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)

The effectiveness of high-potassium cardioplegic solution in the neonatal heart remains controversial. Our previous study indicated that the protection afforded by a cardioplegic solution was inadequate in the neonatal heart. On the hypothesis that oxyradicals were responsible for the ineffectiveness of cardioplegic solution in neonatal heart, the effects of a cardioplegic solution (a modified St. Thomas' Hospital cardioplegic solution) with recombinant human superoxide dismutase on the isolated perfused neonatal guinea pig hearts (within 2 days after delivery, body weight of 60 to 120 g) were studied in comparison with those on the adult hearts (6 to 8 weeks after delivery, body weight of 300 to 500 g). After arrest induced by modified St. Thomas' Hospital cardioplegic solution, hearts were subjected to 120 min of ischemia at 20 degrees C, during which time the cardioplegic solution was injected every 30 minutes. Then the heart was reperfused for 60 minutes at 37 degrees C. Under this condition, the left ventricular developed pressure recovered to 84.4% +/- 4.0% of the preischemic value in the adult heart, whereas the recovery was only 68.1% +/- 3.1% in the neonatal heart. Thiobarbituric acid-reactive substance level, a parameter of lipid peroxidation by oxyradicals, significantly increased during ischemic arrest both in the adult and neonatal heart. However, the increase was much greater in the neonatal heart than in the adult. Cardioplegia with recombinant human superoxide dismutase (300 and 1,000 U/mL) significantly inhibited this accumulation of thiobarbituric acid-reactive substance in the neonatal heart; at 1,000 U/mL, the myocardial function of the reperfused neonatal heart recovered to the level of the adult heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection of neonatal heart by cardioplegic solution with recombinant human superoxide dismutase. 161 Feb 23

The role of lipid peroxidation and endogenous oxygen-derived free radical scavengers on ischemia-reperfusion injury and tissue recovery in rat ulcer model corresponding to the gastric histopathology was investigated. Male Wistar rats weighting 200-250 g were heparinized before occlusion of the celiac axis for 1.5 h. Endogenous CuZn-superoxide dismutase (SOD), Mn-SOD, glutathione peroxidase, fumarase, cytochrome c oxidase, and thiobarbituric acid-reactive compounds as lipid peroxidation products were measured in the gastric tissue at 3 h, and 1, 2, 4, and 7 days after release and in the controls (no occlusion). At 3 h after release, erosion of the gastric mucosa was observed, and gastric ulcers beyond the muscularis mucosae were present in the gastric body 2 days later. Seven days after release, gastric ulcers had disappeared. Activity levels for all five enzymes (CuZn-SOD, Mn-SOD, glutathione peroxidase, fumarase, and cytochrome c oxidase) were low for days 1-4 after release and did not return to control levels by the seventh day. It was observed that the ulcer formation, as evidenced by the histopathology, was significantly related to the levels of endogenous CuZn-SOD, Mn-SOD, glutathione peroxidase, fumarase, and cytochrome c oxidase activities. Thiobarbituric acid-reactive compounds were also low through the entire course of ulcer formation. The study concludes that decreases in the levels of these oxygen-derived free radical scavengers may result in the formation of gastric ulcers; however, endogenous free-radical scavengers may not correspond with tissue recovery. Lipid peroxidation may not be related to ulcer formation.
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PMID:The role of endogenous free radical scavengers on tissue recovery in the experimental ulcer model. 217 May

Ischemia followed by reflow often results in tissue injury. Although reactive oxygens seem to play an important role in the pathogenesis of postischemic reflow-induced tissue injury, the mechanism and an efficient way to inhibit oxidative injury are not known. We studied the mechanism by which hepatic transport function was inhibited by a transient occlusion followed by reflow of the portal vein and hepatic artery by using a superoxide dismutase (SOD) derivative (SM-SOD) which circulates bound to albumin with a half-life of 6 h. Occlusion of the hepatic vessels for 20 min followed by reflow for 60 min significantly inhibited transhepatic transport of cholephilic ligands, such as bromosulfophthalein (BSP) and taurocholic acid. Intravenous administration of SM-SOD markedly inhibited the reflow-induced decrease in transhepatic transport of these ligands. Thiobarbituric acid - reactive metabolites (TBAR) in the liver and plasma remained unchanged during occlusion and reflow, while TBAR in the bile increased significantly. Intravenous injection of SM-SOD inhibited the reflow-induced increase in biliary TBAR. Xanthine oxidase activity in plasma also increased during occlusion and reflow by an SM-SOD-inhibitable mechanism. Polymorphonuclear leukocyte-dependent chemiluminescence of the peripheral blood remained unchanged during occlusion, but increased markedly with time after reflow. SM-SOD also inhibited the increase in chemiluminescence almost completely. These and other results suggested that the superoxide radical and/or its metabolite(s) might play an important role in the pathogenesis of the reflow-induced liver injury and that SM-SOD might be useful for studying the mechanism for tissue injury caused by oxygen toxicity.
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PMID:Inhibition of ischemia and reflow-induced liver injury by an SOD derivative that circulates bound to albumin. 230 17

