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

Brain damage initiated during global ischemia has been shown to be exacerbated by iron-dependent lipid peroxidation during early reperfusion. We hypothesized that other cellular components might be involved in similar free radical reactions. In this study we examined three brain protein fractions and ribosomal RNA for evidence of free radical damage during post-ischemic reperfusion. Global brain ischemia was induced by 20-min cardiac arrest. Dogs were divided into four groups: (1) non-ischemic controls; (2) 20-min cardiac arrest without reperfusion; (3) 20-min cardiac arrest and 2 h reperfusion; (4) 20-min cardiac arrest and 8 h reperfusion. Soluble proteins and proteins from ribosomes and synaptosomes were assayed by a dinitrophenylhydrazine method for carbonyl groups, which are characteristic products of protein peroxidation. The ribosomal RNA was also examined by electrophoresis. When proteins from each fraction were peroxidized in vitro by Fenton reagents, carbonyl content increased as [Fe2+] was increased from 0 to 100 microM. However, following reperfusion there was no significant accumulation of carbonyl content in either the soluble (ANOVA P = 0.92) or ribosome (P = 0.10) protein fractions. There was a significant decrease in the carbonyl content of the synaptosome protein fraction after 8 h of reperfusion (P = 0.03). Similarly, although ribosomal RNA fragmentation was observed in ethidium stained agarose gels following in vitro reaction with Fenton reagents, there was no evidence of ribosomal RNA fragmentation or cross-linking following reperfusion. These results suggest that reperfusion free radical reactions do not involve these cellular proteins or ribosomal RNA.
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PMID:Assessment of free radical-induced damage in brain proteins after ischemia and reperfusion. 131 70

Mechanical ventilation with positive end-expiratory pressure (PEEP) limits hepatic blood flow (HBF) and oxygen delivery (HO2D). Early gut feeding may augment hepatic hemodynamics and avoid relative ischemia in this flow-limited environment. To examine these effects, canines were instrumented with arterial, pulmonary artery, portal, and hepatic vein catheters. Splenectomy and gastrostomy were performed and the hepatic artery and portal vein were encircled with flow probes. All animals underwent lung injury with oleic acid (0.08 ml/kg) followed by the addition of 10 cm H2O PEEP to correct shunt. One group (fed) was then given a bolus elemental feeding (1 kcal/ml, 10 ml/kg) and the Control group, sterile water. Cardiac index (CI), HBF, hepatic oxygen delivery (HO2D), and hepatic oxygen consumption (HO2C) were measured at baseline (T0), after PEEP (T1), and 1 (T2) and 2 hr (T3) after feeding. Data were tested for significant changes between time points in the same group by ANOVA and significant differences were subjected to t testing. PEEP significantly decreased CI, HBF, and HO2D compared to baseline. Subsequently, gut feeding increased HBF to baseline levels and improved HO2D. HO2C also increased but hepatic O2 extraction was unchanged. There was little change noted in the control group over this same period. We conclude that gut feeding augments HBF and HO2D in this flow-limited state and may preserve splanchnic integrity in critical illness.
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PMID:Gut feeding and hepatic hemodynamics during PEEP ventilation for acute lung injury. 140 14

The normal microvascular permeability of the ascending colon in horses and the microvascular permeability of that segment after ischemia and reperfusion were investigated. Microvascular permeability was estimated by the ratio of lymphatic protein to plasma protein concentration (Cl/Cp) at high lymph flow rates in 8 adult horses in 2 equal groups: normal and ischemic (2-hour period). Lymphatic flow rates and lymph and plasma protein concentrations were determined. Intestinal biopsy specimens were obtained at the end of each experiment. Flow independent values were selected and compared by one-way ANOVA, and the mean and SEM of these values were determined. The mean Cl/Cp ratios for the flow independent part of each data set were as follows: normal = 0.36 +/- 0.08; ischemic = 0.70 +/- 0.08. These groups were significantly different (P < or = 0.0001). Microscopic evaluation revealed mild congestion and edema in the normal group. The ischemic group had mild to moderate mucosal degeneration, with moderate to severe congestion and edema. We concluded that ischemia of the ascending colon, when followed by reperfusion, results in a significant increase in microvascular permeability.
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PMID:Microvascular permeability changes in ischemia/reperfusion injury in the ascending colon of horses. 142 57

