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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neuroprotective effects of felbamate were tested in a model of incomplete cerebral ischemia and hypoxia in 7-day-old rat pups. Felbamate pretreatment (300 mg/kg) reduced the surface of infarcted cortex following bilateral carotid ligation, by 42-49% compared to saline and dimethylsulfoxide (DMSO) controls, respectively. The number of necrotic neurons in the dentate gyrus was reduced by 77% over both DMSO controls and saline controls. These results suggest that felbamate deserves further evaluation for its therapeutic potential in hypoxia-ischemia.
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PMID:Felbamate reduces hypoxic-ischemic brain damage in vivo. 160 Oct 70

To determine whether treatment with hyperbaric oxygen (HBO) or dimethyl sulfoxide (DMSO) could mitigate the fatal effects of cerebral ischemia, we anesthetized 68 gerbils with ketamine, ligated the right carotid artery (CA), and placed a snare occluder around the left CA. After 48 hours, 30 gerbils that were neurologically normal or had suffered only mild deficits were subjected to left CA occlusion without anesthesia for periods of 2 to 60 minutes. The onset of circling, posturing, falling, and lethargy began immediately; seizures and coma ensued 4 to 5 minutes later and persisted until release of the left CA occluder. All gerbils recovered after 2-minute staged bilateral CA occlusions. The mortality rate was 33% after both 5- and 10-minute occlusions and 100% after 20- and 60-minute bilateral occlusions. Twelve gerbils were placed in an HBO chamber (100% oxygen at 1.5 atmospheres) for 15 minutes during 20-minute bilateral occlusion; only 2 died (16% mortality rate). Thus, HBO therapy conferred significant protection against death from untreated ischemia (P less than 0.001). Histological examination showed that the extent of patchy bilateral ischemic neuronal damage was much less in surviving gerbils that received HBO therapy than in those that died after 20-minute occlusions. Fourteen gerbils were treated with DMSO, 2.5 g/kg intraperitoneally, during 5- or 10-minute bilateral CA occlusion; 12 died (86% mortality rate). Thus, DMSO provided no protection against fatal cerebral infarction; in fact, the results in the 10-minute reperfusion group suggest that DMSO may have a deleterious effect.
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PMID:Effect of hyperbaric oxygen therapy or dimethyl sulfoxide on cerebral ischemia in unanesthetized gerbils. 371 99

We have previously reported that the combined administration of mannitol and perfluorochemical blood substitutes is evidently effective in protecting the brain from cerebral ischemia. This experimental study was designed to develop more effective method in suppressing brain infarction than the combined treatment of mannitol and PFC. Using the "Canine model of complete ischemic brain regulated with a perfusion method" in which it is possible to control the degree of blood flow to a cerebral hemisphere via a perfusion pump, the effect of eight agents including six kinds as the free radical scavenger on cerebral ischemia was investigated. Eight agents were mannitol, vitamin E (Vit. E), dimethyl sulfoxide (DMSO), vitamin C, glycerol, nizofenone (Y-9179), dexamethasone (Dexa.) and suloctidil (MY-103). After pretreatment with each agent, blood flow was reduced via the pump to 1/10 of the normal state and 1 hour later, return to the normal state was allowed. Subsequent changes in EEG were observed and the effects of the drugs evaluated. In the control group, no recovery of electrical activity was seen, but in six groups among eight treated groups, i.e., treated with mannitol, Vit. E, DMSO, MY-103, Y-9179 and Dexa, gradual emergence of slow waves was observed. And more favorable effects were found when the combined administration of mannitol, Vit. E and Dexa was made in the same experimental schedule as compared with the single administration of each of these drugs. Furthermore in the animals administered with PFC in combination with mannitol, Vit. E and Dexa, flattening of electrical activity could not be seen throughout the period of severe ischemia. Moreover, the power of electrical activity recovered nearly to the preischemic state immediately after recirculation. Although the possible mechanisms are not yet completely clarified, the present results are thought to indicate that this new combination therapy utilizing PFC with mannitol, Vit. E and Dexa may be useful in the treatment of cerebral ischemia.
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PMID:[Experimental study of cerebral protective effect on cerebral ischemia of various antioxidants and other agents. With special reference to the combined treatment of mannitol, vitamin E, dexamethasone and perfluorochemicals]. 632 77