Ischemia and reperfusion is of the greatest importance in the pathology of various diseases. This study was designed to investigate the role of oxygen-derived free radicals and lipid peroxidation in gastric mucosal injury induced by ischemia-reperfusion in rats. Clamping of the celiac artery in rats reduced the gastric mucosal blood flow to 10% of that measured before the clamping. Gastric mucosal injury, such as spotty and linear hemorrhagic erosions, was seen in rats 60 min of the reperfusion following 30 min of ischemia. Thiobarbituric acid (TBA) reactants in the gastric mucosa were increased after the reperfusion. The increase in gastric mucosal lesions and TBA reactants were significantly inhibited by the treatment with SOD+ catalase and allopurinol. These results suggest that oxygen-derived free radicals and lipid peroxidation may play an important role in the pathogenesis of acute gastric mucosal lesions induced by ischemia-reperfusion.
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PMID:[Role of free radicals and lipid peroxidation in gastric mucosal injury induced by ischemia-reperfusion in rats]. 232 34

Studies were made on the influence of vitamin E on the effects of compression injury of the spinal cord associated with ischemia in rats. The motor disturbance induced by spinal cord injury was greatly reduced by vitamin E supplementation. After injury, the spinal cord evoked potentials showed greater recovery of both amplitude and latency in the vitamin E-supplemented group than in the control group. Spinal cord blood flow was promptly restored and remained normal after injury in the vitamin E-supplemented group, but was significantly decreased from 3 h after injury in the control group. Thiobarbituric acid (TBA)--reactive substances in the spinal cord was immediately increased by compression injury in both groups, and after injury it persisted at a high value for 24 h in the control group, but decreased within 1 h in the vitamin E-supplemented group. Pathological examination of the spinal cord showed less damage, such as bleeding and edema, in the vitamin E-supplemented group than in the control group. Vitamin E may have protective effects on the spinal cord by inhibiting damage induced by lipid peroxidation and/or by sustaining the blood flow by maintaining the normal metabolism of arachidonic acid.
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PMID:Protective effect of vitamin E on spinal cord injury by compression and concurrent lipid peroxidation. 275 91

Rats were subjected to cardiac arrest and resuscitation, 90 min of reperfusion, and in situ perfusion fixation. Thiobarbituric acid (TBA) was included in the aldehyde-free perfusion fixative, the TBA reaction was driven in situ by heating, and fluorescence microscopy was utilized to characterize the location of products of the TBA reaction. Absorbance-difference spectra were performed on butanol-extracted brain homogenates to confirm in situ formation of TBA adducts with aldehydic products of lipid peroxidation. Nissl-stained sections revealed good cellular fixation without shrinkage artifacts. Fluorescence was not seen microscopically when TBA was omitted from the perfusion fixative, and little fluorescence was present in normal brains or brains after ischemia only. However, after 90-min reperfusion, intense granular fluorescence was seen in the neuronal perikarya (especially at the base of the apical dendrite) of numerous pyramidal neurons in cortical layers 5 and 6 and in the pyramidal layer of Ammon's horn in the hippocampus. The nuclei of these cells exhibited no fluorescence. Fluorescence was also present in some striatal neurons, but was absent in the adjacent radial bundles. Neither glia nor white matter exhibited similar fluorescence. These observations indicate that neurons in the selectively vulnerable zones of the cortex and hippocampus are early and specific targets of lipid peroxidation during post-ischemic reperfusion.
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PMID:Fluorescent histochemical localization of lipid peroxidation during brain reperfusion following cardiac arrest. 769 May 14

The effect of ischemia-reperfusion, induced by the transient embolic agent degradable starch microspheres (DSMs) on tumor tissue was investigated from the standpoint of active oxygen species. Rabbits with VX2 carcinoma received regional infusion of DSMs by transcatheter angiography, and it was confirmed that DSMs occluded tumor vessels. Blood flow in the tumors decreased rapidly immediately after the DSM treatment and returned to the original level within 40 min. The size of tumors did not change after a single infusion of DMS, while five repeated DSM treatments led to a significant reduction in tumor size. This reduction in tumor size was prevented by the treatment of rabbits with superoxide dismutase and catalase, indicating that the generation of active oxygen species in the tumor was involved in the mechanism of action of DSMs. Thiobarbituric acid-reactive substances also increased in the tumors after DSM infusion, and this increase was also inhibited by treatment with superoxide dismutase and catalase. In conclusion, the antitumor effect of the transient embolic agent DSM is secondary to the phenomenon of ischemia-reperfusion injury. In addition, active oxygen species and lipid peroxidation are possible causes of ischemia-reperfusion injury.
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PMID:Antitumor effect of ischemia-reperfusion injury induced by transient embolization. 792 11

