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

We have studied the effects of the calcium antagonist verapamil on the epicerebral arteriovenous transit time and regional epicerebral circulation of dogs by direct measurement of arterial diameters, fluorescein angiography, and krypton-85 regional epicerebral blood flow analysis. A large craniectomy was performed and vasoconstriction was induced by the subarachnoid injection of human platelet-rich plasma (PRP) pretreated with 25 mu M of ADP to cause maximum aggregation. Once vasoconstriction was established, verapamil (0.1 mg/kg) was topically applied to the perforated arachnoid. The PRP-ADP produced a mean decrease in the arterial diameters of 38.2 +/- 1.6% (p less than 0.01) at 10 minutes after its injection and verapamil produced a mean dilatation of 19.5 +/- 2.5% (p less than 0.01), compared to control values. Regional epicerebral blood flow was 54.9 +/- 3.4 ml/100 g/min in the control state, 34.8 +/- 3.2 ml/100 g/min (p less than 0.01) during vasospasm, and 78.2 +/- 4.5 ml/100 g/min (p less than 0.01) after verapamil. Fluorescein angiography, after verapamil, demonstrated a mean acceleration of the arteriovenous circulation time of 4.5 +/- 0.8 seconds (p less than 0.01) compared to the spasm value. We concluded that the topical application of verapamil can dilate previously constricted cortical arteries and that this dilatation is associated with acceleration of the epicerebral transit time and increased cerebral blood flow.
Stroke
PMID:The effects of calcium antagonism on the epicerebral circulation in early vasospasm. 650 12

The possibility that cerebral ischemia or cerebral hypoxia may initiate a series of free radical reactions in brain tissue lipid constituents was explored by measuring sequential changes in chemiluminescence values and energy metabolism during brain hypoxia in the rat. Brain hypoxia was induced by means of arterial hypoxemia (PaO2 17-22 mmHg), normocapnia (PaCO2 28-38 mmHg) and normotension (MABP 100-140 mmHg). To obtain lowered PaO2, 4% O2--96% N2 mixed gas was used. Analysis of the chemiluminescence spectra for the purpose of luminous mechanism investigation was again attempted. No peroxidation occurred in the pre-hypoxic state since there were no photon counts. Chemiluminescence began to rise in the hypoxic state and remained at a high value in the post-hypoxic state. Specifically in the hypoxic state, the 3 min period showed 231 +/- 35 counts/10 sec X g (n = 5) and the 5 min period showed 154 +/- 62 (n = 19) counts/10 sec X g. In the post-hypoxic state, the 5 min period showed 217 +/- 79 counts/10 sec X g (n = 9) and the 30 min period showed a decrease similar to the pre-hypoxic state. The chemiluminescence spectroanalysis showed five peaks in wavelength at 480 nm, 520-530 nm, 570 nm, 620-640 nm and 680-700 nm. Sequential changes in energy metabolism revealed that hypoxia caused marked brain lactic acidosis, an increase in both ADP and pyruvate, and a fall in glucose. However, all metabolites recovered at 30 min in the post-hypoxic state, which suggests this was reversible brain hypoxia. Sequential changes in chemiluminescence values and energy metabolism imply the occurrence of free radical reaction in the hypoxic and post-hypoxic brain. The spectroanalysis reveals the luminous mechanism as follows: 1 delta g + 1 delta g----23O2 + h mu
Stroke
PMID:Chemiluminescence in hypoxic brain--the first report. Correlation between energy metabolism and free radical reaction. 650 18

Sustained contraction of isolated canine basilar artery was induced by addition of prostaglandin F2 alpha, prostaglandin E2, hemoglobin-containing solution, or serum. Human platelet aggregation was induced by 1.0 microM adenosine diphosphate. The sustained contraction of basilar artery and the aggregation of platelet, particularly its secondary aggregation, were inhibited in a dose-dependent manner by addition of chlorpromazine or amitriptyline; calmodulin antagonist. The molar concentrations at 50% inhibition by chlorpromazine or amitriptyline were 5.9 to 7.7 microM or 28 to 39 microM for the contraction of basilar artery and 57 microM or 111 microM for the secondary aggregation of platelet. The results were discussed mainly on the basis of interaction of psychotropic drugs and Ca2+, calmodulin-dependent enzymes, particularly myosin light chain phosphorylation.
Stroke
PMID:Responses of isolated canine basilar artery and human platelet to chlorpromazine and amitriptyline. 658 79

The extent of the ADP-induced platelet release reaction has been determined in 107 patients admitted to hospital with acute stroke. In 43 of the patients a precise diagnosis was obtained and in those with proven thromboembolic stroke the mean extent of the release reaction was significantly higher than for those with either primary haemorrhagic stroke or those with subarachnoid haemorrhage. Enhanced platelet reactivity was also found in the patients in whom a precise diagnosis could not be obtained, most of whom probably had cerebral infarction. Comparison of the results obtained for patients with stroke with those obtained for individuals who had not experienced a stroke showed that thromboembolic stroke is associated with platelet hyperactivity while haemorrhagic stroke is associated with platelet hypoactivity. The part that abnormalities of platelet behaviour, whether causal or consequential, might play in occlusive stroke and intra-cranial haemorrhage is discussed and the need for large scale prospective studies is emphasised.
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PMID:ADP-induced platelet release reaction in acute stroke. 663 31

