortem dopamine dynamics assessed by voltammetry and microdialysis. 259 Aug 45

1. The relationship of the mesenteric inflammation with intestinal loop deformities was made clear and changes of these deformities were examined with time, using experimental model rabbits. 2. The above rabbit was laparotomized and was caused to develop mesenteritis by applying acetic acid onto sigmoid mesentery and descending colic mesentery, then the abdomen was closed. Subjects were divided into 2 groups (A and B); A group and B group were re-laparotomized 3-7 and 21 days later, respectively and were observed for mesentery and loop appearance, then were extirpated for sigmoid colon and descending colon with mesenterium attached thereto. Roentgenograms were taken first with attachment of mesentery, secondly there-without. Then, the intestinal canal was opened and the mucosal surface was observed, together with bleeding and blood flow disturbance in the depth of the wall in transmitted light. 3. As a result, the following conclusions were obtained: 1) Macroscopically, mesentery was marked with redness for A group and with thickening and twitch due to cicatricial contraction for B group. 2) A group near to the third day showed remarkable shortening, narrowing and marginal irregularity of the loop, which disappeared with time and were scarcely observed for B group; these deformities were considered to involve mesenteric inflammations and ischemia caused by secondary blood flow disturbance. 3) A group near to the 7th day and B group showed remarkable angulation, distortion and coil-like appearance; these deformities are considered to have been caused by thickening (stiffness) of the mesentery and its attachment and twitch-distortion due to cicatricial contraction. 4) Coil-like appearance disappeared upon cutting off the mesentery from the loop.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An experimental study on mesenteritis and deformities of the intestinal canal; with special reference to the changes with time of deformities (angulation, distortion, coil-like appearance)]. 262 49


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