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

The purpose of this study was to determine whether gamma-hydroxybutyrate provides protection against intestinal ischemia/reperfusion injury and to compare its effect with that of allopurinol and vitamin E. Thirty minutes of total regional ischemia, followed by 3 hours of reperfusion, produced intestinal damage that was completely prevented by gamma-hydroxybutyrate pretreatment. Naloxone partially blocked this protective effect. Allopurinol provided only partial protection against this injury, whereas vitamin E provided none. Treatment with gamma-hydroxybutyrate after ischemia but before reperfusion also provided significant protection. This study clearly demonstrates that gamma-hydroxybutyrate provides significant protection against intestinal ischemic injury and that it may do so via an opiate receptor-mediated mechanism.
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PMID:The protective effect of gamma-hydroxybutyrate in regional intestinal ischemia in the hamster. 237 90

The effect of dietary vitamin E on the fetal ischemic distress induced by clamping the uterotubal vessels of pregnant rats was studied. The fetal heart rate was measured by the pulsed doppler technique as an index of fetal distress induced by ischemia. On reperfusion after clamping the vessels for 9 min, the decreased fetal heart rate was restored to normal rapidly and completely in the E-supplemented group, but slowly and incompletely in the E-deficient and control groups. On reperfusion after ischemia, the amounts of lipid peroxides, measured as thiobarbituric acid (TBA)-reactive substances, were greatly increased in the fetal brain and liver and in the placenta of in the E-deficient and control groups, but not in the E-supplemented group. The vitamin E concentrations in fetal tissues were less than 10% of those in the maternal tissues. Significant differences were found in the vitamin E concentrations in the maternal serum and liver in the three groups of rats given diet containing different amounts of vitamin E for 2 weeks. No significant differences were found between the vitamin E-deficient and control groups in the levels of vitamin E in the fetal brain and liver and the placenta, but these levels were significantly lower than those in the E-supplemented group.
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PMID:Protective effect of vitamin E on fetal distress induced by ischemia of the uteroplacental system in pregnant rats. 237 64

Peroxidation of myocardial-membrane phospholipid is considered an important pathogenic component of heart muscle damage in ischemia and reperfusion. The extent to which membrane alpha-tocopherol (vitamin E) in the heart can modulate such damage and protect against it is a matter of controversy. The relative alpha-tocopherol deficit of spontaneously-hypertensive (SH) rat myocardium as compared to the myocardium of the Wistar-Kyoto (W/K) normotensive parent strain prompted use of these animals to identify and characterize any protective antiperoxidant role of endogenous, myocardial-membrane alpha-tocopherol. With exposure to a superoxide- and iron-containing initiator of peroxidation, the membrane complements from the ventricular myocardia of the SH rat and the W/K parent strain were found to have very different peroxidative-injury profiles. SH-rat myocardial membrane demonstrated a marked sensitivity to peroxidation as reflected in the acute onset and rapid progression of phospholipid damage. The greater susceptibility of SH-rat myocardial membrane to free-radical attack could not be explained by inter-strain compositional differences in membrane polyunsaturated fatty acids or fatty aldehydes. Rather, the basis for the enhanced peroxidation was identified as the 3-fold lower alpha-tocopherol content of SH-rat myocardial membrane with respect to the heart-muscle membrane from the normotensive animal. The relative alpha-tocopherol deficit not only increased the susceptibility of SH-rat cardiac membrane to damage under pro-oxidant conditions, but also reduced the efficacy of exogenously supplied antioxidant intervention. These findings demonstrate that membrane alpha-tocopherol tone is a critical protectant of myocardial phospholipid against oxidative injury and acts as a determinant of the course of heart-membrane peroxidative damage.
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PMID:Oxidative injury to myocardial membrane: direct modulation by endogenous alpha-tocopherol. 255 23

We investigated whether vitamin E plays a role in the protection against potential free radical formation and related biochemical changes in hypoxic, ischemic and Ca(2+)-depleted rat heart upon normal reperfusion. In the heart of normally fed rats a decrease in the activity of superoxide dismutase and the capacity of the glutathione system, factors of the cellular protective mechanisms against free radicals, occurred upon exposure to the above mentioned treatments. This decrease was not further enhanced if vitamin E-deficient rat hearts were treated. Vitamin E-deficiency, however, led to detectable peroxidation of lipids if Ca(2+)-depleted or hypoxic hearts were reperfused. Lipid peroxidation was measured as the formation of thiobarbituric acid reactive material, which is readily formed during this process. Reflow after ischemia did not induce lipid peroxidation either in normal or in vitamin E-deficient rat heart. Since changes in Ca(2+)-homeostasis are thought to be primarily responsible for the Ca(2+)-reperfusion injury, a role for Ca(2+)-ions in lipid peroxidative processes, either directly or indirectly, seems indicated. Furthermore the results imply that even a sharp and extensive decrease of reduced glutathione, as seen upon Ca(2+)-repletion after a period of Ca(2+)-depletion, does not necessarily induce peroxidation of lipids in heart tissue. Obviously, vitamin E is very important in the protection of cardiac membranes. Replenishment of the water-soluble protective factors in the heart seems, however, more important during above mentioned treatments, especially since repair of the vitamin E-free radical is dependent on water-soluble factors.
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PMID:The effect of vitamin E-deficiency in isolated rat heart on the cellular defence system against free radicals during normal reperfusion after hypoxic, ischemic and Ca(2+)-free perfusion. 257 38

