cyanide/инфаркт

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Macroscopic enzyme histochemistry in myocardial infarction: use of coenzyme, cyanide, and phenazine methosulphate.

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Transversely sectioned human heart slices, obtained at necropsy from normal subjects and from cases of recent myocardial infarction, were stained with the nitroblue tetrazolium (NBT) dehydrogenase macroreaction for the gross identification of recent myocardial infarction. The addition of

Methylene blue treatment delays progression of perfusion-diffusion mismatch to infarct in permanent ischemic stroke.

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Stroke is a leading cause of morbidity and mortality in the world. Low-dose methylene blue (MB), which has been used safely to treat methemoglobinemia and cyanide poisoning in humans, has energy enhancing and antioxidant properties. We tested the hypothesis that methylene blue treatment delays

Cerebral energy metabolism in cyanide encephalopathy.

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This study documents the effects of an intracarotid artery injection of a lethal threshold amount of KCN (2.5 mg.kg-1) on the energy metabolism and histology of the rat brain. This dose of KCN resulted in a rapid abolition of electroencephalographic activity, which remained essentially absent for up

Both metabolic inhibition and mitochondrial K(ATP) channel opening are myoprotective and initiate a compensatory sarcolemmal outward membrane current.

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BACKGROUND Blockade of oxidative phosphorylation may activate ATP sensitive mitochondrial potassium (mitoK(ATP)) channels. We examined whether both metabolic inhibition and mitoK(ATP) channel openers protect both the whole organ and isolated cells from ischemia. RESULTS Using a Langendorff

Uncoupling of the Electron Transport Chain Compromises Mitochondrial Oxidative Phosphorylation and Exacerbates Stroke Outcomes.

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Mitochondrial dysfunction is known to be implicated in stroke, but the complex mechanisms of stroke have led to few stroke therapies. The present study to disrupted mitochondrial oxidative phosphorylation through a known electron transport chain (ETC) uncoupler, Carbonyl cyanide-4

L-cis diltiazem attenuates intracellular Ca(2+) overload by metabolic inhibition in guinea pig myocytes.

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We have previously demonstrated that treatment with L-cis diltiazem reduced cardiac infarct size in vivo. To examine the effect of L-cis diltiazem on Ca(2+) overload induced by ischemia/reperfusion, we used a model for Ca(2+) overload produced by metabolic inhibition in isolated guinea pig myocytes.

Detection of Mercury in Human Organs and Hair in a Case of a Homicidal Poisoning of a Woman Autopsied 6 Years After Death.

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In the described case of the death of a 53-year-old woman, no toxicological examination was performed directly after death (only an anatomopathological autopsy), although symptoms of serious gastrointestinal disturbances had been present (the woman had been hospitalized twice in the course of

Reactive oxygen species generated by mitochondrial injury in human brain microvessel endothelial cells.

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Generation of reactive oxygen species (ROS) and their detrimental effects on the brain after transient ischemia are widely recognized. We studied ROS production from mitochondria in human brain microvessel endothelial cells (HBEC) under chemical hypoxia. HBEC in confluent conditions were incubated

The Effects of Methylene Blue on Autophagy and Apoptosis in MRI-Defined Normal Tissue, Ischemic Penumbra and Ischemic Core.

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Methylene blue (MB) USP, which has energy-enhancing and antioxidant properties, is currently used to treat methemoglobinemia and cyanide poisoning in humans. We recently showed that MB administration reduces infarct volume and behavioral deficits in rat models of ischemic stroke and traumatic brain

B vitamin therapy for homocysteine: renal function and vitamin B12 determine cardiovascular outcomes.

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Therapy to lower homocysteine with B vitamins does reduce the risk of stroke, if not myocardial infarction. The apparent lack of efficacy of vitamin therapy in most of the large clinical trials was probably determined by the failure to take account of the metabolic deficiency of vitamin B12, which

Intranuclear ubiquitin immunoreactivity in the pigmented neurons of the substantia nigra in fire fatalities.

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To evaluate the significance of immunohistochemical staining of ubiquitin (heat shock protein) in the midbrain for medico-legal investigation of death in fires, we examined forensic autopsy cases of fire fatalities (n = 35) in comparison with controls (n = 27; brain stem injury, acute myocardial

Dihydrolipoate reduces neuronal injury after cerebral ischemia.

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It has been shown in vitro that dihydrolipoate (DL-6,8-dithioloctanoic acid) has antioxidant activity against microsomal lipid peroxidation. We tested dihydrolipoate for its neuroprotective activity using models of hypoxic and excitotoxic neuronal damage in vitro and rodent models of cerebral

[Histochemical demonstration of glial enzyme activity. II. Reagent and neoplastic glia].

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Enzyme activity changes in reagent and neoplastic glia are examined. In the case of reagent glia, considerably increased ADPase, ATPase and AMPase values have been observed in experimental elective parenchymal necrosis in the rat, in hypertrophic astrocytes from recent plaques in multiple necrosis,

Pharmacological studies supporting the therapeutic use of Ginkgo biloba extract for Alzheimer's disease.

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The standardized Ginkgo biloba extract EGb 761(definition see editorial) has been shown to produce neuroprotective effects in different in vivo and in vitro models. Since EGb 761 is a complex mixture containing flavonoid glycosides, terpene lactones (non-flavone fraction) and various other

Nonanticoagulant heparin reduces myocyte Na+ and Ca2+ loading during simulated ischemia and decreases reperfusion injury.

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Heparin desulfated at the 2-O and 3-O positions (ODSH) decreases canine myocardial reperfusion injury. We hypothesized that this occurs from effects on ion channels rather than solely from anti-inflammatory activities, as previously proposed. We studied closed-chest pigs with balloon left anterior

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