Intestinal ischemia was induced and maintained for 60 minutes in male Sprague-Dawley rats weighing 175 to 225 g. Prior to reperfusion, the following drugs were administered via the caudal vena cava: 0.9% NaCl (0.5 ml), superoxide dismutase (SOD; 1,000 IU/kg of body weight), polyethylene glycol-conjugated SOD (PEG-SOD; 1,000 IU/kg), or the 21-aminosteroids, U74006F (3 mg/kg) or U78715G (3 mg/kg). A sham-operated control group was included. Animals from each group were euthanatized at 5 periods of reperfusion: 5 minutes, 30 minutes, 18 hours, 3 days, and 7 days after reperfusion. Fixed tissues were embedded in paraffin, sectioned at 5 microns, and stained with H&E. Villi profiled in cross section were measured from the crypt villus junction to the tip of the villus. The mean villus height for each rat was calculated and compared by two-way ANOVA to determine the effects of time and treatment. Villus height was maintained after 30 minutes of reperfusion in rats of the sham- and U74006F-treated groups; U78715G and SOD treatment attenuated the loss in villus height, and villus height was not maintained in the PEG-SOD- and 0.9% NaCl-treated rats. In all rats, villus height was comparable to, or was greater than villus height in sham-operated controls by 18 hours after reperfusion in all animals and remained constant through 7 days. Administration of the 21-aminosteroids maintained villus height after ischemia and reperfusion. Treatment with PEG-SOD did not maintain villus height to the degree observed in rats treated with SOD.
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PMID:Evaluation of intestinal villus height in rats after ischemia and reperfusion by administration of superoxide dismutase, polyethylene glycol-conjugated superoxide dismutase, and two 21-aminosteroids. 146 14

Neutrophils (PMN) have been implicated as mediators of the "no-reflow" phenomenon seen in skeletal muscle during reperfusion after ischemia. In order to evaluate the PMN contribution to the changes seen in the microcirculation of skeletal muscle after ischemia, we evaluated PMN velocity using in vivo microscopy in a rat model. After the induction of anesthesia, the right iliac and femoral arteries were isolated. The right anterior tibialis muscle was exposed in situ, covered with a plexiglass disc, and perfused with Kreb's solution. Fluorescein-labeled bovine albumin was given intravenously, which identified the capillaries under microscopic magnification as viewed on the video screen. Acridine orange was then administered intravenously, which selectively fluoresced the PMN. The right iliac and femoral arteries were clamped for ischemia intervals of 5, 10, 15, 20, 25, and 30 min. Acridine orange was given immediately after the arteries were unclamped, after 30 min of reperfusion and after 60 min of reperfusion. PMN velocity was determined by the distance traveled by the PMN over time using the videotape and frame-by-frame review. Results demonstrated no change in PMN velocity (mm/sec) after 5 min of ischemia. After 10, 15, and 20 min of ischemia, PMN velocity initially slowed and then recovered, which was not statistically significant. After 25 min of ischemia, PMN velocity decreased significantly, which persisted (P < 0.05 compared to 5-min ischemia by ANOVA). No flow was seen after 30 min of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo microscopy of rat skeletal muscle after ischemia using labelled neutrophils (PMN). 149 88

Peripheral A-delta and C fibers are activated during the production of ischemic or tourniquet pain; however, individual metabolic or molecular factors responsible for neural activation are not known. To elucidate these mechanisms the in vitro corneal nerve preparation was used. Electrophysiologic effects of individual metabolic perturbations associated with ischemia (hypoxia, hypoglycemia, lactic acid, and decreased pH) were investigated on A-delta and C fiber nociceptors. Increased tonic action potential activity occurred in C fibers but not in A-delta fibers after ischemia. The conduction velocity of C fibers was 0.85 +/- 0.2 m/s (mean +/- SD). Under control conditions (n = 43) there was very little fluctuation in the baseline action potential frequency (+/- 3.2%). Hypoxia (n = 12) resulted in a 213 +/- 3.4% (mean +/- SD) increase in C fiber action potential frequency relative to control (P less than 0.001, ANOVA). L-glucose substitution for D-glucose (n = 8) increased C fiber discharge frequency by 653 +/- 28% relative to control (P less than 0.001) as did the combination of hypoxia and L-glucose substitution (n = 6) by 671 +/- 14%. Comparison of hypoxia versus hypoxia and hypoglycemia conditions did not show them to be statistically different (P greater than 0.5). Lactate (10-1000 micrograms/ml) at a pH of 6.9 or 7.4 did not alter the action potential discharge frequency in corneal C fibers (n = 5, P greater than 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of C fibers by metabolic perturbations associated with tourniquet ischemia. 155 Feb 87

Glycine preserves tubular cell integrity under hypoxic and toxic conditions in vitro. It also ameliorates cisplatin nephrotoxicity in vivo. We studied the effect of glycine on tubular necrosis from ischemia reflow and on inner stripe injury in an animal model of radiocontrast nephropathy. In all experiments, glycine (75 mg/100 g/h) increased tubular damage in the inner stripe. In the model of radiocontrast nephropathy, the percentage of medullary thick ascending limb (mTAL) necrosis at 24 hours increased from 22% +/- 6% to 41% +/- 9% or 55% +/- 7% with glycine infusion of 75 or 135 minutes, respectively (mean +/- SE, P less than 0.05, analysis of variance [ANOVA]). Renal function was not significantly affected. In rat kidneys subjected to ischemia reflow, mTAL injury following glycine increased from 1% +/- 0% to 12% +/- 6% (P less than 0.05) and from 8% +/- 5% to 49% +/- 8% (P less than 0.01) 24 hours after 30 minutes and 45 minutes ischemia, respectively. Tubular injury in the inner stripe was maximal in the deep interbundle zone, typical of hypoxic, rather than reperfusion, injury. Prior uninephrectomy increased inner stripe damage, but protected the proximal tubules. Both uninephrectomy and glycine infusion were found to contribute to mTAL necrosis. The infusion of glycine for 1 hour in intact rats increased renal blood flow by 44% and tripled urine volume (P less than 0.01). A parallel increase in glomerular filtration rate GFR; by 22% over 90 minutes) fell short of statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of glycine and hypertrophy on renal outer medullary hypoxic injury in ischemia reflow and contrast nephropathy. 159 7