The author of this report has studied peroxide lipid and evoked potentials of the spinal cord during ischemia and after reperfusion. In addition, he has studied effects of vitamin E (V.E.) upon ischemic spinal cord. The ischemia of the spinal cord was experimentally produced by clamping the thoracic aorta of Wistar rats and subsequently removing the clamps. Wistar rats were given diet containing 2 IU/100 g (control group) or 50 IU/100 g (V.E. group) of alpha-tocopherol acetate for 6 weeks before experiments. In the V.E. group the quantity of thiobarbituric acid reactive substance (TBARS) in the spinal cord after clamp removal was lower than the control group. The V.E. content in the spinal cord indicated a negative correlation to the TBARS values. The evoked spinal potentials in both groups disappeared due to spinal cord ischemia. The control group displayed wave form loss earlier than the V.E. group. It is conceivable that lipid peroxidation correlate to the tissue damage following spinal cord ischemia and reperfusion, and V.E. has the preventive effect to the damage.
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PMID:[Peroxide lipid and evoked spinal potentials in experimental spinal cord ischemia]. 258 41

A study was made of the protective effects of several drugs (mannitol, phenytoin, vitamin E and dexamethasone) on the electrical activities of guinea pig hippocampal neurons in vitro when they were treated with a bathing medium deprived of both oxygen and glucose. Using guinea pig hippocampal slices, antidromic field potentials in the granular cell layer of the dentate gyrus were recorded stimulating mossy fibers. A model of ischemia in vivo in the slices was achieved by removing both oxygen and glucose from the perfusing medium. In standard medium, after 10 min of both oxygen and glucose deprivation, the field potentials exhibited minimum recovery with an amplitude of 6% of the control after 60 min. The protective effect of the drugs was evaluated by recovery of the field potential amplitude of the 60 min post-deprivation response and histological examination of the brain slice tissue. Drugs were added during 30 min of pre-deprivation and during deprivation. In this experiment we demonstrated that (1) phenytoin and vitamin E clearly showed protective action against neuronal damage caused by both oxygen and glucose deprivation in guinea pig hippocampal slices, (2) combined application of these drugs was more effective, and (3) mannitol showed no protective action in vitro. It was also demonstrated that (4) the dentate antidromic field response can be a useful index of cell death.
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PMID:Actions of brain-protecting substances against both oxygen and glucose deprivation in the guinea pig hippocampal neurons studied in vitro. 259 19

The paper studies intensification of lipid peroxide oxidation in separate brain structures (the medulla oblongata, cerebellum, visual and sensomotor cortex), synaptosomal and mitochondrial fractions under hypoxia. It has been established that acute hypoxia increases accumulation of lipid peroxidation (LPO) products, hydroperoxide and malonyl dialdehyde. Intensification of LPO in synaptosomes and mitochondria is more pronounced as compared to the whole structures. Preliminary treatment with antioxidants (vitamin E and ionol) considerably suppressed LPO intensity under both hypoxia and hypoxia with reoxygenation. Intensification of LPO in synaptosomes and mitochondria is suggested to be the key point in structural-functional disturbances of the nervous system under hypoxia and ischemia.
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PMID:[Lipid peroxidation in the synaptosomal and mitochondrial fractions of separate brain structures in hypoxia]. 271 68

Aim of this study was to confirm an increased free radical generation rate during ischemia-reoxygenation, by ultra-weak chemiluminescence detection at the surface of perfused rat heart. We observed that reoxygenation following 30 min global ischemia, induces an increase of ultraweak chemiluminescence emission in isolated perfused heart only if partial depletion of vitamin E is induced by dietary manipulation. Moreover, in normal diet fed rats, vitamin E is partially consumed during global ischemia, but not during reoxygenation. Since chemiluminescence increases during post-ischemic reperfusion, when vitamin E myocardial content is lowered, the most probable free radicals involved are the hydroperoxyl radical derivatives of lipids. These radicals, indeed, are known both to produce photoemission by disproportion and to react with vitamin E. On the other hand, the nature of the reaction that consumes vitamin E during ischemia is still obscure. Accordingly, the basal level of vitamin E myocardial content seems to be a key factor for protecting the heart against reoxygenation injury and its consumption during ischemia could be a determinant of myocardial sensitivity to oxidative stress during reperfusion.
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PMID:Increased ultra weak chemiluminescence emission from rat heart at postischemic reoxygenation: protective role of vitamin E. 275 89

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

The effect of two different combined treatments with vitamin E acetate and vitamin C on infarct size and recovery of regional myocardial function was investigated in ischemic, reperfused porcine hearts. The left anterior descending coronary artery was distally ligated in 30 thoracotomized pigs for 45 minutes followed by 3 days of reperfusion. Infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic (dye technique) myocardium. Regional myocardial function was assessed by sonomicrometry. Ten pigs received vitamin E acetate (12 gm intravenously three times for 1 week) before ischemic and vitamin C (4.4 gm intravenously) before reperfusion (therapy A). Another 10 pigs were treated with vitamin E acetate (12 gm intraarterially) and vitamin C (4.4 gm intravenously) during ischemia (therapy B). An additional 10 pigs served as a control group. Global hemodynamics did not differ significantly among the groups before and during ischemia. Mean plasma concentrations of vitamin E amounted to 107 micrograms/ml in group A, 16 micrograms/ml in group B, and 0.9 micrograms/ml in the control group at the onset of reperfusion. Therapy A reduced the size of the infarct from 73 +/- 12% to 47 +/- 16% of the region at risk (p less than 0.005) and improved regional systolic shortening from 0 +/- 7% to 11 +/- 6% at 3 days after reperfusion (p less than 0.01). Therapy B decreased the size of the infarct to 64 +/- 9% of the region at risk (p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined treatment with vitamins E and C in experimental myocardial infarction in pigs. 280 74


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