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

In the present study the hypothesis is tested that hypoxia causes morphological damage to the inner mitochondrial membrane and that this damage can be reversed by modification of the reoxygenated perfusate. Using the working rat heart model, hearts in group I (n = 40) were subjected to a 30 min normothermic, normoxic phase and a 90 min hypoxic phase, followed by 60 min reoxygenation. Hearts in group II (n = 32) were also subjected to a 30 min normoxic and a 90 min hypoxic phase. However, after 30 min of reoxygenation 1.5 mmol/l 2-mercaptopropionylglycine (MPG) was injected in the reoxygenated solution in order to test its ability to improve mitochondrial function. Mitochondrial function was assessed by measuring oxygen uptake (ST3), ST4, respiratory control index (RCI), ADP/O and oxidative phosphorylation rate (OPR). In addition mechanical function (heart rate, aortic and coronary flow, cardiac output, stroke volume) was monitored along with ultrastructural parameters. 90 min of hypoxia caused a deterioration of all parameters with persistent impairment in hemodynamic, morphologic and biochemical functions after 60 min of reoxygenation (group I). The role of the ATP-synthetases in the pathogenesis of oxygen-paradox is discussed. In contrast, the MPG-enriched reoxygenated solution (group II) improved hemodynamics, ultrastructure and mitochondrial function significantly (alpha = 0.05). It is concluded from these data that the ATP-synthetases are damaged during oxygen-deficiency and that MPG may be a useful drug for protecting the inner mitochondrial membranes during reoxygenation.
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PMID:Improvement of myocardial function after global hypoxia by protection of the inner mitochondrial membrane. 295 43

Effects of S-adenosyl-L-methionine (SAMe) on experimental cerebral ischemia were investigated using two different ischemic models. Cerebral energy metabolites (ATP, lactate, c-AMP) and brain water content were measured. It is reported that SAMe accelerates synthesis of phosphatidyl choline and increases erythrocyte membrane fluidity. Complete ischemia was produced by heart excision using wistar kyoto rats. SAMe (100 mg/kg, I.P.) was administered twice at one hour and immediately before inducing ischemia. The brain of rats were irradiated by microwave to stop the enzyme activity exactly 60 seconds after inducing ischemia and brain energy metabolites were measured. Recirculation model was produced by one hour recirculation following two hours ischemia induced by clipping of bilateral common carotid arteries using stroke-prone spontaneously hypertensive rats. SAMe (100 mg/kg, I.V.) was administered twice one hour after clipping and ten minutes after recirculation. The brain metabolites and water content were measured one hour after recirculation. In the complete ischemia, ATP and c-AMP levels were statistically high in the SAMe treated group compared to the untreated group (vehicle). But there was no statistical difference in lactate between the treated group and the untreated group. In the recirculation model, lactate elevation was suppressed in the SAMe treated group compared to the vehicle group with statistical difference, but there was no difference in ATP and c-AMP. Also, there was no difference in water content between the treated and the untreated group. SAMe protected energy failure in ischemia and accelerated recovery from ischemia. It is indicated that this agent is beneficial for treatment of cerebral ischemia in the acute stage.
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PMID:[Effects of S-adenosyl-L-methionine on experimental cerebral ischemia]. 299 May 9

Glucagon has been shown to increase further the enhanced tolerance for hypoxia of mice with elevated blood ketones and to stimulate ketone utilization by rat brain slices, suggesting that glucagon may affect brain metabolism. In addition to stimulating gluconeogenesis, glucagon alters the metabolism of mitochondria isolated from liver and heart. This study was designed to test whether glucagon can act directly and selectively on brain mitochondrial substrate oxidation. Mitochondria were isolated from normal murine brains using differential centrifugation through Ficoll gradients. Glucagon (3.6 microM) stimulated respiration in the presence of glutamate, and glutamate plus beta-hydroxybutyrate, but not in the presence of glutamate plus malate, succinate or beta-hydroxybutyrate alone. With glutamate as the substrate the hormone significantly increased State 3 oxygen consumption rates from control values of 91 mol O2/mol of cytochrome aa3/min to 117 mols O2/mol/aa2/min (p less than 0.0001), and also increased State 4 rates slightly but significantly. Glucagon did not change mitochondrial respiratory control ratios, but increased estimated rates of ATP synthesis from 434 (control) to 597 mols ADP consumed/mol aa3/min (p less than 0.0001). The data indicate that in vitro glucagon has a direct and substrate-specific stimulatory effect on isolated brain mitochondria. These substrate-specific effects were not altered when respiration was studied in the presence of postmitochondrial supernatant or exogenous 3',5'-cyclic AMP, indicating that glucagon, in addition to an in vivo action via activation of membrane-bound adenylate cyclase, can act, at least in vitro, directly and selectively on brain mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke
PMID:Substrate-specific stimulation by glucagon of isolated murine brain mitochondrial oxidative phosphorylation. 300 83