A beneficial effect of dimethyl sulfoxide (DMSO) in the treatment of acute focal cerebral ischemia has not been proven. In the present study, two established experimental models of acute focal cerebral ischemia were treated with DMSO. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. No improvement of EEG findings, erythrocyte transit, regional cerebral blood flow (rCBF), blood-brain barrier permeability, or morphological findings were demonstrated in the DMSO-treated cats. In a second study, 15 conscious adult baboons underwent temporary left MCA occlusion (6 or 12 hours) using an implanted occluding device. Seven baboons were not treated and 8 baboons received continuous intravenous infusions of DMSO for 10 hours beginning 30 minutes after occlusion. Four of the baboons that were treated with DMSO also were treated with pentobarbital coma for 96 hours starting 4 hours after occlusion. Analysis of the neurological scores after 1 week survival indicated that treatment with DMSO alone and DMSO and pentobarbital coma did not improve the outcome. Morphological changes were similar in the 3 groups. The findings of our investigation indicate that DMSO is ineffective in treating acute focal cerebral ischemia.
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PMID:Ineffectiveness of DMSO in treating experimental brain ischemia. 657

Aiming whether intraperitoneal administration of disulfiram (tetraethyl thiuram disulfide, DS) achieves potentially therapeutic drug concentrations in brain tissue, the behaviour of blood-brain barrier (BBB) to 14C-labelled DS in cerebral ischemia with and without simultaneous administration of dimethylsulfoxide (DMSO) was studied in Mongolian gerbils subjected to left common carotid artery (CCA) occlusion. The results indicated that: (a) the permeability of DS through the BBB was significantly enhanced in the ischemic brain during the initial 30 min duration after DS administration; (b) administration of DMSO increased the entry of DS into the ischemic brain five-fold during the first 30 min and it was significantly higher even at the 60 min sampling period; (3) in general, the content of DS in the brain was quickly reduced with time.
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PMID:Distribution of disulfiram in brain after carotid ligation in gerbils. 663 26

Hyaluronidase has been shown clinically and experimentally to reduce the effects of tissue ischemia in myocardial infarction and hemorrhagic shock. Dimethyl sulfoxide (DMSO) has been shown to reverse the effects of cerebral ischemia in the primate model. A caudally based dorsal skin flap in the rat was used to study the effects of these two drugs in physiological doses on skin flaps, and to investigate their mechanisms of action. This study demonstrates that both hyaluronidase and DMSO, which are nontoxic in physiological doses, can increase the surviving length of an experimental skin flap. It is hypothesized that these substances exert their effect by decreasing tissue edema and by aiding in the transport of nutritive substances to the flap during its acute phase.
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PMID:The effect of hyaluronidase and dimethyl sulfoxide (DMSO) on experimental skin flap survival. 663 21

Recent evidence suggests that platelet-activating factor plays a role in ischemia-induced neural injury. The Pulsinelli-Brierley four-vessel occlusion model was used to study the effect of a synthetic platelet-activating factor antagonist, BN 50739, and its solvents, either dimethyl sulfoxide or hydroxypropyl-beta-cyclodextrin, on cerebral ischemia-reperfusion. Rats were subjected to either 30 min of ischemia or 30 min of ischemia followed by 60 min of recirculation. Changes in the brain mitochondrial free fatty acid pool size, fatty acyl composition of phospholipids, and respiratory function were monitored. When the BN 50739 (2 mg of BN 50739/kg of body weight i.v.) was administered at the onset of recirculation, it significantly reversed the ischemia-induced accumulation of mitochondrial free fatty acids and loss of polyunsaturated fatty acyl chains from phosphatidylcholine and phosphatidylethanolamine while simultaneously improving mitochondrial respiration. Dimethyl sulfoxide alone decreased the mitochondrial level of malonyldialdehyde and total free fatty acid pool size, but there was no improvement in mitochondrial respiration. Hydroxypropyl-beta-cyclodextrin was reported to be pharmacologically inactive and capable of dissolving BN 50739. However, hydroxypropyl-beta-cyclodextrin alone also caused a significant increase in content of cerebral mitochondrial membrane free fatty acids and hydrolysis of phosphatidylcholine in normoxic control animals. The overall effect of BN 50739 on mitochondrial structure and energy metabolism supports the hypothesis that platelet-activating factor may play a key role in ischemia-induced cerebral injury.
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PMID:Effect of the platelet-activating factor antagonist BN 50739 and its diluents on mitochondrial respiration and membrane lipids during and following cerebral ischemia. 815 41

