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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A laser diffraction system was used to study the deformation of RBC. This work indicated: 1. There was a decreased tendency accompanied with age increased, especially at pre-elderly period. 2. The deformability of patients with acute ischemic stroke was significantly decreased. This result emphasized that DI value should be considered as a peculiar index for diagnosis and treatment. 3. Abnormal calcium accumulation in RBC may play a crucial role in governing RBC deformability. It provided one of the basis of potential therapy of calcium antagonist. 4. The quantitative relation of deformation and SOD activity of RBC need to be researched.
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PMID:[Experimental study of erythrocyte deformation]. 147 41

To determine the efficacy of direct versus systemic administration of human recombinant superoxide dismutase (rt-SOD) in acute myocardial ischemia and reperfusion, the following experimental model was applied. Twenty-one dogs were subjected to 30 minutes normothermic global ischemia caused by the occlusion of the ascending aorta followed by 60 minutes reperfusion. To eliminate collateral blood flows during the ischemia, bipulmonary hilus were cross clamped. The dogs were randomly assigned to three groups: group A (n = 7), 12 ml of normal saline was injected through the aortic root into the coronary artery 1 minute prior to reperfusion, in addition to a 30 minute continuous infusion of 50 ml of saline into the cardiopulmonary bypass circuit beginning just after reperfusion; group B (n = 7), rt-SOD (10,000 U/kg) dissolved in 12 ml saline was administered by bolus injection through the aortic root and an additional 30,000 U/kg of rt-SOD dissolved in 50 ml of saline was injected into the cardiopulmonary bypass circuit as the same manner as the group A; group C (n = 7), the treatment was similar to the group B except the bolus injection of rt-SOD was into the cardiopulmonary bypass circuit. The left ventricular stroke work index (LVSWI) was determined by a right heart bypass technique and expressed as a percent recovery of pre-occlusion state. Morphologic structures were observed by the electron microscope. The coronary sinus blood was assessed for malondialdehyde (MDA) measured by TBA method and creatine phosphokinase (CPK). The percent of recovery of LVSWI after 60 minutes reperfusion was superior in group B (121 +/- 82%) than groups A (24 +/- 38%*, *p less than 0.05) and C (52 +/- 21%*). In group B, the myocardial cell structure had a normal appearance in most areas, but swollen mitochondria and disrupted myofibrils were observed in groups A and C. Serum MDA levels did not change in all groups. Increasing CPK levels after reperfusion were less in group b than group A. These results suggest that an adequate concentration of rt-SOD in the interstitial fluid or cell surface at the time of reperfusion may be required to prevent reperfusion injury.
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PMID:[Effective administration method of recombinant superoxide dismutase in acute myocardial ischemia and reperfusion]. 221 72

To determine which biochemical entity of the red cell is responsible for preventing augmented postischemic myocardial oxygen consumption (MVO2), 28 canine hearts instrumented with ultrasonic dimension crystals underwent simultaneous determination of stroke work (SW) and MVO2 during incremental volume loading on right heart bypass before and 30 min after 2 hr of 10 degrees C cardioplegic arrest with unmodified oxygenated crystalloid cardioplegia (OC), OC with histidine of equal buffering capacity as 18% hematocrit blood (OC + H), or OC with 200 units/ml of superoxide dismutase and catalase (OC + SOD/C). In all groups, the slope of the linear SW vs end-diastolic volume relationship, Mw, and the slope of the linear SW vs MVO2 relationship, Me, were unchanged after cardioplegic arrest. The intercept of the SW vs MVO2 relationship, Eo, was augmented an average of 22.2% in the OC group, but both OC + H and OC + SOD/C prevented this subtle expression of ischemic injury. The characteristic of the red cell most likely responsible for the myoprotective efficacy of blood cardioplegia is buffering capacity; however, since the effects of tissue acidosis are partially mediated by free radicals, the use of free radical scavengers can also ameliorate ischemic damage incurred during cardioplegic arrest.
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PMID:Upgrading acellular to sanguineous cardioplegic efficacy. 273 17