The susceptibility to cerebral ischemia was studied in stroke-resistant spontaneously hypertensive rats (SHRSR) treated by a long-term antihypertensive treatment, and compared with untreated SHRSR and Wistar rats (WR). Male SHRSR, aged 8 weeks, were divided into two groups and a long-term antihypertensive treatment for 4-6 weeks was started on one group (treated SHRSR: T-SHR) while the other group was left untreated as control (untreated SHRSR: U-SHR). The changes of blood pressure were checked on these rats. The prior treatment of hypertension was achieved by administration of hydroflumethiazide (120 mg/kg/day) and captopril (15-30 mg/kg/day) orally for 4-6 weeks by mixing in drinking water. All the experiments were performed at the age of 12-16 weeks and WR of similar age served as normotensive untreated control. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and blood pressure was always checked before BLCL. The survival ratio was observed from 1 hour to 24 hours after BLCL. The regional cerebral blood flow (rCBF) were measured before and 4 hours after BLCL periodically. The brain energy metabolites were measured 4 hours after BLCL. rCBF were measured at the thalamus by the hydrogen clearance method. ATP concentrations were determined by luciferine-luciferase method, c-AMP was measured by RIA and lactate by enzymatic method. The brain water content was measured by freeze-dry method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of long-term prior antihypertensive treatment on cerebral ischemia induced by bilateral common carotid artery ligation in SHRSR]. 300 93

The Wistar rat, with a blood pressure range of 120-160 mmHg, and two strains of spontaneously hypertensive rats (SHR), stroke-prone (SHRSP, range 210-270 mmHg) and stroke-resistant (SHRSR, range 160-240 mmHg), were used to determine the degree of damage after ischemic insult induced by bilateral carotid artery ligation (BLCL). The survival rate and McGraw Stroke Index correlated well with the degree of hypertension. After BLCL, impairment of cerebral blood flow is abrupt and residual flow is near zero in rats with initial blood pressures greater than 200 mmHg. A markedly deteriorated aerobic metabolism, as measured by the concentrations of ATP, c-AMP and lactate, is seen to precipitate in rats with initial blood pressures greater than 180 mmHg and severe edema occurs if the pressure is more than 160 mmHg. The degree of hypertension that produces high vulnerability to stroke and severe damage to the brain after ischemic insult is indicated as beginning at about 180 mmHg.
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PMID:Susceptibility to ischemic insult in hypertensive rats: correlation between degree of ischemia and hypertension. 301 58

Lateral cilia of Mytilus edulis gill arrest upon mechanical stimulation, the result of calcium influx. A mechanical stimulus that deflects these cilia toward the effective stroke, and is normally sufficient to cause transient arrest in beating lateral cilia or transient movement into the recovery stroke in quiescent cilia, initiates beating in Ca2+ ionophore-arrested cilia at 9-15 Hz, for periods as long as 30 s. This movement is restricted to the stimulated cilia and the beat pattern appears constrained in the first half of the beat cycle. Application of dopamine causes ciliary arrest in the presence (but not absence) of Ca2+ and mechanical stimulation will also activate such cilia to beat. In the presence of ATP, mechanical stimulation of detergent-permeabilized lateral cell models arrested in the presence of 50 microM Ca2+ will also cause activation comparable in frequency, duration, and beat pattern to that seen in Ca2+-arrested cells, but the initiation is more difficult. Upon application of ionophore in Ca2+-free (EGTA) seawater, the cilia become quiescent, stopped at the end of the recovery stroke. Mechanical stimulation will cause activation of beat, with a similar range of frequencies and duration as in Ca2+-arrested lateral cilia, but the beat pattern is normal and cilia of adjacent cells may also beat, presumably initiated by mechanical coupling. Gently lifting cilia at their basal ends, using small, slow movements of a mechanical probe, will initiate several beat cycles in quiescent lateral cilia but will cause Ca2+-arrested cilia to 'snap' into the effective stroke and back.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanical stimulation activates beating in calcium-arrested lateral cilia of Mytilus edulis gill. 309 98

