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

Platelet-activating factor (PAF) is metabolized by a specific enzyme, PAF acetylhydrolase, which may play an important role in the manifestation of the biological activities of PAF in vivo. The activity of PAF acetylhydrolase in plasma of patients with ischemic stroke was higher than that in healthy controls. The incidence of irreversible platelet aggregation in response to PAF, as well as to ADP, was found to be higher in patients than in controls. The patients whose platelets responded with irreversible aggregation to PAF displayed a higher activity of plasma PAF acetylhydrolase than those with only reversible aggregation. In controls, PAF acetylhydrolase activity correlated positively, although weakly, with LDL-cholesterol, which may reflect the major role of LDL in carrying this enzyme. However, since there was no significant difference in plasma levels of lipids and apoproteins between patients and controls (except for apo B) and there was no significant relationship between the enzyme activity and the levels of other lipids and apoproteins, it is unlikely that increased plasma level of PAF acetylhydrolase activity in stroke patients is accounted for by an abnormality of lipoprotein metabolism. Platelet hyperfunction may be associated with augmented generation of PAF, which, in turn, may bring about the induction of the inactivating enzyme, PAF acetylhydrolase.
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PMID:Activity of platelet-activating factor (PAF) acetylhydrolase in plasma from patients with ischemic cerebrovascular disease. 339 78

148 patients with various forms of cerebrovascular disease (CVD) were studied by means of a multiparametric analysis of in vitro platelet aggregation, based on the following six parameters: ADP and epinephrine primary and secondary aggregation thresholds and percent maximum aggregation induced by optimal concentrations of ADP and epinephrine. These patients were assigned to four study groups, according to clinical diagnosis supported by CT scan, of transient ischemic attack and reversible neurological deficit (TIA-RIND), or completed stroke, in the presence or absence respectively of antiplatelet medical treatment at the time of the study. A statistically significant increase of the in vitro platelet aggregation was found in 44.4% of the untreated TIA-RIND patients and in 33.9% of the untreated stroke patients. However this last group showed a higher percentage of very marked hyperaggregation. Differences between the two treated study groups and controls were not significant. No difference was found in collagen- and ristocetin-induced aggregation between the patient groups and the controls.
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PMID:A multiparametric index of platelet in vitro aggregation in cerebrovascular disease. 342 15

Platelet shape was examined in freshly fixed whole blood, using phase contrast microscopy, from 7 patients post-myocardial infarction, 9 patients undergoing elective angiography for the investigation of angina, and 17 patients with stroke. Platelet shape was abnormal in 29/33 patients and in 20 of them the distribution of platelet shape did not resemble that produced by known platelet activators, by venipuncture techniques known to produce platelet activation, nor by shearing platelet-rich plasma. In particular, the proportion of spherical platelets is too high relative to the proportion of smooth discoid shaped platelets. Addition of platelet-poor plasma from a patient post-myocardial infarction to normal platelet-rich plasma did not reproduce the abnormality in platelet shape. In contrast, for patients post-myocardial infarction platelet shape was normal in platelet-rich plasma, but the platelets were hypersensitive to ADP-induced aggregation. Incubation of citrated whole blood at 37 degrees C resulted in an incomplete disappearance of the spherical platelets suggesting that the abnormal distribution of platelet shape consists of both a reversible and a more persistent abnormality. The reversible portion of the platelet shape abnormality seen in patients with stroke and coronary artery disease may be related to venipuncture-induced platelet activation; however, the nature of the persistent abnormality in platelet shape is presently unknown.
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PMID:Unusual properties of platelet shape in coronary and cerebral artery disease. 367 35

