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

Reduce nicotinamide adenine dinucleotide (NADH) fluorescence was recorded from an avascular area on the squirrel monkey cortex prior to, during, and after focal incomplete ischemia. By using the instrumentation described, stable recordings were obtained free from hemoglobin artifact and with only minimal photodecomposition. Pentobarital was compared to urethane and halothane as the anesthetic agent and was found acceptable for these types of studies in the dosages used. NADH levels were constant prior to ischemia, increased during ischemia, returned to pre-ischemic levels after restoration of blood flow, and then increased greatly at death produced by anoxia. The use of the infrared microscope for semiquantitative measurements of cortical blood flow throughout the duration of these acute studies was investigated and found to the reliable.
Stroke
PMID:Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 1. animal preparation, instrumentation, and validity of model. 16 72

The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.
Stroke
PMID:Reduced nicotinamide adenine dinucleotide fluorescence and cortical blood flow in ischemic and nonischemic squirrel monkey cortex. 2. effects of alterations in arterial carbon dioxide tension, blood pressure, and blood volume. 16 73

Acute changes in the redox state of NADH in the cerebral cortex of cats were investigated following occlusion of the middle cerebral cortex (MCA) and were correlated with alterations of regional cerebral blood flow in the ischemic cortex determined autoradiographically. Arterial occlusion was accomplished via the transorbital approach. Cortical fluorescence and reflected light signals were recorded from the central MCA territory by means of a beam-splitting fluorometer, and a fluorescence signal corrected for alterations in intravascular hemoglobin was derived. Following arterial occlusion, there was a rapid increase in cortical NADH fluorescence, peaking within 30 to 70 seconds at 20% to 40% of full scale. This was followed by a slow linear decline in fluorescence over the next several minutes. The behavior of cortical NADH fluorescence was unaffected by replacement of the ambient air over the cortical surface with nitrogen. Mean regional blood flow values in the most ischemic gyri two to 15 minutes following arterial occlusion were 21% to 23% of the corresponding values in the opposite, nonischemic hemisphere. In individual animals, peak NADH fluorescence values following arterial occlusion correlated with the extent of blood flow reduction in the affected ischemic gyri (P less than 0.05).
Stroke
PMID:Pyridine nucleotide redox state and blood flow of the cerebral cortex following middle cerebral artery occlusion in the cat. 17 77

The changes induced by phenobarbital in cerebral enzymatic activities of the Krebs' cycle (citrate synthase, malate dehydrogenase) and electron transfer chain (total NADH-cytochrome c reductase and cytochrome oxidase) were studied. In addition, the activity of lactate dehydrogenase of acetylcholine esterase and of glutamate dehydrogenase was also studied. These enzymatic activities were evaluated in the homogenate in toto and in a crude mitochondrial fraction from rat brain. The modifications in some of these activities indicate that several new metabolic situations occur in brain tissue after phenobarbital treatment.
Stroke
PMID:Effect of phenobarbital on cerebral energy state and metabolism. Enzymatic activities. 23 Jun 18

Focal brain ischemia was produced in halothane-anesthetized Mongolian gerbils by occluding the right common and the left external carotid artery. Ninety minutes after vascular occlusion the following regional hemodynamic and metabolic parameters were evaluated in adjacent cryostat sections taken from seven different coronal planes of each brain: cerebral blood flow (CBF), glucose utilization (CMRG), and the tissue content of ATP and glucose. NADH fluorescence was recorded from the surface of the cryostat block. In addition, tissue slices were taken from each brain to determine the rate of phosphorylation of 2-deoxyglucose in ischemic and nonischemic regions. Depending on the density of ischemia, the following metabolic disturbances were observed. At CBF values below 35 ml x 100 g-1 x min-1 CMRG increased and at values below 25 ml x 100 g-1 x min-1 it declined sharply. Glucose content declined when CBF was below 35 ml x 100 g-1 x min-1 and ATP fell at CBF below 20 ml x 100 g-1 x min-1. At 10 ml x 100 g-1 x min-1 ATP was completely depleted. NADH fluorescence was found elevated at flow rates that caused an increase of glucose utilization and was maximal when CBF stopped. The ischemic thresholds for the initial increase in CMRG and the complete depletion of ATP content represent the metabolic equivalent of the penumbra zone and provide a basis for the evaluation of therapeutic procedures for the treatment of stroke.
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PMID:Threshold relationship between cerebral blood flow, glucose utilization, and energy metabolites during development of stroke in gerbils. 139 69

