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

Intriguing questions have recently been raised regarding the applicability of direct observations of the pial microcirculation to the behavior of the total cerebral microcirculation. Operating under the assumption that arteriolar tone and, thus, cerebrovascular resistance is, to some extent, directly related to the intrinsic energy metabolism of the arteriolar wall, a comparative histochemical analysis of cerebral microvessels, both pial and parenchymal, was undertaken. Reactions were chosen on the bases of representation of substrate and of enzymes of glycolysis, the hexose monophosphate shunt, beta-oxidation of fat, Krebs cycle, cytochrome system and ATP hydrolysis. Three metabolically distinct segments of the cerebral microvasculature were delineated with the pial vessels showing strong capacities for glycolysis, beta-oxidation of fats and utilization of glucose through the hexose monophosphate shunt. Microvessels of the gray matter have a qualitatively similar metabolic profile but the capacities of each pathway are lower when compared to pial arterioles. Arterioles of the white matter demonstrate the weakest energy-yielding capacities.
Stroke
PMID:Metabolic profiles of canine cerebrovascular tree: a histochemical study. 14 24

In a clinically applicable cat stroke model, 16 purpose-bred adult animals were used to evaluate the beneficial effects of two treatment regimens: isovolemic hemodilution with either a perfluorocarbon emulsion or dextran 40 (a glucose polymer). Animals that received these treatment regimens were then compared with a control group of untreated animals. Focal cerebral infarctions were produced by transorbital ligation of the left middle cerebral artery. The randomly allocated treatment arms of the study were instituted 3 hours after ligation of the middle cerebral artery, thereby simulating a human clinical situation. In vivo mitochondrial metabolic activity of the peri-infarct cerebral tissue was continually assessed by means of a multiwavelength near-infrared spectrophotometer. This allowed measurement of cellular oxygenation at the cytochrome aa3 level, the terminal member of the cytochrome chain. Sequential proton-based magnetic resonance imaging was used to measure intracerebral water in vivo. Cardiac output, oxygen consumption/delivery, chemical, histologic, and rheologic parameters were also assessed. The data collected were analyzed by group means and standard statistical analyses, which revealed that the group treated with the perfluorocarbon emulsion had both less brain edema in the early post-infarct period (p less than 0.05), as well as a higher level of oxidation of cytochrome aa3 (p less than or equal to 0.025). This evidence supports the premise that isovolemic hemodilution with an oxygen-carrying hemodiluent may be beneficial in the treatment of ischemic strokes.
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PMID:Beneficial effects of isovolemic hemodilution using a perfluorocarbon emulsion in a stroke model. 171 44

The case of 12 years-old boy with seizures, headache, severe vomit and focal neurological signs is reported. These episodes had several recurrences and regression with little neurologic deficits. In the investigation it was found: lactic acidosis; stroke like episodes and calcification in the basal ganglia on computerized axial tomography; ragged red fibers on muscle biopsy and decreased of cytochrome C oxidase in the muscle tissue. A revision about mitochondrial disorders with involvement of the central nervous system and muscle is made, with emphasis on diagnosis and recognition of MELAS.
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PMID:[MELAS (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes): report of a case]. 283 Aug 68

To assess the residual effects of transient cerebral ischemia on mitochondrial oxidative metabolic function, changes in the reduction/oxidation state of cytochrome a,a3 and relative local blood volume were measured in situ from the exposed cerebral surface of rat brain before and after 10 minutes of carotid artery ligation. During the ischemic interval, cytochrome a,a3 became reduced and electrocortical activity was abolished. During the first 20 minutes of reperfusion cytochrome a,a3 was hyperoxidized beyond baseline with eventual recovery to the original steady state. Electrocortical activity returned more slowly. Increased energy demand induced by electrical stimulation of the cortex produced transient oxidation of cytochrome a,a3. The amplitude of this oxidative response was decreased during the first 30 minutes of reperfusion. During the first 2 hours of reperfusion the time required for re-reduction of the oxidative response was lengthened despite the recovery of baseline mitochondrial redox state. These data demonstrate residual metabolic dysfunction after transient ischemia not apparent under "resting" conditions but evident when the system is required to perform additional "work." We speculate this metabolic dysfunction could be due to relative substrate limitation.
Stroke
PMID:Disparate recovery of resting and stimulated oxidative metabolism following transient ischemia. 627 54

