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

Aqueous solutions of engine exhaust condensation products were derived from cars powered by diesel or four-stroke gasoline engines (with and without three-way catalytic converter). The cars were operated on a static test platform. Samples of the different exhaust solutions accumulated in a Grimmer-type distillation trap (VDI 3872) during standard test programs (Federal Test Procedure) were incubated with important biomolecules. As indicators of reactive oxygen species or oxidative destruction, ascorbic acid, cysteine, glutathione, serum albumin, the enzymes glycerinaldehyde phosphate dehydrogenase and xanthine oxidase, and the oxygen free-radical indicator keto-methylthiobutyrate were used. During and after the incubations, oxygen activation (consumption) and oxidative destruction were determined. Comparison of the oxidative activities of the different types of exhaust condensates clearly showed that the exhaust condensate derived from the four-stroke car equipped with a three-way catalytic converter exhibited by far the lowest oxidative and destructive power.
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PMID:Oxidative destruction of biomolecules by gasoline engine exhaust products and detoxifying effects of the three-way catalytic converter. 128 38

Plasma homocyst(e)ine (the sum of free and bound homocysteine, homocystine, and the mixed disulfide homocysteine-cysteine, expressed as homocysteine) levels were determined by high performance liquid chromatography in 214 patients with symptomatic (claudication, rest pain, gangrene, amputation) lower extremity arterial occlusive disease and/or symptomatic (stroke, cerebral transient ischemic attacks) cerebral vascular disease and in 103 control persons. Mean plasma homocyst(e)ine was significantly higher in patients than in controls (14.37 +/- 6.89 nmol/ml vs 10.10 +/- 2.16, p less than 0.05). Thirty-nine percent of patients (83 of 214) had plasma homocyst(e)ine values greater than control mean + 2 standard deviations. Plasma homocyst(e)ine values were contrasted to age, male sex, diabetes, hypertension, smoking, renal failure, and plasma cholesterol. No difference was found in the incidence and/or level of any of these risk factors when patients with normal plasma homocyst(e)ine were compared to those with elevated plasma homocyst(e)ine, both by univariate and multivariate analysis. Patients with elevated plasma homocyst(e)ine were more likely to demonstrate clinical progression of lower extremity disease and of coronary artery disease, but not of cerebral vascular disease than were patients with normal plasma homocyst(e)ine, and the rate of progression was more rapid (p = 0.002). Progression of lower extremity disease as assessed in the vascular laboratory was also more common in patients with elevated plasma homocyst(e)ine (p = 0.01). We conclude that elevated plasma homocyst(e)ine is an independent risk factor for symptomatic lower extremity disease or cerebral vascular disease or both. Symptomatic patients with lower extremity disease and with elevated plasma homocyst(e)ine also appear to have more rapid progression of disease.
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PMID:The association of elevated plasma homocyst(e)ine with progression of symptomatic peripheral arterial disease. 198 84

Homocyst(e)ine refers to the sulfur-containing amino acids homocysteine, homocystine, and homocysteine-cysteine mixed disulfide, which normally exist in plasma in both the free and protein-bound forms. Marked hyperhomocyst(e)inemia is associated with well-recognized complications of occlusive thrombotic events and a characteristic syndrome. It is less clear whether mild to moderate elevations in plasma homocyst(e)ine concentrations (i.e., 1.5-5-fold increases) also represent a risk factor for stroke and, if so, whether it is independent of other recognized risk factors. To examine these questions we compared the plasma homocyst(e)ine levels in 41 patients with acute strokes, 27 patients with transient ischemic attacks, 31 patients with recognized risk factors for but no recent symptoms of cerebrovascular disease, and 31 normal volunteers (controls). Plasma homocyst(e)ine concentration was moderately but significantly higher in the patients than in the controls (p less than 0.0001). Approximately 30% of the patients had homocyst(e)ine levels higher than the controls. No relation was found between homocyst(e)ine concentration and other recognized stroke risk factors or stroke type; however, a positive correlation was found between serum uric acid and plasma homocyst(e)ine levels. These data suggest that a moderately elevated plasma homocyst(e)ine concentration may be an independent risk factor for cerebrovascular disease.
Stroke 1990 Apr
PMID:Elevated plasma homocyst(e)ine concentration as a possible independent risk factor for stroke. 232 39

