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

Changes in cerebral cortex concentrations of high-energy phosphates, glycolytic metabolites, citric acid cycle intermediates, associated amino acids, and ammonia, were studied after 5, 15 and 30 min of incomplete ischemia in rats anesthetized with 70% N2O or 150 mg.kg-1 of phenobartibal. Previous results have shown that with this type of ischemia (bilateral carotid artery occlusion combined with reduction in blood pressure to 50 mm Hg) cortical blood flow is reduced to below 10% of nitrous oxide values, whether animals are anesthetized with 70% N2O or 150 mg.kg-1 of phenobarbital. In animals under 70% N2O, changes in tissue concentrations of phosphocreatine, ATP, ADP and AMP were similar to those previously obtained in complete ischemia. However, some glucose remained in the tissue, and the lactate concentrations gradually rose to reach excessive values. Changes occuring in glycolytic and citric acid cycle intermediates were similar to those seen in complete ischemia but, after 30 min, there was some reduction in the pool size of amino acids. In those animals given phenobarbital and which lost all EEG activity during ischemia, changes in cerebral metabolites were virtually identical to those observed in nitrous oxide-anesthetized animals. However, some animals exposed to 5 or 15 min of ischemia had some remaining EEG activity. In these, cerebral energy state was significantly less deranged, and levels of glycogen, glucose and pyruvate were higher.
Stroke
PMID:Effects of phenobarbital in cerebral ischemia. Part I: cerebral energy metabolism during pronounced incomplete ischemia. 2 84

Circulating platelet aggregates formed in vivo were serially measured, and platelet-aggregation thresholds were determined in vitro in 82 patients with acute cerebral ischaemia. The percentage of aggregated platelets was increased in 53 patients with completed stroke (30.9% +/- 2.0) and in 29 patients with transient ischaemic attacks (34.1% +/- 2.3), all studied within 10 days of the acute event. These values were higher (P less than 0.001) than levels of aggregated platelets in 30 patients with non-vascular neurological disease (16.8% +/- 2.3). The percentage of aggregated platelets returned to normal 10 days to 6 wk after acute cerebral ischaemia. Aspirin and dipyridamole did not affect either the increase in or subsequent normalisation of circulating-platelet-aggregate levels in these patients. Platelet-aggregation sensitivity to adenosine diphosphate and adrenaline was also increased in patients with acute cerebral ischaemia, but this abnormally resolved during convalescence. Platelet activation is abnormal in acute cerebral ischaemia but usually returns to normal with or without anti-platelet therapy. This activation of platelets may contribute to the clinical manifestations of occlusive vascular disease.
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PMID:Platelet activation in acute cerebral ischaemia. Serial measurements of platelet function in cerebrovascular disease. 6 34

Adenosine and adenine compounds (AMP, cyclic AMP, ADP and ATP) markedly dilated feline and human pial arteries in vitro, the effect being more prominent with increasing tone of the vessel (active tonic contraction induced by prostaglandin F 2 alpha or serotonin). In contrast, the various adenine compounds were unable to produce any dilation of extracranial arteries tested (branches of lingual, external maxillary, and superficial temporal arteries). The degree of dilatation depended upon the perivascular potassium concentration, so that low potassium increased Emax and reduced ED50 values. Possible involvement of adenine compounds in the vasodilatory phase of the migraine attack is discussed.
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PMID:Adenine compounds: cerebrovascular effects in vitro with reference to their possible involvement in migraine. 21 63

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Employing optical density methods, platelet aggregation in response to 1.275, 1.7, and 3.4 micrometer adenosine diphosphate was tested in 46 patients with migraine and 46 controls matched by age, sex, and race. The migraine patients demonstrated platelet hyperaggregability when compared with controls, as manifested by a lower threshold for the platelet-release reaction and increased platelet stickiness following aggregation. There was no correlation of platelet hyperaggregability with the severity of migraine or with the occurrence of migraine-associated neurologic symptoms, suggesting that platelet hyperaggregability is a concomitant feature of the migraine syndrome but not dependent on the occurrence of the actual headache. As platelet hyperaggregability may predispose to development of intravascular platelet aggregates or mural thrombi, the hyperaggregability found here may help explain the increased incidence of stroke and heart attack in migraine patients that has been reported elsewhere.
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PMID:Platelet aggregability in migraine. 56 34

Platelet aggregability was measured using the screen filtration pressure (SFP) method in 50 elderly healthy people, 93 persons with essential hypertension, 166 patients with cerebral thrombosis at the recovery stage (more than two months after onset), and 74 patients with cerebral hemorrhage at the recovery stage. SFP by 3 muM ADP in the healthy persons, the hypertensive patients, and the patients in the recovery stages of hemorrhage and thrombosis were 148.7 +/- 53.5, 176.2 +/- 74.4, 189.8 +/- 58.3 and 206.3 +/- 58.9 mm Hg, respectively. The differences of the SFP between the Healthy and each of the diseased groups were statistically significant (P less than 0.01 to 0.05). Meanwhile, SFP of nine patients with cerebral thrombosis and 18 patients with hemorrhage was measured during their time course of disease from the onset to 180 days. SFP in the acute stage of thrombosis showed an increase and a gradual decrease during the time course, while SFP in the acute stage of hemorrhage showed the opposite -a decrease and a gradual increase. A statistically significant difference was observed between both groups within 30 days from onset (P less than 0.001). Screen filtration pressure in the acute stage of hemorrhage showed 95.2 +/- 17.7 mm Hg in nine survival cases and 194.0 +/- 96.2 mm Hg in nine deaths with ten days from the onset. The difference was statistically significant (P less than 0.001). Such results suggest a role of platelets in cerebral thrombosis and hemorrhage and a usefulness in differential diagnosis of both diseases.
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PMID:Platelet aggregability measured by screen filtration pressure method in cerebrovascular diseases. 96 Jan 62