Stroke-prone spontaneously hypertensive rats (SHRSP) were treated with food admixed, 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)-1- piperazinyl]methyl)isoquinoline (Ro 22-4839), a novel cerebral circulation improver, for a period of 15 weeks starting from 5 weeks of age at an average daily dose of 30.6 or 66.0 mg/kg. As compared with normotensive Wistar Kyoto rats, SHRSP in the control group rapidly developed severe hypertension (244 mmHg at the end of the experiments) accompanied with deterioration of cardiovascular parameters including left ventricular hypertrophy, reduction in pumping ability and increase in peripheral vascular tone. At 20 weeks of age (i.e. at the end of experiments), 75% of SHRSP developed stroke signs and concomitant cerebral edema evidenced by the increases in water and sodium contents in the brain. These stroke symptoms were accompanied with a profound externalized shape change of erythrocytes after in vitro treatment with Ca2+ and ionophore A23187, an increased plasma level of thiobarbituric acid reacting substance (TBARS), a measure of lipid peroxides, and a decreased sensitivity of platelets to ADP. The long-term treatment with Ro 22-4839 prevented the progress of stroke and cerebral edema, although the deteriorated cardiovascular parameters were not prevented by the treatment. This compound was also found to prevent the hypersusceptibility of erythrocyte membrane to Ca2+-ionophore and Ca2+, the hypoaggregability of platelets and the elevated plasma TBARS in SHRSP. These results indicate that the beneficial effects of Ro 22-4839 in SHRSP may be attributable to its calmodulin antagonistic and anti-lipid peroxidative actions but not to its hypotensive action.
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PMID:Preventive effects of the cerebral circulation improver 6,7-dimethoxy-1-(3,4-dimethoxybenzyl)-4-([4-(2-methoxyphenyl)- 1-piperazinyl]methyl)isoquinoline on stroke symptoms in stroke-prone spontaneously hypertensive rats. 367 71

In normothermic cats, cerebral blood flow was arrested for 1 hour followed by blood recirculation for 5-6 hours. Functional recovery was evaluated by qualitative and quantitative EEG analysis, and metabolic recovery by measuring metabolite and electrolyte levels in tissue samples taken from the cerebral cortex. In 5 out of 12 animals EEG activity did not recover after ischemia (group I); in 3 animals, intermittent EEG activity (group II) and in 4 animals continuous EEG activity returned during the observation period (group III). In group I the energy state was severely disturbed and an increase of calcium was detected, in group II this disturbance was much less pronounced, and in group III changes in energy metabolism and ion concentration were absent with the only exception of lower ADP levels. During recovery, the total intensity of EEG correlated positively with ATP (p less than 0.01) and inversely with lactate (p less than 0.05), and the intensity of the delta band inversely with sodium content (p less than 0.05). The results obtained demonstrate that electrophysiological recovery after prolonged ischemia is closely correlated with the restoration of the energy state and of electrolyte homeostasis of the brain. The inverse relationship of EEG intensity with lactate and sodium are interpreted as evidence for the adverse effects of ongoing post-ischemic glycolysis, resulting in the activation of the H+/Na+ antiporter for the regulation of intracellular pH.
Stroke
PMID:Relationship between metabolic recovery and the EEG prolonged ischemia of cat brain. 381 Jul 16

Endothelium of cerebral surface vessels (pial arterioles and venules) was injured with a light/dye technique in anesthetized mice. This induced platelet aggregation at the site of injury. The onset of aggregation was monitored through a microscope in mice given angiotensin II acetate, 4 micrograms i.v. 30 minutes earlier. Aggregation latency was compared with that in vehicle treated (saline) mice. Angiotensin II caused a highly significant delay in aggregation within the arterioles which was not related to a change in shear rate of blood. Angiotensin II added to platelet rich plasma, failed to influence the aggregation produced by subsequent addition of 0.5 microM ADP or 0.5 mM sodium arachidonate. Angiotensin is a well known stimulator of prostacyclin synthesis or release, and angiotensin has been reported to inhibit platelet aggregation ex vivo by increasing prostacyclin in the effluent superfusing the mass of aggregating platelets. Our data represent the first report of an antiaggregating effect of angiotensin II in vivo in an intact microvascular bed. The data is consonant with the literature describing increased prostacyclin levels following angiotensin II infusion. The antiaggregating effect of angiotensin in cerebral microvessels may help explain a recent observation describing increased survival of gerbils treated with angiotensin following carotid ligation.
Stroke
PMID:Angiotensin delays platelet aggregation after injury of cerebral arterioles. 381 Jul 22