Platelet aggregation in the post-acute phase of 48 patients with cerebral thrombosis was measured to see if any specific type of cerebral infarction is associated with enhanced platelet aggregation. All patients were examined with cerebral angiography and computed tomography (CT). Stenotic lesions in major cranial arteries were analyzed by measuring the apparent diameter. Severe stenosis was defined as 75 per cent constriction or more. Enhanced aggregation of platelets (secondary aggregation at 1 microM ADP or less) was present in 5 of 25 patients (20%) who had severe vessel stenosis or occlusion. CT examination frequently revealed both cortical and deep involvement. On the other hand, 13 of 23 patients (57%) with less stenotic lesions showed enhanced aggregation and that was statistically significant (p less than 0.05). Many patients of this group had persistent hypertension and small deep infarctions. Platelet aggregation was also measured in 20 hypertensive control subjects without stroke. Four of them (20%) showed enhanced aggregation. These findings suggest that a combination of enhanced platelet aggregation and hypertension increases the risk of small deep infarctions accompanied by mild stenotic changes of the major cranial arteries.
Stroke
PMID:Platelet aggregability in cerebral thrombosis--analyzed for vessel stenosis. 665 4

A variety of platelet function tests were performed in patients with four forms of obstructive cerebrovascular disease (CVD); transient ischemic attacks (TIA), reversible ischemic neurological deficit (RIND), cerebral infarct, and cerebral embolism of cardiac source in rheumatic valvular heart disease (RVHD). Platelet studies included platelet aggregation induced by ADP and ristocetin, spontaneous platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and percentage of large platelets (megathrombocytes). Serial testing was carried out in acute stroke patients. The effect of aspirin therapy was also evaluated. A clear difference in results was observed between patients with cardiogenic embolism and those with other forms of CVD. In patients with TIA, RIND, and cerebral infarct, platelet aggregation, both induced and spontaneous, was enhanced along with elevation of plasma VIII:vWF and PAEF, and increased percentage of megathrombocytes. In patients with cardiogenic embolism, however, these studies were negative except for percent megathrombocytes. This value was increased in the embolic patients with RVHD in comparison with non-embolic patients with RVHD. Increase in platelet aggregation to ADP and percent megathrombocytes developed slowly over a week following stroke. Induced and spontaneous platelet aggregation, and percent megathrombocytes could be normalized with 600 mg aspirin p.o. These studies suggest that a systemic increase of hyperaggregable platelets and of plasma activators of platelet function exists in thrombotic CVD and may be related to its pathogenesis, while local hemodynamic factors may be more important in the thrombogenesis of cardiogenic embolism.
Stroke
PMID:Platelet function tests in thrombotic cerebrovascular disorders. 665 25

It is shown that the amount of ATP in rats under hypothermia up to heat stroke lowers and that of ADP and AMP somewhat rises. Ionol administration normalizes the ATP level and increases the ADP and AMP contents. Inhalation of CO2 and especially administration of ionol contribute to a higher resistance of the animals to hyperthermia.
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PMID:[Influence of hyperthermia and protective effect of ionol and carbon dioxide gas on ATP, ADP and AMP content of the rat brain]. 678 22

Most earlier studies of platelet function in stroke patients have been performed in the acute phase and are hampered by diagnostic insecurity. A sample of totally 67 young adults below the age of 55, with ischemic cerebrovascular disease (TIA and minor stroke) were investigated at a late stage after acute disease and compared to 20 healthy controls. Patients with atherosclerotic signs at cerebral angiography had significantly (p less than 0.05) higher platelet factor 3 availability than angionegative patients. Unexpectedly, female patients compared to male patients had significantly (p less than 0.05) larger ADP-release after stimulation with collagen in vitro. Furthermore, when female patients were compared to female controls a significantly (p less than 0.05) increased platelet factor 3 availability was found. The results indicate that platelets in female patients may have an increased tendency to aggregate in vivo. Patients had significantly (p less than 0.01) shortened platelet cyclooxygenase regeneration half times (PRT). This was correlated to high levels of factor VIII related antigen (r=0.59) and high levels of factor VIII biological activity (r=0.67), indicating that platelets may be consumed by platelet adhesion and mural thrombi formation in abnormal vessel walls. PRT appears to be a reliable method to assess platelet function in vivo and to optimize aspirin dose and dose intervals in the individual.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. II. Abnormalities in platelet ADP release, platelet cyclooxygenase regeneration time and platelet factor 3 availability. 681 Apr 97

Routine blood analysis, platelet counts, number of circulating platelet aggregates (CPA) and platelet aggregation in vitro against adenosine-diphosphate (ADP), epinephrine and collagene were studied in 45 healthy controls, in 10 hospitalized patients with other neurological diseases than stroke and in 12 patients with transient ischemic attacks (TIA) before and after prophylactive treatment with anticoagulants (AC) or antiplatelet drugs (APD). Except for lower hemoglobin and hematocrit levels in women, sex, smoking, oral contraceptives of pregnancy did not significantly influence the routine blood parameter. Smoking females taking oral contraceptive had an increased number of CPA and the most easily induced aggregation in vitro. Patients with TIA had no significant differences in blood or platelet findings versus the healthy controls (except smoking females on oral contraceptives) or the non-stroke patients, even though individual patients could have high numbers of CPA and an easily induced platelet aggregation in vitro. Treatment with AC did not influence platelet function, whereas APD therapy decreased the number of CPA and inhibited the secondary platelet aggregation in vitro.
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PMID:Comparison between induced platelet aggregation and circulating platelet aggregates as platelet function tests in patients with transient ischemic attacks. 707 82

The frequency of irreversible induced PA (IPA) by ADP or EN has been studied in 246 stroke patients. Compared to an age and sex matched control group IPA was more frequent in patients with CVD. Eighty six patients were referred to treatment of IPA with ASA or pentoxifylline or both compounds as combined treatment. ASA as well as PO were found to satisfactorily influence IPA however, the best therapeutic results have been achieved by combined treatment.
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PMID:Special therapeutical aspects of cerebrovascular disease. 718 12


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