A 24-year-old male had a deficiency of the complex I (NADH coenzyme-Q-reductase) of the mitochondrial respiratory chain, which clinically presented as a mitochondrial encephalomyopathy, with lactic acidosis and stroke-like episodes (MELAS syndrome). The encephalopathic episodes were preceded by migraine and were characterized by focal deficit signs, motor partial seizures and hypodense areas in the CT scan. An echocardiographic diagnosis of hypertrophic cardiomyopathy without intracavitary thrombi was made. It is suggested that hypertrophic cardiomyopathy is caused by the mitochondrial abnormalities that have been reported in the myocardium, and that migraine and cerebral infarctions are associated with abnormalities in the mitochondria from the endothelium and smooth muscle fibres of the cerebral small arteries and arterioles.
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PMID:[Complex I (NADH coenzyme-Q-reductase) deficiency, MELAS syndrome and hypertrophic cardiomyopathy]. 190 55

A 7-year-old girl with normal psychomotor development during infancy began to have easy fatigability about 3 years of age. At the age of 5 years, she developed respiratory distress and became unconscious when the serum lactate and pyruvate levels were markedly elevated and a blood gas analysis showed respiratory and metabolic acidosis. Thereafter, she had similar episodic respiratory problems with lactic acidosis. Her muscle biopsy showed a myopathic pattern and numerous ragged-red fibers in an approximately half of muscle fibers. Lipid droplets were slightly to moderately increased in amount mostly in the ragged-red fibers. A biochemical analysis on the isolated mitochondria from the biopsied sample showed markedly decreased NADH cytochrome c reductase activity with no specific but rather uniformly decreased subunits of complex I by the immunoblotting method. She was diagnosed as having the myopathic form of complex I deficiency because she and her relatives with similar muscle symptoms had no central nervous system symptoms such as progressive mental deterioration, convulsions and stroke-like episodes. Diagnosis of complex I deficiency was further confirmed by an oxograph study; the oxygen consumption was not detectable when malate and pyruvate were added as the substrates in the isolated mitochondria. Although stroke-like episodes and convulsions are commonly seen in complex I deficiency, episodic respiratory distress as seen in the present patient has not been described in the literature.
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PMID:[A case of complex I deficiency with episodic respiratory distress]. 211 95

A typical case of mitochondrial encephalomyopathy with lactic acidemia and stroke-like episodes (MELAS) was reported. The main clinical manifestations consisted of short stature, psychomotor deterioration, sensorineural deafness, and hemiparesis. The laboratory findings disclosed abnormal lactic acid tolerance abnormal EEG, VEP, AEP, SEP, and MCV. The CT scan showed multiple intracerebral infarcts, basal ganglia calcifications, and cerebral atrophy. A muscle biopsy was performed. The frozen sections with modified gomori trichrome stain revealed ragged-red-fiber which reacted strongly positive in NADH-TR stain. The electron microscopy revealed subsarcolemmal aggregation of mitochondria of various sizes with paracrystalline inclusions, abnormally arranged cristae, and osmiophilic dense-bodies in their matrices.
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PMID:[Mitochondrial encephalomyopathy. Report of a case]. 234 80

To investigate the molecular abnormality in the mitochondria from various tissues of an autopsied patient exhibiting mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, we have examined the enzymatic activity, iron-sulfur cluster, and subunit composition of the NADH-ubiquinone oxidoreductase (complex I). Rotenone-sensitive NADH-cytochrome c reductase activity was found to be decreased in all the tissues examined. A detailed study of the liver mitochondria has shown that NADH-ubiquinone oxidoreductase activity was greatly diminished. Analysis of the electron paramagnetic resonance spectra of the liver submitochondrial particles revealed a disproportionate deficiency of iron-sulfur clusters in the complex I segment of the respiratory chain. Signals from the clusters N-2 and N-3 diminished more drastically than those from clusters N-1b and N-4. Immunoblotting analysis showed that the 75-kD, 51-kD, and several other subunits were markedly diminished among multiple subunit polypeptides of complex I. These findings suggest that the underlying bases for mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes are defects, at least, in the complex I subunits containing a flavin and/or iron-sulfur cluster(s), which resulted in deficiencies of some iron-sulfur clusters.
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PMID:Disproportionate deficiency of iron-sulfur clusters and subunits of complex I in mitochondrial encephalomyopathy. 249 47

Heat stroke was induced in intact rats in a thermal chamber (45 degrees C) and simultaneously a group of animals was subjected to overheating for the same time but was given intraperitoneal injections of ionol (120 mg/kg) for 2 days and 30 minutes before exposure in the chamber. Significant increase of the concentration of intermediates--lactate, pyruvate, malate, glutamate, ammonia--and decrease of the alpha-ketoglutarate content occurred in the renal tissue in animals of both groups. The NAD/NADH ratio in the cytoplasm and mitochondria reduced essentially, to a greater degree in animals given ionol injections. The last named were distinguished by higher survival and lower degree of hyperthermia.
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PMID:[The effect of ionol on oxidative-reductive processes in the kidney during heat stroke]. 261 12


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