9 beta-Methyl carbacyclin (9 beta Me; ciprostene) is a synthetic, chemically stable analogue of prostacyclin (PGI2; epoprostenol). The platelet anti-aggregating and cardiovascular effects of 9 beta Me have been compared to PGI2 in anaesthetized monkeys and dogs. In addition, their haemodynamic effects have been compared in open-chest anaesthetized dogs and conscious dogs. Intravenous infusion of 9 beta Me and PGI2 to the anaesthetized monkey resulted in a dose-dependent hypotension, tachycardia and inhibition of ex vivo ADP-induced platelet aggregation. 9 beta Me was 72 times less active than PGI2 both as a hypotensive and anti-aggregating agent. Intravenous infusion of 9 beta Me and PGI2 to the anaesthetized beagle dog resulted in a qualitatively similar haemodynamic profile. Thus both substances induced a dose-dependent hypotension accompanied initially by a slightly increased heart rate, a dose-dependent increase in cardiac output, stroke volume and an increased peak LV dP/dt. At the higher doses studied, the initial increases in the parameters measured were succeeded by dose-dependent falls. 9 beta Me was 76 times less active than PGI2 as a hypotensive agent. In the anaesthetized greyhound, a dose-dependent anti-aggregating and hypotensive effect was seen with either drug, with 9 beta Me being 23 and 40 times less active than PGI2, respectively. Intravenous infusion of 9 beta Me and PGI2 to the conscious beagle dog induced a dose-dependent hypotension and a variable effect on heart rate. 9 beta Me was 33 times less active than PGI2 as an hypotensive agent. The duration of the hypotensive response induced by 9PMe was not significantly different from that induced by PGI2 in either monkey or beagle dog.
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PMID:The cardiovascular and platelet actions of 9 beta-methyl carbacyclin (ciprostene), a chemically stable analogue of prostacyclin, in the dog and monkey. 389 65

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in pial arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .02) by estradiol treatment in young (2 month old) mice. The same treatment had the opposite effect in 4-6 month old mice and significantly delayed the onset of aggregation (p = .01). When platelet rich plasma (PRP) was prepared, aggregation by sodium arachidonate was always inhibited in PRP from estradiol treated mice, irrespective of age. Estradiol treatment had no effect on aggregation induced ex vivo by ADP. Thus the enhanced aggregation observed in pial arterioles of young estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. The data are discussed in light of the literature suggesting enhancement of ischemic vascular disease, including strokes, in patients receiving estrogens, and especially high doses of estrogens.
Stroke
PMID:Effects of estradiol on platelet aggregation in cerebral microvessels of mice. 393 2

The effects of ethanol ingestion on ADP-induced platelet aggregation and associated thromboxane formation were studied in the platelet-rich plasma of 10 healthy male volunteers, each serving as his own control. Ethanol caused a transient decrease in threshold concentration of ADP to produce irreversible aggregation. Over a wide range of ADP total platelet aggregation was increased. In the presence of irreversible aggregation, formation of thromboxane B2 rose from 303 +/- 56 to 950 +/- 212 fmol per 10(7) platelets (p less than 0.01). The effects lasted as long as ethanol was present in blood, did not significantly correlate to blood ethanol levels and exhibited great individual variation. It remains to be proved, whether these observations could contribute to the increased risk of ischemic brain infarction associated with acute ethanol ingestion.
Stroke
PMID:Acute ethanol ingestion increases platelet reactivity: is there a relationship to stroke? 396 61

Intravascular platelet aggregation induced by ADP injection into the carotid artery of rabbits caused ipsilateral cerebrovascular injuries. We have observed the details of these in vivo vascular changes under the electron microscope. Intracytoplasmic vacuole (1.0-2.0 micron in diameter) formation and partial deendothelialization followed by platelet thrombus formation were characteristic changes in the middle cerebral artery. These vacuoles did not contain horseradish peroxidase (HRP) which was used as a marker of vascular permeability change. Compared with these phenomenon, increased vesicular (0.05-0.2 micron in diameter) transport was prominent, and vacuole formation was rarely seen in small vessels, namely, capillaries and arterioles in the cortex. Endothelial cell damage seemed to be more prominent in large arteries, but only the smaller vessels show marked extravasation of HRP-reaction product and perivascular edema. Blood levels of TXB2 and 6-keto PGF1 alpha were significantly increased 3 min after the ADP injection and returned to pre-injection levels at 60 min after. These results suggest that vasoactive substances resulting from platelet activation may play an important role in producing cerebrovascular injuries caused by platelet aggregation induced with ADP.
Stroke
PMID:Cerebrovascular injuries induced by activation of platelets in vivo. 397 62


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