To investigate correlations between energy supply and mechanical work in the frog's myocardium in true anoxia, the stroke volume, systolic and diastolic volumes and the parameters of velocity of contraction and relaxation of frog hearts were compared to the levels of high energy phosphates and the delivery of lactate. During perfusion with N2 saturated Ringer solution, stroke volume, systolic contractility and diastolic relaxation decrease till a contracture. High preload produces a dilatation growing up to the contracture after retarded and weakened relaxation. The ATP-content decreases during the first quarter of the experiment to 60%. CP decreases continuously to 15%, ADP and AMP remain constant. There is a production of lactate increasing considerably with the onset of contracture. The measured glycolysis is not sufficient for production of mechanical work. The effect of anoxia on the action potential and the reduction of the sequestration of Ca++ and of the break of actomyosin bridges following the decrease of ATP are considered as causing the series of the mechanical events.
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PMID:[Effect of anoxia on energy supply and isotonic work performance in the myocardium of the frog]. 102 37

Biphasic collagen-induced platelet aggregation, resembling that induced by epinephrine, was noted in platelet-rich plasma (PRP) of 11 stroke and 1 coronary disease patients. Similar pattern of aggregation was not observed in normal PRP. The occurrence of the biphasic collagen aggregation does not appear to relate to platelet count, smoking habit, medication, or other abnormalities such as hypertension, diabetes, and elevated serum lipid levels. However, platelets of these patients were very sensitive to aggregating agents including epinephrine and adenosine diphosphate. The concentration of collagen that elicited biphasic aggregation in these platelets was too weak to aggregate platelets of normal subjects. We believe that the release threshold of these platelets is reduced to such an extent that minute amounts of collagen, which would be insufficient to induce release from normal platelets, are capable of inducing release from these platelets. Both phases of collagen induced aggregation are probably resulted from the activation of the release mechanism.
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PMID:Characterization and significance of collagen induced biphasic aggregation of human platelets. 119 59

Adenosine diphosphate (8 mg per minute for five minutes) was infused into the carotid artery of 63 rabbits. The effects were twofold: systemic hypotension and platelet aggregation in the cerebral circulation. As a consequence of the last effect, platelet emboli were produced which occluded cerebral arteries in a number and size sufficient to cause cerebral ischemia. Areas of focal ischemia were observed through a cranial window, and documented with antipyrine autoradiography. Platelet thrombi were almost entirely transient, being fragmented and removed within a very short time of cessation of ADP infusion. Consequently, no permanent tissue damage ensued. This experimental model approaches the spontaneous transient ischemia attacks (TIAs) in man, demonstrating that these can be caused by pure platelet emboli. A high cholesterol diet administered for two months prior to ADP infusion did not enhance the effect of the procedure or make the platelet aggregation and the following ischemia longer in duration or more severe.
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PMID:Animal model of TIA: an experimental study with intracarotid ADP infusion in rabbits. 119 26

Acetylsalicylic acid (ASA) inhibits thromboxane production and hence platelet aggregation. However, individual variations in platelet aggregability and serum thromboxane B2 (TxB2) concentration after a low dose of ASA (40 mg/day) have been reported. To clarify this issue, we studied plasma thromboxane levels and platelet aggregation in 43 ischemic stroke patients. Of the 22 patients who received 100 mg of ASA daily, dissociation between inhibitory effects of ASA on the plasma TxB2 level and threshold concentrations of adenosine diphosphate was found in three cases after one month of drug administration, and in three cases after six, 12 and 18 months of ASA therapy. This dissociation also developed in two patients after one month and six months, respectively, of treatment in the 21 patients who received 300 mg of ASA daily. The dissociation between the inhibitory effects on plasma TxB2 and the circulating platelet aggregate ratio was found in two cases after taking medication for one month, and in four cases after six, 12, 18 and 24 months of therapy in the 100 mg ASA group. In the 300 mg ASA group, dissociation was noted in two cases after one month of medication, and in two cases after six and 12 months of medication. In these patients, although their TxB2 levels were inhibited to almost unmeasurable levels, platelet aggregation was still not inhibited. This ASA inhibitory dissociation phenomenon on platelet function may be due to the low dose of ASA, individual differences in platelet function in response to ASA therapy, or factors other than those involved in the cyclooxygenase system.
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PMID:Dissociation of inhibitory effects of low-dose ASA on thromboxane production and platelet aggregation in ischemic stroke patients. 136 90


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