Bromocriptine, a dopamine D2 receptor agonist, has widely been used for patients with Parkinson's disease. In this study, we examined its neuroprotective effects against neuronal damage in the CA1 subfield of the hippocampus following experimental cerebral ischemia in the Mongolian gerbil. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries for 3 min. Bromocriptine, at a dose of 0.3 or 3 mg/kg, was injected i.p. 30 min before the onset of ischemia. Histopathological observations showed that neuronal damage to hippocampal CA1 neurons, which was seen 7 days after ischemia in vehicle-treated animals, was prevented by bromocriptine treatment. Immunohistochemical staining for copper/zinc superoxide dismutase and manganese superoxide dismutase decreased markedly in the CA1 neurons of vehicle-treated animals 2 days after ischemia when histological neuronal destruction was not yet seen, but was well preserved in bromocriptine-treated animals. The present findings show that bromocriptine protects against ischemia-induced neuronal damage, and that the mechanism of the neuroprotection may relate to the preservation of SODs. Bromocriptine, which was recently shown to be a potent free radical scavenger, may have a potent neuroprotective action against disorders including ischemic stroke.
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PMID:Bromocriptine protects against delayed neuronal death of hippocampal neurons following cerebral ischemia in the gerbil. 775 51

Increased levels of CuZn superoxide dismutase (SOD-1) are cytoprotective in experimental models of neurological disorders associated with free radical toxicity (e.g. stroke, trauma). Targeted delivery of SOD-1 to central nervous system neurons may therefore be therapeutic in such diseases. The nontoxic C-fragment of tetanus toxin (TTC) possesses the nerve cell binding/transport properties of tetanus holotoxin and has been used as a vector to enhance the neuronal uptake of proteins including enzymes. We have now produced a recombinant, hybrid protein in Escherichia coli tandemly joining human SOD-1 to TTC. The expressed hybrid protein (SOD:Tet450) has a subunit molecular mass of 68 kDa and is recognized by both anti-SOD-1 and anti-TTC antibodies. Calculated per mol, SOD:Tet450 has approximately 60% of the expected SOD-1 enzymatic activity. Analysis of the hybrid protein's interaction with the neuron-like cell line, N18-RE-105, and cultured hippocampal neurons by enzyme immunoassay for human SOD-1 revealed that SOD:Tet451 association with cells was neuron-specific and dose-dependent. The hybrid protein was also internalized, but there was substantial loss of internalized hybrid protein over the first 24 h. Hybrid protein associated with cells remained enzymatically active. These results suggest that human SOD-1 and TTC retain their respective functional properties when expressed together as a single peptide. SOD:Tet451 may prove to be a useful agent for the targeted delivery of SOD-1 to neurons.
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PMID:CuZn superoxide dismutase (SOD-1):tetanus toxin fragment C hybrid protein for targeted delivery of SOD-1 to neuronal cells. 779 32

We studied free radical, lipid peroxide (LPO) and antioxidant levels of blood in three cases with mitochondrial encephalomyopathy. Case 1 was a 17-year-old man with MELAS. Serum vitamin E levels were decreased and LPO levels were increased after stroke-like episodes in case 1. Case 2 was a 68-year-old woman with MELAS and a maternal elder aunt of case 1. She showed an elevated serum LPO levels (6.58 nmol/ml) in the absence of stroke-like episode and serum CoQ10 level was 0.54 microgram/ml before therapy. By CoQ10, idebenone and tocopherol nicotinate therapy, serum LPO levels decreased gradually in parallel with the decrease of lactate and pyruvate levels. Free radicals were measured in case 2 and controls by spin trapping method. Hydroxyl radical and C center radical were increased and H radical was normal in blood. But these free radicals in serum were all normal. Her serum antioxidants revealed an elevated percent inhibition of SOD and a decreased transfferin level. Case 3 was a 52-year-old woman with MERRF. She showed an elevation of serum LPO (12.8 nmol/ml). Her serum antioxidants revealed an elevated vitamin E and ceruloplasmin levels and percent inhibition of SOD.
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PMID:[Free radical, lipid peroxide and antioxidant in mitochondrial encephalomyopathy]. 795 20