Progesterone (PROG) is a neurosteroid, possessing a variety of functions in the central nervous system. Exogenous PROG has been shown to reduce secondary neuronal loss in conjunction with attenuated brain edema after cerebral contusion and to reduce brain edema after focal cerebral ischemia. In the present study, we assessed the neuroprotective potential of PROG in a model of focal cerebral ischemia in the rat. Forty-eight male Wistar rats were randomly assigned to 4 groups, i.e. pretreatment with water soluble PROG, or dimethyl sulfoxide (DMSO) dissolved PROG, or DMSO as control or delayed treatment with DMSO dissolved PROG. Middle cerebral artery occlusion (MCAO) was induced by insertion of an intraluminal suture and reperfusion was performed by withdrawing the suture. Pretreatments were initiated 30 min before MCAO via intraperitoneal injection. Delayed treatment was initiated upon reperfusion following 2 h of MCAO. Infarct volume, body weight loss, and neurological deficit were measured 48 h after MCAO. Pre- and delayed treatment with DMSO dissolved PROG resulted in a 39% (P < 0.05) and 34% (P < 0.05) reduction in cerebral infarction, respectively, along with decreased body weight loss and improved neurological function as compared to control animals, whereas no statistically significant reduction in infarct volume by water soluble PROG was found. We demonstrated that administration of PROG to the male rat before or 2 hours after onset of MCAO reduces ischemic cell damage and improves physiological and neurological function 2 days after stroke. These results suggests potential therapeutic properties of PROG in the management of stroke.
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PMID:Progesterone is neuroprotective after transient middle cerebral artery occlusion in male rats. 890 74

Endogenous adenosine released locally during cerebral ischemia is neuroprotective, and agents which decrease adenosine inactivation may potentiate its protective effects. The effects of 5'-deoxy-5-iodotubercidin (5'd-5IT), an inhibitor of the adenosine-catabolizing enzyme, adenosine kinase, were studied in male Wistar rats subjected to 2 h of transient middle cerebral artery occlusion. 5'd-5IT or the vehicle (10% DMSO in saline) was administered i.p. 30 min before, and 2 h and 6 h after the induction of middle cerebral artery occlusion. The infarct volume was determine using 2,3,5-triphenyltetrazolium chloride staining 48 h after middle cerebral artery occlusion. The infarct volume was significantly reduced in rats treated with 1.85 mg/kg x 3 (57% reduction, P < 0.001) or 1.0 mg/kg x 3 (34% reduction, P < 0.05), but not 0.3 mg/kg x 3 5'd-5IT compared to vehicle-treated rats. The reduction of infarct volume was accompanied by a significant improvement in behavioral measures of neurological deficit. These data further support a role of adenosine in neuroprotection and suggest that adenosine kinase inhibition may be a useful approach to the treatment of focal cerebral ischemia.
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PMID:Adenosine kinase inhibition protects brain against transient focal ischemia in rats. 905 45

Dimethylsulfoxide (DMSO) is a common vehicle used for many drugs used in neuroprotective experiments. DMSO has many biological effects, including antiinflammatory, antioxidant, and local anesthetic effects that could be neuroprotective. To determine if DMSO is neuroprotective in ischemia, DMSO (0, 0.01, 0.03, 0.1, 0.3 and 1.0 ml) was administered intraperitoneally 30 min prior to permanent middle cerebral artery (MCA) occlusion in the rat. Twenty-four hours after MCA occlusion, brains were removed and sectioned. Mean infarction volume was significantly reduced in rats treated with 0.1, 0.3 and 1.0 ml of DMSO compared to saline controls. There was no acute effect of drug treatment upon arterial blood gasses or mean blood pressure. These results suggest that DMSO is neuroprotective in focal cerebral ischemia. Investigators must use appropriate controls when DMSO is used as a vehicle.
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PMID:Dimethylsulfoxide (DMSO) treatment reduces infarction volume after permanent focal cerebral ischemia in rats. 946 72


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