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

The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.
Stroke
PMID:The effect of a simulated subarachnoid hemorrhage on cerebral blood flow in the monkey. 0 Aug 20

Microsurgical and microscopic methods were employed in guinea pigs to expose, observe, and measure response characteristics of cerebral cortical pial microvessels and microcirculation to traumatic and nontraumatic experimental subarachnoid hemorrhage. Bleeding produced by vascular micropuncture was associated with a 44.3% arteriolar constriction. Topical application of homologous blood alone produced a 33.2% vasoconstriction. Observed microcirculatory flow characteristics subsequent to such microvascular changes were consistent with those known to be associated with cerebral cortical infarction. These changes could be prevented or reversed by topical application of the alpha adrenergic blocker, phenoxybenzamine. Topical pretreatment with the beta adrenergic blocker, propranolol, prevented blood-induced spasm, but did not reverse such spasm once it had been established. A chemo-mechanical mechanism is suggested as underlying the vasoconstriction association with rupture of pial microvessels. It is thought that consideration of such microvascular characteristics, in conjunction with those known to be associated with larger intracranial vessels, adds to current knowledge of the pathophysiology of subarachnoid hemorrhage and may be extrapolated to bear future clinical import.
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PMID:Pial microcirculation in subarachnoid hemorrhage. 23 72

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

Prinzmetal's variant of angina occurred in a 48-year-old man who sustained two attacks of subarachnoid hemorrhage within 10 days. The first anginal pain started at the same time that the second cerebrovascular accident developed, but subsequent anginal episodes were not accompanied by other symptoms or signs that indicated new development of subarachnoid hemorrhage. Twelve days later, when nuchal rigidity was fairly improved, the episodes of chest pain ended. A vasospasm of the large coronary arteries--probably due to the derangement of the autonomic nervous system caused by subarachnoid hemorrhage--was presumed to contribute to the occurrence of the variant angina. Based on this case and on review of the literature, we propose that coronary arterial spasm is one of several causes of the cardiac changes seen in subarachnoid hemorrhage.
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PMID:Prinzmetal's variant angina associated with subarachnoid hemorrhage: A case report. 43 81

The cat basilar artery was exposed using the transclival approach. After administration of 5% ethanol via intravenous infusion, vasospasm was produced by applying the animal's fresh arterial blood to the exposed artery. The resultant vasospasm was of markedly reduced intensity and duration as compared to vasospasm in control animals. In ethanol-treated animals with spasm induced from non-autogenous fresh arterial bloof free of ethanol, a reduction in the duration of vasospasm was noted although the initial intensity of spasm was similar to control animals. There was no anti-spasm effect if the ethanol infusion followed the production of vasospasm.
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PMID:Effect of intravenous ethanol on cerebral vasospasm produced by subarachnoid blood. 50 94

A model for production of spasm of the anterior cerebral artery in primates is presented. The model consists of injection of 0.35 cc of fresh blood into the chiasmatic cistern through the optic canal after orbital exenteration. Clinical and angiographical follow-up is possible. The clinical appraisal of acute and chronic changes can be accomplished in the awake animal.
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PMID:A model for spasm of the anterior cerebral artery. 81 46

Cerebral vasospasm was produced in the dog basilar artery by topically applied five-day-old clotted autologous blood, but not by freshly drawn blood. The spasm was reversed by methysergide, an antiserotonin agent. However, vasospasm was not produced by five-day-old clotted autologous blood from dogs pretreated with reserpine. This suggests platelet serotonin or a similar, unidentified substance as the vasospastic element in dog blood responsible for experimental vasospasm from topically applied whole blood. Other experimental data support these findings.
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PMID:Reserpine and cerebral vasospasm. 83 51

A marked pleocytosis and increase in the levels of prostaglandin F2a (PGF2a) and prostaglandin E2 (PGE2) were noted in cerebrospinal fluid of dogs within two hours following the intracisternal injection of thrombin. Quantitation of the prostaglandins (PG's) was done by gas chromatography-mass spectroscopy using deuterated PGF2a and PGE2 as internal standards. Whereas the levels of these prostaglandins were below the sensitivity of the method in control animals, a marked increase was noted following thrombin. PGF2a levels were 15-21 ng/ml and the PGE2 levels were 55-72 ng/ml. This concentration of the PG's is adequate to cause spasm of the cerebral vessels and could explain the spasm which occurs following the intracisternal injection of thrombin. These two effects, a pleocytosis and elevation of PG levels, may be specific to thrombin.
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PMID:Pleocytosis and elevation of prostaglandins F2a and E2 in cerebrospinal fluid following intracisternal injection of thrombin. 84 88

The contractile effects of thromboxane A2 (TxA2), a labile arachidonic acid metabolite, were studied in arterial smooth muscle strips. TxA2 was generated upon the addition of 255 nM prostaglandin cyclic endoperoxide H2 to human platelet particles in the muscle bath. Using the isometric contaction produced by 40 mM K+ in isotonic saline as the reference contraction, bovine middle cerebral artery strips contracted to 153 +/- 14% of the reference response while bovine coronary and porcine coronary, renal and common carotid strips contracted to 47 +/- 3, 26 +/- 5, 43 +/- 2 and 2 +/- 1% of reference, respectively. The cerebral artery response to the TxA2 generating system was as great as the maximum response to prostaglandin F2alpha and two times the maximum response to 5-hydroxytryptamine. Because TxA2 is formed by brain tissue and released from aggregating platelets, it may be important in the pathogenesis of spasm associated with injured brain tissue or pathologic changes leading to platelet aggregation.
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PMID:Cerebral arterial smooth muscle contraction by thromboxane A2. 89 44

Percutaneous transluminal angioplasty (PTA) has become an established treatment for peripheral, renal and coronary vascular disease, where the success rate approaches 90% with complications occurring in less than 5% of patients. There has been a reluctance to recommend PTA of the internal carotid artery (ICA) because of concern about the risks of cerebral embolism. However, there are now a number of reports of technically successful PTA for ICA stenosis, as well as stenosis of other brachiocephalic arteries, demonstrating an improvement in vessel diameter and contour. Complications to date include transient neurological symptoms, asymptomatic carotid dissection and arterial spasm, but the risk of permanent stroke seems to be relatively low. The risks of embolization may be reduced by anticoagulation and avoiding arteries with obvious thrombus or ulceration. Current technical difficulties are likely to be surmounted by improvements in catheter design. PTA is most suitable for smooth ICA stenosis causing haemodynamic symptoms, fibromuscular dysplasia, surgically inaccessible stenosis, and patients with medical risk factors increasing the risks of carotid endarterectomy, such as ischaemic heart disease. Only brief admission is required, avoiding the surgical and anaesthetic risks of carotid endarterectomy. The preliminary results are encouraging enough to set up a randomized trial to determine the risks and benefits. It remains to be seen whether alterations in the calibre or contour of the vessel wall will reduce subsequent stroke. Whether cerebrovascular PTA will enter general use will depend on the balance of the risk-benefit equation.
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PMID:Balloon angioplasty for cerebrovascular disease. 135 77


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