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

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

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

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

The effect exerted on the partially ischaemic heart when administering 0.9 mg/kg L-3-(beta-hydroxy-alpha-methylphenethylamino)-3'-methoxypropiophenone (oxyfedrine, ildamen) approx. 10 min after i.v. application of 0.05 mg/kg digoxin was tested on 20 dogs previously anaesthetized with propiomazine-pentobarbital. The following parameters were studied and subsequently compound with the results of former trials of ours' without digoxin premedication: aortic pressure (ASP, ADP), left-ventricular pressure (LVSP, LVEDP), heart rate (HR), cardiac output (HMV), stroke volume (SV), dp/dtmax, dp/dtmax/IP, t-dp/dtmax, blood flow in the normal and partially ischaemic myocardium, the latter being measured with heat conductance probes and labelled microspheres. ASP and ADP show the same reduction--as compared with the control value--both after the administration of oxyfedrine with and without digoxin premedication. After digoxin premedication oxyfedrine led to a somewhat less marked reduction of LVSP; on premedication with digoxin LVEDP was slightly increased whereas it was reduced after additional administration of oxyfedrine as was also the case without digoxin pretreatment. The increase in HR after oxyfedrine is almost the same as without digoxin pretreatment. Also the increase in HMV and the SV lowering are not influenced by digoxin. By administration of oxyfedrine dp/dtmax is always increased by the same amount, starting from the already increased value after digoxin premedication, which is probably an additive effect. The same applies to the quotient dp/dtmax/IP. After oxyfedrine the time t-dp/dtmax is lowered by the same amount, irrespective of a digoxin premedication. Oxyfedrine does not produce a further increase in the heat conductance values after previous application of digoxin; when measuring the blood flow with labelled microspheres the same result was found, which means that by previous administration of digoxin the circulatory effect of oxyfedrine is obviously inhibited. Summing up one can say that by combining the active principles digoxin and oxyfedrine the function parameters of the heart can be influenced only positively.
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PMID:[The action of oxyfedrine on haemodynamics, inotropism and blood perfusion of the partially ischaemic myocardium after digoxin premedication. Studies on anaesthetized dogs (author's transl)]. 719 64

Cerebral hypoxia-oligemia was produced by lowering of the arterial PO2 to 30 mm Hg and by right common carotid artery occlusion in rats who were pretreated with intravenous Krebs' solution, gamma-hydroxybutyrate (GHB) (500 mg/kg) or gamma-butyrolactone (GBL) (300 mg/kg). At 0.5 h exposure the right cerebral hemisphere of animals receiving Krebs', GHB or GBL showed equivalent decreases of ATP and phosphocreatine and increase of ADP, AMP and lactate which indicated that these depressant drugs had no beneficial effect on the energy metabolism of the acutely hypoxic-oligemic brain. In a second series of rats in which Krebs' solution, GHB or GBL were administered to animals during the early recovery period from 0.5 h hypoxic-oligemic exposure, the brain metabolic patterns of the right hemisphere indicated that GHB retarded the restitution of energy phosphates and the oxidation of the accumulated lactate; whereas, GBL led to a delayed metabolic deterioration. It is concluded that GHB and GBL do not beneficially alter cerebral energy metabolism during acute hypoxia-oligemia and that their administration during restitution may result in metabolic alterations which suggest an unfavorable effect.
Stroke
PMID:Effects of gamma-hydroxybutrate and gamma-butyrolactone on cerebral energy metabolism during exposure and recovery from hypoxemia-oligemia. 739 64

The hemodynamic changes which occur when clamping and unclamping the aorta during reconstructive surgery might be a threat to the elderly patient with concomitant cardiac disease. In addition, the cross-clamping induces a temporary ischemia of the legs, with severe metabolic derangement after the release of the aortic clamp. We have studied the effect of a intraoperative adrenergic block (phenoxybenzamine plus metoprolol) on the central circulation and the skeletal metabolism in 14 patients undergoing aortic reconstruction to treat occlusive arteriosclerotic disease. Cardiac output, heart rate, arterial and pulmonary artery pressures, and cardiac filling pressures, as well as femoral venous blood flow were studied. Biopsy specimens of the lateral vastus muscle and blood samples from the radial artery and iliac vein were taken before aortic clamping, and before, 30 minutes, four and 16 hours after the aorta was unclamped, as well as five days postoperatively. In addition, intramuscular temperature and pH were measured. Glycogen, glucose, lactate, pyruvate, ATP, ADP, AMP, phosphocreatine (PCr) and creatine (Cr) contents of the muscle and lactate and pyruvate concentrations in iliac venous and radial arterial blood were determined using enzymatic fluorometric techniques. Mean arterial blood pressure (MAP) averaged 80 mmHg before clamping, chiefly because of the low systemic vascular resistance (SVR), and left ventricular stroke work (LVSW) was normal. At clamping MAP, SVR, LVSW, remained unchanged. MAP and LVSW were unaffected even though SVR decreased slightly after the aorta was unclamped and resulted in an increased cardiac output, mainly due to a higher stroke volume. No major change in the pulmonary circulation was observed. During clamping the muscle lactate/pyruvate ratio increased, intramuscular pH and femoral venous blood flow decreased indicating insufficient tissue perfusion. Energy charge (EC), the adenylate (ATP + ADP + AMP) and creatine (PCr + Cr) pools were, however, unchanged. In spite of a restored blood flow to the legs, a severe metabolic derangement of the muscle was observed after declamping, with lowered EC, ATP + ADP + AMP and PCr + Cr indicating cellular damage. No improvement in the condition of the cells was observed 16 hours after operation. In conclusion, we found that by using neurolept anesthesia and an intraoperative adrenergic block in combination with a differentiated fluid therapy the central circulation stabilized and was largely unaffected by the clamping and unclamping procedures. In spite of the improved central hemodynamics no favorable effect on the skeletal muscle metabolism was observed.
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PMID:Temporary incomplete ischemia of the legs induced by aortic clamping in man: effects on central hemodynamics and skeletal muscle metabolism by adrenergic block. 745 55


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