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

The gut organs are vulnerable to injury during shock because of ischemia and reperfusion of the microcirculation. These injuries result in upper GI hemorrhage, liver dysfunction, and pancreatic and mesenteric necrosis. Toxic mediators, released via lymph drainage and with reperfusion, contribute to the failure of other organs and the development of refractory shock. Until single organ perfusion can be measured, the primary goal of care is to maintain systemic perfusion. Secondary goals are to decrease hydrogen ion accumulation, minimize pancreatic stimulation, remove hepatotoxic agents, and reduce blood bacteria. Gut ischemia is simply one piece of the puzzle in the multiple organ response to reduced systemic oxygenation and perfusion that characterizes the clinical syndrome of shock.
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PMID:Gastrointestinal complications in shock. 219 30

Efforts to reduce reperfusion injury have focused on exogenous therapies; however, endogenous attenuation of reperfusion injury can be induced by a single sublethal dose of endotoxin (ETX) prior to ischemia. The purposes of this study were to investigate (i) the early neutrophil-endothelial (PMN-EC) adherence, (ii) the associated myocardial oxidant stress, (iii) the relationship of oxidant stress to antioxidant enzyme activity, and (iv) the correlation of increased antioxidant enzyme activity to myocardial recovery following ischemia/reperfusion (I-R) injury at 36 hr. Rats were administered a sublethal dose (2% of LD50) of endotoxin (500 micrograms/kg, ip, Salmonella typhimurium). At 6 hr, myocardial neutrophil accumulation (histology), hydrogen peroxide (H2O2) levels, and myocardial tissue glutathione (glutathione and oxidized glutathione) levels were determined. At 24 hr myocardial tissue glutathione levels and catalase (CAT) activity were assayed. At 36 hr, myocardial tissue superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase, and glucose-6-phosphate dehydrogenase (G-6-PD) were assayed. At 36 hr, hearts were subjected to a standard (20 min, global, 37 degrees C) ischemic insult followed by reperfusion. At 40 min of reperfusion, ventricular function was assessed (ventricular balloon; ventricular developed pressure +dP/dt, and -dP/dt).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of endogenous tissue antioxidant enzyme activity attenuates myocardial reperfusion injury. 219 33

Twenty hogs were administered the following procedures before, during, and after overdistraction of the spinal column at T5-T6: somatosensory (SEP) and neurogenic-motor evoked potentials (NMEPs), hydrogen clearance procedures, Stagnara wake-up tests, and aortic-injection of silastic plastic. To ensure that overdistraction was possible, a nonosseous, circumferential osteotomy was made at T5-T6 and distraction applied in one-ratchet increments using Harrington instrumentation. Overdistraction was maintained for 3, 5, 6, 10, 15, 20, 25, or 30 minutes. Results indicated that the duration of overdistraction, as represented by lost NMEPs, was always correlated with the animal's clinical status on wake-up test. If overdistraction was maintained more than 6 minutes, 100% of the animals demonstrated positive wake-up results; if maintained between 5 and 6 minutes, 75% demonstrated positive wake-up results; and if maintained less than 5 minutes, only 25% demonstrated positive wake-up results. Time-to-loss of the NMEPs and SEPs, after onset of overdistraction, fell within two groups: slow and fast. In the slow group, it required slightly more than 20 minutes (mean = 20.6) for the potentials to be lost, while in the fast-loss group data were lost in slightly less than 4 minutes (mean = 3.6). Blood flow studies and inspection of the spinal cord revealed that the mechanism of action for the slow group appeared to be ischemia of the spinal cord that extended several centimeters above and below the site of maximum distraction. In the fast-loss group, it appeared that gross structural damage, with some very localized ischemia, were the mechanisms of actions influencing the integrity of the spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between duration of spinal cord ischemia and postoperative neurologic deficits in animals. 221 5