Ventricular pressure-volume area (PVA) is a specific area in the pressure-volume diagram, which represents the total mechanical energy generated by each contraction, consisting of stroke work and mechanical potential energy at end-systole. Animal experiments have shown that PVA is correlated linearly with the ventricular oxygen consumption (Vo2) per beat under a variety of loading conditions in a stable contractile state. The slope of the Vo2-PVA line has been shown to remain constant in different contractile states, implying a constant stoichiometry between Vo2 and PVA. As a first step to understand the nature of this Vo2-PVA relation, we devised a new crossbridge (CB) model to theoretically relate PVA with the total enthalpy change associated with the ATP hydrolysis for all CB cycles. One of the most important assumptions on which this model analysis depended was that the time-varying elasticity model could simulate the instantaneous pressure-volume relation. The result of this analysis implied that the empirical linear Vo2-PVA relation could be attributed to the energy balance between energy input and output of the chemomechanical transduction associated with CB cycles during a ventricular contraction.
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PMID:Crossbridge model compatible with the linear relation between left ventricular oxygen consumption and pressure-volume area. 317 77

We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced greater than or equal to 1 hour before ischemia and was maintained during 1.5-2 hours of recirculation in nine cats; four cats were subjected to hyperthermia without cerebral ischemia, six to hyperthermia during recirculation (after return of intracellular pH to preischemic values), and 14 to normothermic ischemia and recirculation. Our data indicate that preischemic hyperthermia results in an intracellular cerebral pH during recirculation significantly lower than that in normothermic cats. In hyperthermic cats beta-ATP and phosphocreatine (PCr) concentrations and the ratio of PCr to inorganic phosphate failed to return to preischemic levels during recirculation in contrast to normothermic cats. Hyperthermia without ischemia and hyperthermia during recirculation had no significant effect on intracellular pH. Thus, preischemic hyperthermia has a detrimental effect on metabolic recovery after transient global cerebral ischemia.
Stroke 1988 Dec
PMID:Effect of mild hyperthermia on recovery of metabolic function after global cerebral ischemia in cats. 320 11

Adenosine, administered intravenously (0.25 mg/kg-1/min-1) to rabbits with experimental myocardial infarction, produced a drop in arterial pressure and total peripheral resistance, normalized stroke volume, increased ATP content at the margin of the infarcted area, and reduced LDG activity and increased SDG activity in the ischemized region.
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PMID:[Hemodynamic and metabolic effects of adenosine in experimental myocardial infarction]. 323 Jul 62

We have briefly reviewed the broad range of applications of NMR spectroscopy to metabolism in tissues and biological fluids. Most of these studies are in the exploratory stage, though the potential of NMR for non-invasive and non-destructive monitoring of certain important substrates and reaction pathways is considerable. The limitations of the technique lie in its relative insensitivity and the rather restricted range of substances that it can detect, as well as the current expense. So far, the main clinically useful applications have been in the diagnosis and monitoring of treatment of certain inborn errors of metabolism, namely those that result in altered energy of pH states or the abnormal accumulation of significant amounts of metabolites in body fluids. It might be expected that as localization techniques improve, clinically useful information will be obtained in a wide range of ischaemic or hypoxic states, e.g. stroke and myocardial infarction. The possibility of producing a detailed spatial image of metabolite concentrations (e.g. ATP), in the way that NMR imaging techniques currently do using features of the water proton resonance, is attractive and the initial results are very encouraging (Bogusky et al, 1986; Bailes et al, 1987; Blackledge et al, 1987).
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PMID:NMR as a metabolic tool. 333 Apr 36


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