Elevations in intracellular calcium during myocardial ischemia have been implicated in the development of lethal cardiac arrhythmias. The calcium antagonist, flunarizine, has been shown to suppress the accumulation of intracellular calcium and has been proposed to protect against triggered activity due to calcium overload. Using 13 mongrel dogs with healed myocardial infarctions, ventricular fibrillation (VF) was induced by a 2 min coronary occlusion during exercise. This exercise plus ischemia test consistently induced VF during control (C, vehicle) presentations. Pretreatment with flunarizine (2.5 mg/kg i.v.) completely suppressed VF in all the animals (P less than 0.001 Chi-squared). Flunarizine (F) elicited significant (P less than 0.01 ANOVA) reductions in left ventricular (LV) systolic pressure (C 143.2 +/- 12.0 F 92.3 +/- 10.5 mm Hg), LVdP/dt max (C 4256 +/- 251.9, F 1784 +/- 297.2 mm Hg/s) and heart rate (C 118.8 +/- 7.4, F 104.7 +/- 9.0 beats/min). Since heart rate can contribute significantly to the development of VF, the exercise plus ischemia test was repeated with heart rate held constant with ventricular pacing (n = 3, 230.0 +/- 10 beats/min). Flunarizine pretreatment still prevented VF under these conditions.
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PMID:The calcium channel antagonist, flunarizine, protects against ventricular fibrillation. 160 Oct 65

We have previously demonstrated that elevated intraischemic glutamate levels are insufficient, of themselves, to engender ischemic damage. Glycine and gamma-aminobutyric acid (GABA), which modulate glutamatergic activity, may also play a significant role. We compared ischemia-induced changes in glutamate, glycine, and GABA release in a selectively vulnerable region (dorsolateral striatum) to the changes occurring in a region, although rendered ischemic, is usually spared with 20 min ischemia (anterior thalamus). Regional extracellular neurotransmitter levels were measured by microdialysis before, during, and after 20 min of global ischemia induced by 2-vessel occlusion plus systemic hypotension in the rat (n = 5). Similar ischemia-induced increases in glutamate, GABA, and glycine were observed in both striatum and thalamus (19-25 fold, 43-52 fold, and 3-4 fold, respectively). During recirculation, both glutamate and GABA returned to baseline in both regions by 30 min of reperfusion. Glycine levels remained two-fold higher than baseline in the striatum but fell to baseline in the thalamus. To derive a quantitative descriptor reflecting the composite magnitude of aminoacid neurotransmitter changes with ischemia, we defined the 'excitotoxic index' as: [glutamate] x [glycine]/[GABA]. While increases in the excitotoxic index during ischemia were similar for striatum and thalamus, a marked and highly significant increase was found in the striatum compared to the thalamus at early (1 h = 91.5 +/- 27.4 and 25.1 +/- 6.3, P less than 0.01, ANOVA) as well as later recirculation times (2 h = 111.3 +/- 30.9 and 20.9 +/- 3.6, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Excitotoxic index--a biochemical marker of selective vulnerability. 167 23

Neutrophils (PMN) have been implicated as mediators of the reperfusion injury which occurs in skeletal muscle after ischemia. This study was performed to measure PMN phagocytosis and chemotaxis after 3 hr of ischemia followed by 1 hr of reperfusion in a model where a significant reperfusion injury occurred. Baseline blood samples were drawn from an ear artery from New Zealand white rabbits for PMN and serum. The right iliac and femoral arteries were clamped for 3 hr which resulted in a severe clinical reperfusion injury. Just prior to clamp release, blood was harvested from the right iliac vein. After 1 hr of reperfusion, blood was again harvested from the right iliac vein. Phagocytosis was measured by the percentage ingestion of zymosan beads by the PMN. The zymosan beads had been opsonized with baseline (b), ischemia (i), or reperfusion (r) serum. Results for phagocytosis revealed no difference for (b) PMN when opsonized by (b), (i), or (r) serum. A significant increase was seen in (i) PMN phagocytosis when (i) or (r) serum was present. Also, a significant increase in (r) PMN phagocytosis was seen when (i) serum was present (ANOVA: F = 14.47; P = 0.0002). Chemotaxis was evaluated by the number of PMN migrating across a filter. Serum obtained from (b), (i), and (r) blood samples served as the chemoattractants. Significant increases in chemotaxis were observed for (b), (i), and (r) PMN when (i) serum was used as the chemoattractant (ANOVA: F = 7.11; P = 0.0025). We conclude: (1) Rabbit PMN harvested after ischemia and reperfusion demonstrated increased phagocytosis when (i) serum was present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neutrophil (PMN) phagocytosis and chemotaxis after reperfusion injury. 174 Sep 37


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