Cystatin C, a protein inhibitor of lysosomal cysteine proteinases, was demonstrated by immunohistochemical techniques to be present in the birefringent amyloid deposits of the small arteries in the cerebrum, cerebellum, and leptomeninges of 10 Icelandic individuals with hereditary cerebral hemorrhage with amyloidosis. Specimens from other organs were investigated in one of the patients, and amyloid angiopathy characterized by an immunoreactivity of cystatin C was found in a submandibular lymph node. No immunoreactivity of amyloid fibril protein AA, kappa or lambda immunoglobulin light chain, or prealbumin was observed. Significantly low cerebrospinal fluid concentrations of cystatin C were found in all 9 investigated individuals with hereditary cerebral hemorrhage with amyloidosis. The concentrations of beta 2-microglobulin, albumin, and IgG in the cerebrospinal fluid were within normal limits. Isoelectric focusing showed that cystatin C from the cerebrospinal fluid of 9 patients with hereditary cerebral hemorrhage with amyloidosis had an isoelectric point identical to that of normal individuals. This investigation demonstrates that hereditary cerebral hemorrhage with amyloidosis may be diagnosed by two laboratory methods: immunohistochemical investigation of cystatin C in brain tissue specimens and quantitation of cystatin C in cerebrospinal fluid.
Stroke
PMID:Immunohistochemical characterization of the amyloid deposits and quantitation of pertinent cerebrospinal fluid proteins in hereditary cerebral hemorrhage with amyloidosis. 243 60

Highly elevated concentrations of homocysteine measured as homocysteine or cysteine-homocysteine mixed disulfide (MDS) are found in plasma and urine in subjects with inherited abnormalities of the methionine metabolism. These subjects have a high incidence of arteriosclerotic vascular complications during childhood. Homocysteine causes endothelial cell injury and cell detachment that initiates the development of arteriosclerosis. The present study demonstrates a significantly elevated mean plasma MDS concentration in 19 patients with arteriosclerotic cerebrovascular disease compared to 17 controls. Our findings suggest that moderate homocysteinemia might be a risk factor for arteriosclerotic cerebrovascular disease.
Stroke
PMID:Moderate homocysteinemia--a possible risk factor for arteriosclerotic cerebrovascular disease. 650 11

We previously reported that N-acetyl-L-cysteine (NAC), an oxygen free-radical scavenger, can increase the oxygen extraction capabilities during endotoxic shock when blood flow is progressively reduced. In the present study, we investigated whether the protective effects of NAC are related to an improvement in regional blood flow following endotoxemia. Fourteen anesthetized, saline-infused and ventilated dogs were divided into two groups: 7 dogs received NAC (150 mg/kg, followed by a 20 mg/kg.h infusion), and the other 7 dogs served as a control time-matching group. Thirty minutes later all the dogs received Escherichia coli endotoxin (2 mg/kg) i.v. A saline infusion was started 30 min after endotoxin challenge to restore pulmonary artery occlusion pressure to baseline and maintain it constant. Regional blood flow was measured by ultrasonic volume flowmeter. In the control group, arterial pressure, left ventricular stroke work index and systemic vascular resistance remained lower than baseline. Mesenteric, renal and femoral arterial blood flow increased but only femoral blood flow returned to baseline levels. In the NAC group, cardiac index and left ventricular stroke work index remained higher and systemic and pulmonary vascular resistance were lower than in the control group. Blood flow in mesenteric, renal and especially femoral arteries was higher than in the control group. Fractional blood flow increased only in the femoral artery. PaO2 and PvO2 had similar courses in the two groups. A higher venous admixture was associated with a higher cardiac index and a lower pulmonary vascular resistance in the NAC group. Oxygen delivery and oxygen-uptake were higher in the NAC-treated than in the control animals throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of N-acetyl-L-cysteine on regional blood flow during endotoxic shock. 758

A substantial number of adults and half of the children with acquired immunodeficiency syndrome (AIDS) suffer from neurological manifestations. Among the various pathologies reported in brains of patients with AIDS is neuronal injury and loss, although neurons themselves do not appear to be infected by HIV-1. There is growing support for the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons via a potentially complex web of interactions between macrophages (or microglia), astrocytes, and neurons. HIV-infected monocytoid cells, especially after interacting with astrocytes, secrete neurotoxic substances. Not all of these substances are yet known, but they may include eicosanoids, platelet-activating factor, quinolinate, cysteine, cytokines, and free radicals. Macrophages activated by HIV-1 envelope protein gp120 also appear to release similar toxins. Some of these factors can lead to increased glutamate release or decreased glutamate reuptake. A final common pathway for neuronal suceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca2+ channels and N-methyl-D-asparate (NMDA) receptor-operated channels, and therefore offers hope for future pharmacological intervention. This review focuses on clinically tolerated calcium channel antagonists and NMDA antagonists with the potential for trials in humans with AIDS dementia in the near future.
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PMID:Neuronal injury associated with HIV-1 and potential treatment with calcium-channel and NMDA antagonists. 770 21