A new histofluorescence method by HPAA (p-hydroxyphenyl acetic acid) for free radicals in the brain tissue was devised to study neuronal damage induced by ischemia. Cerebral ischemia was produced in rats by injection of plastic microspheres and arachidonic acid (AA) into the right carotid artery. The concentration of malondialdehyde (MDA; free radical) in cerebral cortex of aminotriazol (an H2O2-dependent inhibitor of catalase) treated rats 2 h after stroke was 6.33 times the level before infarction, while the concentration of MDA in h-r SOD (free radical-scavenging enzyme) treated rats 2 h after stroke was significantly lower than in untreated rats. The histochemical findings demonstrated marked H2O2 production around blood vessels occluded by microspheres in the cerebral cortex of the aminotriazole treated rats 2 h after stroke together with disruption of the BBB. Light microscopical findings demonstrated extensive edematous changes in the aminotriazole treated rats 2 h after stroke, while pathological damage in SOD treated rat brains was absent or minimal. We conclude that free radicals are formed during ischemia, and that AA appears to be a major source of activated oxygen radicals. The findings indicate that SOD is protective against ischemia-induced neuronal damage.
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PMID:Histochemical demonstration of free radicals (H2O2) in ischemic brain edema and protective effects of human recombinant superoxide dismutase on ischemic neuronal damage. 797 74

A rapid increase in the need to explore the molecular basis of cellular function and injury in the central nervous system has led neuroscientists to employ transgenic mouse technology. The successful making of transgenic mice (Tg) overexpressing human CuZn-superoxide dismutase (SOD-1) activity has made it possible to investigate the role of oxygen free radicals in ischemic and traumatic brain injury in a molecular fashion. It has been demonstrated that the 3-fold increase in SOD-1 transgene activity in SOD-1 Tg mice offers protection against cerebral ischemia and reperfusion in two different models of focal cerebral ischemia, as compared to nontransgenic wild-type littermates. Studies involving traumatic brain injury have also demonstrated that acute injuries, including brain edema and blood-brain barrier permeability, are significantly reduced in SOD-1 Tg mice. Furthermore, chronic neurological deficits, such as beam walking, beam balance, and body weight, are significantly improved in these transgenic animals following traumatic brain injury. In addition to the SOD-1 Tg mice being a useful tool for the study of CNS injury, targeted disruption of the mouse gene for mitochondrial manganese SOD (SOD-2) has been successful. These SOD-2 knockout mutant mice, in addition to the recently developed knockout mutants of neuronal nitric oxide synthase (NOS), are believed to offer a unique opportunity to elucidate the oxidative mechanisms in brain injury following stroke and trauma.
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PMID:Transgenic mice and knockout mutants in the study of oxidative stress in brain injury. 859 9

1. Enzyme activities and contents of manganese and copper-zinc superoxide dismutase (Mn-, Cu/Zn-SOD) and oxygen free-radical scavengers were determined in the myocardium (right, left ventricle) and brain (cerebral cortex, hippocampus) of 15 and 31 week old stroke-prone spontaneously hypertensive rats (SHRSP). 2. In 15 week old SHRSP myocardium, both Mn- and Cu/Zn-SOD activities were higher but in 31 week old SHRSP, these were lower than that in Wistar-Kyoto (WKY) rats. Further, correlation between Mn-SOD content and activity in 31 week old SHRSP myocardium showed that specific activity was lower than that in WKY. 3. In 15 and 31 week old SHRSP cerebral cortex and hippocampus, SOD content and activity showed a tendency to be lower than that in WKY. 4. These results indicate that enzymatically inactive or low-active Mn-SOD protein exists in SHRSP myocardium, and that the alteration of SOD may be one of the causative factors for the vulnerability of the myocardium and brain against O2-radicals.
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PMID:Regional distribution of superoxide dismutase in the brain and myocardium of the stroke-prone spontaneously hypertensive rat. 907 37

Regional distribution and age-related change of Mn-, Cu/Zn-superoxide dismutase (SOD) and constitutive type of nitric oxide synthase (NOS) activities in the brain were determined using stroke-prone spontaneously hypertensive rats (SHRSP). In the hippocampus (HIP), Mn- and Cu/Zn-SOD activities in SHRSP of 31-week-old were significantly lower than those of 15-week-old or normotensive rats (WKY). From Mn-SOD immunohistochemical staining of several subfields of the HIP, our results suggested that SHRSP hippocampal CA1 was more vulnerable to oxidative stress compared with WKY and other subfields. In the 31-week-old SHRSP cerebral cortex (CC), the activities of Mn-, Cu/Zn-SOD and NOS were significantly lower than those in WKY. At this age, most of the SHRSP developed cerebral injuries. These observations indicated that hypertensive vascular disease observed in the SHRSP CC resulted from the decreased antioxidant capacity that is closely associated with the development of stroke and, in turn, shortened life span.
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PMID:Age-related change of antioxidant capacities in the cerebral cortex and hippocampus of stroke-prone spontaneously hypertensive rats. 1050 47


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