Rats were subjected to a 30 minute period of combined hypoxia (F1o2 = .08) and hemorrhagic hypotension (MAP = 30 mm Hg), then resuscitated by restoration of F1o2 = .30 and reinfusion of shed blood and saline. Intracranial blood volume, hemoglobin saturation, and the cytochrome alpha, alpha 2 redox state were monitored through the intact skull during hypoxic hypotension and after resuscitation utilizing reflectance spectrophotometry. Although resuscitation returned arterial blood pressure, arterial pO2, and hemoglobin saturation toward normal, a sustained, significant (p less than .005) reduction in cytochrome alpha , alpha 2 remained. A parallel series of rats was subjected to identical hypoxic hypotension. At designated intervals the animals were sacrificed to determine brain ATP, ADP, and inorganic phosphate (P1). The data are discussed in terms of relationships between high energy phosphate metabolism and recorded changes in cerebral cytochrome alpha , alpha 2 redox state.
Stroke
PMID:Failure of brain cytochrome alpha , alpha 3 redox recovery after hypoxic hypotension as determined by in vivo reflectance spectrophotometry. 627 81

A 4-year-old boy presented with developmental delay, aggressive behavior, and incoordination. His EEG showed a diffuse encephalopathy. At age 10 he developed convulsions and severe migraine-like headaches. Muscle wasting, arreflexia, and lactic acidemia following exercise were noted. Electromyography was myopathic and nerve conduction studies revealed a peripheral neuropathy. Muscle biopsy demonstrated variation in fiber size and an excess of lipid droplets. He than had several stroke-like episodes and periods of unconsciousness, associated with severe metabolic acidosis. Muscle cytochrome C oxidase was abnormally low. This boy displayed the classical clinical and biochemical features of MELAS syndrome, namely Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes. Treatment included carnitine, vitamin C, vitamin K, riboflavin, coenzyme Q10, and corticosteroids. He died at the age of 14 years following an episode of seizures, coma, and gastrointestinal hemorrhage. This is the first reported case of MELAS syndrome in Israel.
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PMID:MELAS syndrome: peripheral neuropathy and cytochrome C-oxidase deficiency: a case report and review of the literature. 772 60

1. The hepatic metabolism of 3-[-2(phenylcarbamoyl) ethenyl]-4,6-dichloroindole-2-carboxylic acid (GV150526), a novel glycine antagonist for stroke, was investigated. 2. After a single intravenous administration of 800 mg GV150526 to healthy volunteers, six metabolites were observed. The major metabolites detected in human plasma have been shown by mass spectrometry to be glucoronides and one sulphate conjugate. 3. After incubation of GV150526 for 6 and 24 h with human liver slices, three glucuronide metabolites were observed. After incubation of GV150526 with pooled human liver microsomes, only one metabolite was observed, with the same molecular weight and HPLC retention time as the synthetic standard GV217053 (GV150526 hydroxylated on the para-position of the phenyl ring). 4. GV150526 hydroxylase enzyme kinetics--a step before sulphation--was determined using pooled human microsomes and was shown to be catalysed by cytochrome P4502C9. Glucuronidation kinetics towards GV150526 using microsomal preparations were also determined. Glucuronidation of GV150526 was observed with UGT1A1 cDNA-expressed protein, but not with UGT1A6. 5. The above enzyme kinetic data were used to calculate intrinsic clearance after scaling-up and hepatic clearance were calculated. Since GV150526 has a high plasma protein binding capacity, the effect of GV150526 binding to microsomal protein was determined. Thus, enzyme kinetic data were corrected, plotting the free (unbound) concentration of GV150526 versus enzymatic velocities: apparent Vmax did not alter significantly but apparent Km was approximately 10-fold lower. Correlation of these corrected enzyme kinetic data to predict clearance with in vivo clearance of GV150526 was good when both fu(plasma) and fu(microsomes) were included in the clearance calculations.
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PMID:Human hepatic metabolism of a novel 2-carboxyindole glycine antagonist for stroke: in vitro-in vivo correlations. 1105 63