Epilepsy complicates severe head trauma. Development of persistent seizures appears to correlate with the extent of trauma. Although early reports suggested that prophylactic administration of antiepileptic drugs would prevent epileptogenesis, controlled studies have failed to corroborate this assumption. Head trauma initiates a sequence of responses that includes altered blood flow and vasoregulation, disruption of the blood-brain barrier, increases in intracranial pressure, focal or diffuse ischemia, hemorrhage, inflammation, necrosis, and disruption of fiber tracts. The presence of an intracranial hematoma has a robust association with the development of post-traumatic epilepsy. Extravasation of blood is followed by hemolysis and deposition of heme-containing compounds into the neuropil, initiating a sequence of univalent redox reactions and generating various free radical species, including superoxides, hydroxyl radicals, peroxides, and perferryl ions. Free radicals initiate peroxidation reactions by hydrogen abstraction from methylene groups adjacent to double bonds of fatty acids and lipids within cellular membranes. Intrinsic enzymatic mechanisms for control of free radical reactions include activation of catalase, peroxidase, and superoxide dismutase. Steroids, proteins, and tocopherol also terminate peroxidative reactions. Tocopherol and selenium are effective in preventing tissue injury initiated by ferrous chloride and heme compounds. Treatment strategies for prevention or prophylaxis of post-traumatic epilepsy must await absolute knowledge of mechanisms. Antioxidants and chelators may be useful, given the speculation that peroxidative reactions may be an important component of brain injury responses. However, potential treatment strategies involving gamma-aminobutyric acid (GABA) agonists, NMDA receptor antagonists, and barbiturates need further scientific assessment.
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PMID:Post-traumatic epilepsy: cellular mechanisms and implications for treatment. 222 73

Blood flow of the colon and the ileum was measured before and after intestinal devascularization by laser Doppler velocimetry and the hydrogen gas clearance technique in 10 dogs in order to evaluate the clinical usefulness of laser Doppler velocimetry. The submucosal blood flow of the colon and the ileum measured by the hydrogen gas clearance method was significantly decreased, as was the subserosal blood flow of both sites measured by laser Doppler velocimetry. There was a linear relationship between the flow values using the two methods both in the colon (r = 0.7192, p less than 0.001) and in the ileum (r = 0.7646, p less than 0.001). These data suggested laser Doppler velocimetry may be a useful method to assess the degree of intestinal ischemia because of its noninvasiveness and good correlation with submucosal blood flow by the hydrogen gas clearance technique.
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PMID:Comparison of blood flow assessment between laser Doppler velocimetry and the hydrogen gas clearance method in ischemic intestine in dogs. 224 Mar 85

Blood granulocyte-mediated reactions involving generation of oxygen-derived free radicals have recently been shown to be capable of causing injury to the lungs. These findings suggest a similar mechanism also to be involved in the development of pulmonary ischemia/reperfusion injury. In the present study, therefore, the effects of three oxygen-derived free radical scavengers, superoxide dismutase (SOD; 1 mg/kg), catalase (20,000 IU/kg) and allopurinol (45 mg/kg), were evaluated during reperfusion in a rabbit model after 2 h normothermic ischemia of the lung. During reperfusion, ischemic lungs were found to have an elevated pulmonary vascular resistance, increased total and extravascular lung water content, and decreased arterial oxygen tension (PaO2) compared to control animals. SOD and catalase, but not allopurinol, were able to reduce pulmonary injury by lowering the pulmonary vascular resistance, but could not prevent pulmonary damage as shown by total lung water (TLW) or PaO2. It is concluded that oxygen-derived free radicals such as hydrogen peroxide and the superoxide anion may play an important role in precipitating pulmonary injury after ischemia. The failure of xanthine oxidase inhibition (allopurinol) to exert protective effects may suggest that oxygen-derived free radical generation following pulmonary ischemia occurs predominantly via leukocyte-mediated reactions.
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PMID:Pulmonary reperfusion injury: evidence for oxygen-derived free radical mediated damage and effects of different free radical scavengers. 228 47

Striatal microdialysis was performed in rats subjected to 20 min of transient forebrain ischemia produced by occlusion of the carotid arteries during hemorrhagic hypotension. Extracellular changes of dopamine, serotonin, and their metabolites were monitored before, during, and after the ischemic insult at 10-min intervals by on-line HPLC analysis. During ischemia, extracellular dopamine increased dramatically (156 times baseline), as did 3-methoxytyramine (3-MT), whereas 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) decreased (15-25% of baseline). Upon reperfusion, dopamine was cleared from the extracellular fluid within 40 min and reached a stable level (70% of baseline). DOPAC and HVA increased (250-330%) transiently and reached their maximum 1 h following reperfusion, whereas 3-MT decreased to undetectable levels within 20 min. Although baseline levels of serotonin were not detectable, serotonin and 5-hydroxyindoleacetic acid showed a qualitatively similar temporal pattern to dopamine and its acid metabolites. Killing rats by cervical dislocation produced changes in extracellular dopamine, serotonin, and their metabolites that were almost identical to those seen during ischemia. Pargyline pretreatment 2 h before ischemia had marginal effects on the postischemic clearing of dopamine. The pargyline pretreatment, however, did increase the survival rate of rats subjected to ischemia, and this protective effect might be due to the pargyline-induced blockade of the post-ischemic monoamine oxidase-mediated increase in dopamine metabolism and the concurrent production of the potentially neurotoxic molecule, hydrogen peroxide.
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PMID:Effects of transient forebrain ischemia and pargyline on extracellular concentrations of dopamine, serotonin, and their metabolites in the rat striatum as determined by in vivo microdialysis. 230 12