Because oxygen free radicals have been implicated in the endothelial cell damage and in the myocardial depression occurring during severe sepsis, we investigated whether N-acetyl-L-cysteine (NAC) could influence the oxygen extraction capabilities during an acute reduction in blood flow induced by cardiac tamponade after endotoxin challenge. Sixteen anesthetized, saline-infused, and ventilated dogs received Escherichia coli endotoxin (2 mg/kg) 30 min before tamponade was induced by repeated bolus injections of warm saline into the pericardial space. Thirty minutes before endotoxin administration, nine dogs received NAC (150 mg/kg, followed by a 20 mg.kg-1.h-1 infusion); the other seven dogs served as a control group. The NAC group maintained higher cardiac index, oxygen delivery (DO2), and left ventricular stroke work index, but lower systemic and pulmonary vascular resistance, than the control group. The oxygen uptake (VO2) levels at critical DO2 (DO2crit) were identical in the two groups. However, DO2crit was significantly lower in the NAC than in the control group (8.1 +/- 1.7 vs. 10.8 +/- 1.8 ml.kg-1.min-1, P < 0.01). Critical oxygen extraction ratio and the slope of the VO2-to-DO2-dependent line were higher in the NAC than in the control group (72 +/- 14 vs. 53 +/- 15% and 0.80 vs. 0.56, respectively; both P < 0.05). The peak lactate and the maximal tumor necrosis factor (TNF) levels were lower in the NAC than in the control group (5.2 +/- 0.4 vs. 7.6 +/- 0.4 mM, and 0.14 +/- 0.03 vs. 1.21 +/- 0.58 ng/ml, respectively; both P < 0.01). NAC significantly increased glutathione peroxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effects of N-acetyl-L-cysteine in endotoxemia. 820 75

The mechanisms underlying cell damage in stroke or during experimental brain ischemia are not fully understood. L-Cysteine, an excitotoxic amino acid that could contribute to tissue damage, is normally found in relatively low levels in brain (ca. 0.05 mumol/g), compared to the cysteine-containing tripeptide, glutathione (GSH, ca. 1.5 mumol/g). We have observed that during brain ischemia in gerbils, levels of cysteine rise 10-13-fold over an 8 h period to 0.66 and 0.62 mumol/g, respectively, in the ischemic hippocampus and striatum. At the same time, levels of GSH fall by 0.84 and 0.94 mumol/g, respectively. The elevated free cysteine may be derived largely from GSH. The levels of cysteine found in ischemic brain are similar to those reported after parenteral administration of neurotoxic doses of L-cysteine to perinatal rats. The remarkable increase in cysteine during brain ischemia, coupled to its neurotoxic properties, may play a role in aspects of brain damage during or following brain ischemia.
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PMID:Brain ischemia markedly elevates levels of the neurotoxic amino acid, cysteine. 849 46

The noradrenergic neurotransmitter (-)-norepinephrine (1) is very easily oxidized at physiological pH to an o-quinone (2) that normally cyclizes and subsequently oxidatively polymerizes to black melanin. In this investigation it is demonstrated that L-cysteine (CySH) can divert the melanin pathway by efficiently scavenging o-quinone 2 to give, initially, 5-S-cysteinylnorepinephrine (6) and 2-S-cysteinylnorepinephrine (7). These cysteinyl conjugates are appreciably more easily oxidized than 1 to o-quinones that, in part, are further attacked by CySH to give 2,5-bi-S-cysteinylnorepinephrine (8), an even more easily oxidized compound. The o-quinone intermediates formed upon oxidation of 6-8 can also undergo facile intramolecular cyclizations to bicyclic o-quinone imines that oxidize the cysteinyl conjugates from which they are derived in a reaction sequence that leads initially to a number of dihydrobenzothiazines. At least two of these compounds, 7-(1-hydroxy-2-aminoethyl)-3,4-dihydro-5- hydroxy-2H-1,4-benzothiazine-3-carboxylic acid (9) and 8-(1-hydroxy-2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1, 4-benzothiazine-3-carboxylic acid (10) are lethal when administered into the brains of mice. The in vitro chemical pathways elucidated in this investigation might be of relevance to the depigmentation and degeneration of neuromelanin-pigmented noradrenergic cell bodies in the locus ceruleus in Parkinson's Disease and to the degeneration of noradrenergic nerve terminals in Alzheimer's Disease and following transient cerebral ischemia (stroke).
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PMID:Oxidation chemistry of (-)-norepinephrine in the presence of L-cysteine. 864 60


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