dimethyl sulfoxide/infarction

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Regulatory effect of Dimethyl Sulfoxide (DMSO) on astrocytic reactivity in a murine model of cerebral infarction by arterial embolization.

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BACKGROUND The pathophysiology of cerebral ischemia is essential for early diagnosis, neurologic recovery, the early onset of drug treatment and the prognosis of ischemic events. Experimental models of cerebral ischemia can be used to evaluate the cellular response phenomena and possible

Protective effect of dimethyl sulfoxide on acute myocardial infarction in rats.

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Dimethyl sulfoxide (DMSO) is an organic compound widely used as solvent in biological studies and as vehicle for drug administration. DMSO has been shown to possess several biological effects, including antioxidant, anti-inflammatory, antinociceptive effects, and it has been proposed to be

Treatment of cerebral infarction with dimethyl sulfoxide in the mongolian gerbil.

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Dimethyl sulfoxide (DMSO) has been reported to have beneficial effects in the treatment of central nervous system trauma, possibly due to its reported anti-inflammatory, antiedemic, anticoagulate, diuretic, hypothermic, vasodilatory, and respiratory stimulatory effects as well as an ability to

[Modeling myocardial infarct by applying dimethyl sulfoxide to the anterior surface of the heart].

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The effect of dimethyl sulfoxide (DMSO) on cerebral infarction in the Mongolian gerbil.

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Reduction of myocardial infarct size in rabbits by a novel indole derivative with antioxidant and free radical scavenging properties.

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We investigated the cardioprotective efficacy of a new compound, 3-[(1H-1-indolyl)methyl] -4-amino 4,5-dihydro-1H,1,2,4 triazole-5-thione (C6458). The effect of C6458 on the reduction of the infarct size and its protective ability against oxidative damage of the myocardium after ischemia-reperfusion

Isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin.

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BACKGROUND Volatile anesthetics are known to protect the heart against ischemia-reperfusion injury. The authors tested whether anesthetic preconditioning with isoflurane is mediated via activation of the transcription factor hypoxia inducible factor 1 (HIF-1) and evaluated the role of mammalian

Treatment of acute focal cerebral ischemia with dimethyl sulfoxide.

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The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats

Effects of intravenous dimethyl sulfoxide on ischemia evolution in a rat permanent occlusion model.

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Dimethyl sulfoxide (DMSO) has a variety of biological actions that suggest efficacy as a neuroprotectant. We (1) tested the neuroprotective potential of DMSO at different time windows on infarct size using 2,3,5-triphenyltetrazolium staining and (2) investigated the effects of DMSO on ischemia

Differential role of Pim-1 kinase in anesthetic-induced and ischemic preconditioning against myocardial infarction.

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BACKGROUND Ischemic preconditioning (IPC) and anesthetic-induced preconditioning against myocardial infarction are mediated via protein kinase B. Pim-1 kinase acts downstream of protein kinase B and was recently shown to regulate cardiomyocyte survival. The authors tested the hypothesis that IPC and

The Role of Cyclooxygenase-1 and -2 in Sevoflurane-Induced Postconditioning Against Myocardial Infarction.

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Cyclooxygenase (COX)-2 mediates ischemic pre- and postconditioning as well as anesthetic-induced preconditioning. However, the role of COX-1 and -2 in anesthetic-induced postconditioning has not been investigated. We evaluated the role of COX-1 and -2 in sevoflurane-induced postconditioning in vivo.

Cardioprotective properties of dimethyl sulfoxide during global ischemia-reperfusion of isolated rat heart.

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Cardioprotective properties of dimethyl sulfoxide (DMSO) were studied in the isolated rat heart model. Intraperitoneal administration of DMSO to animals for 3 days before the experiment, but not addition of DMSO to the perfusate, reduced infarction size. Both intraperitoneal and intracoronary

The effect of hyaluronidase and dimethyl sulfoxide (DMSO) on experimental skin flap survival.

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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

Protective effects of methyl prednisolone and dimethyl sulfoxide in experimental middle cerebral artery embolectomy.

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Acute arterial embolism continues to be a major cause of stroke morbidity in children and young adults. Potential therapy modalities include medical management and/or cerebral revascularization. The canine middle cerebral artery (MCA) was embolized by means of a pliable cylinder, 8 mm long by 1.6 mm

Protective effect of necrostatin-1 on myocardial tissue in rats with acute myocardial infarction.

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The aim of this study was to investigate the protective effect of necrostatin-1 on myocardial tissue of acute myocardial infarction (AMI) rats and to provide a basis for necrostatin-1 for the treatment of acute myocardial infarction. AMI rats (45) were established by ligating the anterior descending

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