The resumption of blood flow to organs following ischemia may cause a further increase in tissue damage through an increase in peroxidation of lipids in cell membranes. An experimental study was conducted to investigate the prevention of reperfusion injury after testicular torsion through changes in the lipid peroxide content of the testis. Adult male albino rats were divided into 11 groups, each containing 10 rats. One group served to determine base values of the lipid peroxide content of the testis and kidney; 3 groups were subjected to unilateral testicular torsion lasting 1, 3 and 5 hours; 3 groups were subjected to detorsion following torsion lasting 1, 3 and 5 hours; 3 groups were treated with allopurinol before detorsion following torsion lasting 1, 3 and 5 hours; and 1 group underwent sham operation as a control. Thiobarbituric acid reactive products of lipid peroxidation (TBAR) were assessed in testicular and renal tissues. Testicular torsion caused a significant increase in TBAR in the testis (p < 0.01), but not in the kidneys. Detorsion caused a further significant increase in testicular TBAR (p < 0.01). Pretreatment with allopurinol prevented this further increase (p < 0.01). It is concluded that, biochemically, reperfusion injury occurs in the testis following detorsion after testicular torsion of 720 degrees lasting as long as 5 hours. Pretreatment with allopurinol before detorsion prevents such reperfusion injury.
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PMID:The effect of allopurinol pretreatment before detorting testicular torsion. 818 3

A Cypridina luciferin analog (CLA), considered to be a sensitive and specific agent for the assay of superoxide, was assessed in isolated hearts for its effects on ischemia/reperfusion injury. Hearts of anesthetized male Wistar rats were isolated and perfused with a modified Krebs-Henseleit bicarbonate buffer to serve as non-recirculating working heart preparations. After 15 min of perfusion to achieve stability, they underwent 20 min of global ischemia and were then reperfused for 30 min with or without 250 microM of CLA, dissolved in the perfusate. The incidence of ventricular fibrillation was only 13% in the CLA group, whereas it was 88% in the controls. The CLA treatment was further associated with significantly increased left ventricular developed pressure and cardiac output; and in contrast, the left ventricular end-diastolic pressure was significantly reduced, as compared with the control group. Thiobarbiturate reacting substance content in the hearts of the CLA group was significantly decreased (27.5 +/- 2.4 versus 36.9 +/- 9.7 mumol/g dry weight). This study thus indicates that CLA may be useful for alleviating ischemia/reperfusion injury (reperfusion-induced arrhythmia and damage to heart function) involving free radicals.
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PMID:Cypridina luciferin analog reduces the incidence of ischemia/reperfusion-induced ventricular fibrillation. 827 31

The peroxidation of lipids and changes in the activities of related enzymes, such as xanthine-xanthine oxidase (XOD), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) in the gastric mucosa were studied in rat model of ischemia-reperfusion with pylorus ligation. Myeloperoxidase (MPO), a marker enzyme of leucocytes, was also studied. Thiobarbituric acid reactive substances (TBA RS) in gastric mucosa were significantly increased by clamping the celiac artery for 30 min and reperfusion for 60 min after 3 h of pylorus ligation. XOD activity in gastric mucosa increased with the development of gastric mucosal injury. Allopurinol significantly suppressed XOD activity but did not inhibit mucosal injury or the increase in TBA RS. MPO activity in the gastric mucosa was significantly increased by gastric mucosal injury. Famotidine significantly inhibited the increase in MPO activity in gastric mucosa, while allopurinol did not. SOD and GSH-px activities in the gastric mucosa were decreased significantly by gastric mucosal injury. SOD activity was normal following treatment with famotidine and allopurinol. Moreover, GSH-px activity recovered to the normal level with famotidine and allopurinol treatment. These findings suggest that oxygen radicals and lipid peroxidation can cause gastric mucosal injury by ischemia-reperfusion in the pylorus-ligated rat. The generation of oxygen free radicals may be derived mainly from activated polymorphonuclear leukocytes (PMN), and the decrease in SOD and GSH-px activity in gastric mucosa seems to aggravate mucosal injury by free radicals and lipid peroxidation.
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PMID:Role of lipid peroxidation in gastric mucosal lesions induced by ischemia-reperfusion in the pylorus-ligated rat. 839 87


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