The generation of oxygen radicals and lipid peroxidation may be factors in the cerebral damage secondary to ischaemia of the cerebrovascular disease, as in stroke. Five traditional Chinese medicinal prescriptions were investigated for their antioxidant activity: Shiee Fuu Jwu Iu Tang (TCMP1), Oh Yaw Shuen Chin Saan (TCMP2), Buu Yang Hwan Wuu Tang (TCMP3), Sheau Shiuh Ming Tang (TCMP4), and Chir Hwu Jia Long Guu Muu Lih Tang (TCMP5). Anti-lipid peroxidation, anti-superoxide formation and free radical scavenger activity were determined by the FeCl2--ascorbic acid-induced lipid peroxidation effects on lipids in-vitro, xanthine oxidase inhibition, cytochrome C system and an electron spin resonance spectrometer, respectively. The results showed that TCMP5 had greater anti-lipid peroxidation and anti-superoxide formation activity than the other prescriptions. TCMP4 had the greatest free radical scavenging effect, TCMP5 showed the greatest superoxide radical scavenger activity and TCMP3 showed the greatest hydroxyl radical scavenger activity. Tests were also performed to evaluate the effects of the five prescriptions on blood lipid in-vivo. The test showed that the prescriptions decreased the level of total cholesterol and LDL-cholesterol in serum in high cholesterol-fed rats. From these results, it seems probable that these prescriptions may be effective in the prevention and therapy of stroke and ischaemia.
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PMID:Anti-hypercholesterolaemia, antioxidant activity and free radical scavenger effects of traditional Chinese medicine prescriptions used for stroke. 1118 47

The efficacy of pre-, intra-, and postoperative prevention of hemodynamic disorders by creatinine phosphate, cytochrome C, and glutamic acid was evaluated in 61 coronary patients with decreased myocardial contractility. All these agents exerted a positive inotropic effect in coronary patients with ejection fraction below 0.4, increasing the stroke volume and left-ventricular ejection fraction without modifying heart rate. Glutamic acid is not recommended for preoperative treatment, because it increases oxygen consumption by the myocardium above the reserve potential of the coronary bed. Cytochrome C is the most effective drug for preoperative treatment. Intraoperative preischemic protection of the myocardium by cytochrome C in coronary patients during high risk operations prevents the development of unfavorable hemodynamic complications during induction and maintenance of anesthesia before artificial circulation, provides favorable recovery of cardiac activity, decreases the incidence of severe arrhythmias, promotes a rapid and full-value recovery of myocardial contractile function after ischemia, and decreases the incidence of acute heart failure.
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PMID:[Prevention of disorders of myocardial contractile function in patients with ischemic heart disease during aortocoronary shunting]. 1145 65

Besides necrosis, apoptosis is the other major mode of cardiomyocyte loss in ischemic cardiovascular disease. In the present study, we examined the hypothesis that nitric oxide (NO) protects myocardial function by improving myocardial microcirculation and attenuating cardiomyocyte apoptosis in a rat model of myocardial ischemia/reperfusion (MI/R). The left main coronary artery of anesthetized male rats was ligated for 40 min, followed by 4 h reperfusion. Four groups of animals were studied: sham operated control + saline; sham operated control + N(W)-nitro-L-arginine methyl ester (L-NAME); MI/R + saline; MI/R + L-NAME (10 mg/kg, iv, 10 min prior to reperfusion). Results show that MI/R caused a decrease in mean arterial blood pressure (MABP), cardiac index (CI), and stroke volume index (SVI). Inhibition of NO synthesis by L-NAME attenuated plasma NO levels, but increased MABP and SVR in sham control rats and rats subjected to MI/R, and further depressed left ventricular function in rats subjected to MI/R as indicated by decreased CI and SVI. Furthermore, administration of L-NAME to rats subjected to MI/R enhanced cardiomyocyte apoptosis as indicated by a significant increase in DNA fragmentation compared to rats with MI/R alone. Histological study revealed that L-NAME caused arterial constriction and congestion of red blood cells in arteries and capillaries in the peri-ischemic areas of the hearts in rats subjected to MI/R and, interestingly, also in the sham control rats. Data suggest that the mechanism of increased reperfusion injury may be attributable to a "no-reflow" phenomenon induced by L-NAME, resulting in increased cardiomyocyte apoptosis secondary to ischemia and enhanced cytochrome-c release from mitochondria. In addition, cardiac injury may be increased due to the augmented oxygen consumption of cardiomyocytes caused by the increased SVR and afterload. These results suggest that endogenous NO may act to improve myocardial microvascular perfusion, reduce SVR, and limit cardiomyocyte apoptosis, thereby, attenuating myocardial dysfunction induced by MI/R.
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PMID:L-NAME enhances microcirculatory congestion and cardiomyocyte apoptosis during myocardial ischemia-reperfusion in rats. 1190 Mar 36


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