Since hydrogen peroxide (H2O2) can react with ferrous iron (FE++) to form the more toxic hydroxyl radical (OH) in vitro, and since H2O2 is generated brain xanthine oxidase (XO) during ischemia/reperfusion (I/R), we hypothesized that gerbils depleted of iron by dietary restriction or treated with iron chelators would be less susceptible to I/R injury. We found that gerbils fed a low iron diet for 8 weeks had decreased brain and serum iron levels, less neurologic deficits, and decreased brain edema after temporary unilateral carotid ligation (ischemia) and then reperfusion than gerbils fed a control standard iron diet. In addition, brains from gerbils treated with iron-free deferoxamine (an iron chelator), but not iron-loaded deferoxamine, had decreased (P less than .05) brain edema following ischemia and reperfusion. The results indicate that iron may contribute to cerebral ischemia/reperfusion damage.
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PMID:Iron depletion or chelation reduces ischemia/reperfusion-induced edema in gerbil brains. 230 92

The effect of neocuproine on cardiac injury was studied using retrogradely perfused isolated rat hearts in two experimental systems. In the first system, where hydrogen peroxide-induced damage was studied, neocuproine at the range of 40-175 microM provided protection at the level of 70-85%, as demonstrated by the reduced loss in the peak systolic pressure (P), in +dP/dt and in -dP/dt. In the second system, where ischemia/reperfusion-induced arrhythmias were studied, neocuproine (42 microM) provided a marked protection against cardiac injury as demonstrated by the lowering of the incidence in irreversible ventricular fibrillation, by decreasing the duration of ventricular fibrillation and by the concomitant increase of the duration of normal sinus rhythm, and by improving the post-ischemic recovery of P, +dP/dt and -dP/dt. Free radicals have already been implicated as causative agents in cardiac injury resulting from either hydrogen peroxide or ischemia followed by reperfusion. Additionally, iron and copper have already been shown to drastically exacerbate the injurious effects of free radicals. Thus, the results reported here with neocuproine, a highly effective chelator for both iron and copper, as well as with adventitious copper and with the combination of neocuproine and copper, are in accord with the mediatory role of transition metals in enhancing the deleterious effects induced by free radicals.
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PMID:The protective role of neocuproine against cardiac damage in isolated perfused rat hearts. 233 93

The purpose of this study was to determine the changes in cardiac interstitial fluid (ISF) purine metabolites during 90 min of regional myocardial ischemia. To collect ISF metabolites and measure local coronary blood flow (CBF), cardiac microdialysis probes were implanted into the left anterior descending artery (LAD) and left circumflex artery (LC) perfused myocardium of chloralose-urethane anesthetized dogs (n = 7). Regional ventricular wall thickness was measured in the LAD and LC perfused regions with sonomicrometric crystals, using systolic wall thickening (SWT) as an index of regional ventricular function. Regional myocardial ischemia, produced by occlusion of the LAD, resulted in a decrease in CBF (hydrogen clearance) from 77.3 +/- 12.4 to 10.9 +/- 4.4 ml/min/100 g (P less than 0.05), and systolic wall thinning (control SWT = 15.5 +/- 2.2%; ischemic SWT = -6.8 +/- 1.7%). ISF adenosine was transiently elevated in the ischemic region, obtaining a maximum sixfold increase after 15 min of ischemia. Inosine, hypoxanthine, and to a lesser extent xanthine, composed the majority of metabolites which accumulated in the ISF of the ischemic region, accounting for greater than 95% of the total purine metabolites in the ISF after 20 min of ischemia. Despite the marked increase in ISF inosine, hypoxanthine, and xanthine levels, ISF uric acid levels did not increase in the ischemic region. Although CBF and SWT did not change in the nonischemic LC perfused area, there were small transient increases (two- to fourfold) in ISF adenosine, inosine, and hypoxanthine levels. In summary, these data demonstrate that purine metabolites accumulate rapidly in the ISF during myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interstitial purine metabolites during regional myocardial ischemia. 235 25


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