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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental traumatic abscesses were produced in rhesus monkeys by intracerebral injection of nutrient agar contaminated with Staphylococcus epidermidis, and metastatic abscesses were induced by intracarotid embolization of silicone cylinders contaminated with Staphylococcus epidermidis. All monkeys underwent preoperative and serial postoperative carotid angiography. Traumatic abscesses produced early capsular blushes and progressive anterior cerebral artery displacements. Metastatic abscesses induced transient midline shifts but no capsular stains. Postmortem studies on the monkeys showed that mean capsular thickness and segmental wall vascularity of the traumatic and metastatic abscesses were significantly different (p less than 0.001), despite equal abscess ages and similar abscess volumes. In comparison to traumatic abscesses, metastatic abscesses demonstrated reduced inflammatory cell infiltration and retarded collagen formation around proliferating capsular vessels. Brain surrounding the metastatic abscesses demonstrated ischemic changes. The results suggest that 1) capsular blushes during cerebral angiography are secondary to vascular proliferation within the capsule and not to compression of surrounding brain, 2) vascular staining reflects capsular thickness, 3) capsular vascularity contributes to collagen formation, 4) encapsulation is dependent upon the integrity of surrounding brain, and 5) adjacent cerebral ischemia may impede inflammatory responses involved in capsule formation.
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PMID:Role of vascular proliferation on angiographic appearance and encapsulation of experimental traumatic and metastatic brain abscesses. 41 22

A 49-year-old man had for 30 years suffered from severe recurrent thromboembolism with leg-vein thrombosis, pulmonary emboli, mesenteric infarction, cerebrovascular accident, cerebral vein thrombosis, portal vein thrombosis and femoral artery occlusion requiring leg amputation. In addition to moderately increased clotting activation with single-fold positive demonstration of fibrin monomers and a D-dimer concentration of 1 mg/l platelet aggregation was increased and could not be influenced by aspirin, 300 mg daily. Despite aspirin there were recurrent transitory attacks of cerebral ischaemia. Fibrin monomers were threefold positive and D-dimer concentration was increased to 4 mg/l (elevated clotting activation). Ticlopidine administration (250 mg daily) reduced adenosine diphosphate-induced platelet aggregation by 30% without effect on collagen-induced platelet aggregation. In parallel to these changes the patient's general condition clearly improved: fibrin monomers were no longer demonstrated and the D-dimer level fell to 0.5 mg/l.
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PMID:[Recurrent thromboembolism due to increased acetylsalicylic acid-resistant platelet aggregation]. 188 75

Acute myocardial infarction is most commonly initiated by fissuring of an atheromatous plaque. Through such fissures the blood is exposed to thrombogenic constituents of the intima, causing thrombotic obstruction of the coronary artery. Why plaque fissuring occurs is not known. Our investigation is to establish which types of plaque undergo fissuring by relating their mechanical with their cellular and biochemical properties; and to quantify the distribution of fissures. Results so far indicate that fissures occur predominantly in plaques with lipid pools in one segment of intima, and that the commonest single site of fissuring is that of maximal stress concentration as predicted by computer modelling. The results also suggest that arterial spasm at the immediate site of fissuring is not involved, as more than half the fissures occur at sites where there is no residual medial smooth muscle. Obstructive coronary thrombosis is initiated in most cases by plaque fissure with local haemorrhage which induces intravascular platelet aggregation. Recent observations with novel techniques have provided evidence that platelet aggregation in vivo is initiated by ADP and potentiated by thromboxane A2 and thrombin, with actual contribution of exposed collagen still undetermined. These observations provide an explanation for the limited effectiveness of any simple platelet-inhibiting drug, including Aspirin, by itself whenever arterial, eg. coronary or cerebral thrombosis is initiated by haemorrhages into atheromatous plaques. On the other hand, Aspirin is significantly effective when myocardial infarction follows unstable angina and when strokes follow transient episodes of cerebral ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary thrombosis: pathogenesis and prevention. 210 21

We studied 23 patients suffering cerebral ischemia who also had laboratory evidence of either a lupus anticoagulant (LA) or an abnormal anticardiolipin antibody (ACA). Four patients had lupus or a lupus-like illness, three had drug-induced lupus, and 16 had no overt evidence of collagen-vascular disease. Cerebral ischemic events were multiple in 71% of the patients; two patients presented with multi-infarct dementia. Recognized cerebrovascular disease risk factors were present in 57% of the patients. The partial thromboplastin time was prolonged in only 35% of the patients. An LA was identified in 15 of 21 patients tested, and an elevated ACA titer was identified in 10 of 12 patients tested. Simultaneous assays for LA and ACA were discordant in eight of 10 patients tested. LA- and ACA-associated brain ischemia is often recurrent, but other risk factors for cerebrovascular disease are often present. The laboratory findings in such patients may display considerable heterogeneity.
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PMID:Lupus anticoagulants, anticardiolipin antibodies, and cerebral ischemia. 249 72

A new canine model of focal cerebral ischemia has been developed employing intravascular delivery of microfibrillar collagen via femoral catheterization. In 13 dogs, dose-effect studies showed neurologic deficits (ranging from mild hemiparesis to death) related to the dose of microfibrillar collagen delivered. In another 10 dogs, 0.5 ml of 60 mg/ml microfibrillar collagen was injected into the common carotid artery; neurologic assessment over 48 hours revealed a survivable stroke syndrome in seven dogs, death at 40 hours in one dog and at less than 12 hours in another, and no clinical effect in one dog. The eight surviving dogs were sacrificed at 48 hours; nine of the 10 dogs had middle cerebral artery distribution infarcts (two grossly hemorrhagic and five grossly nonhemorrhagic) on histologic examination. Angiography in three dogs demonstrated no significant major vascular occlusion. All seven dogs with survivable strokes demonstrated a dense hemiparesis at 24 hours that improved to ambulatory status at 48 hours. The use of microfibrillar collagen to produce middle cerebral artery strokes in dogs provides a new opportunity to study cerebral ischemia without surgery involving the cervical or cranial vasculature. Dogs have larger brains than other common animal models and thus are more amenable to study with imaging modalities. A model with a measurable but survivable insult provides an opportunity for short- and long-term clinical follow-up and for the investigation of therapeutic interventions.
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PMID:Microfibrillar collagen model of canine cerebral infarction. 279 67

We describe a series of experiments in which a subhuman primate model was used to create temporary and permanent cerebral ischemia by three separate mechanisms. In the first group of five baboons, a hemodynamic model was produced by creating unilateral and bilateral carotid stenotic lesions of varying degrees with and without associated reduction in systemic perfusion pressure. Only global ischemic changes and no focal changes resulted. In the second group of three baboons, a macroembolic model was produced by introducing solid particulate material into the extracranial circulation. No reversible contralateral focal neurologic changes resulted. In the third group of 11 baboons, cerebral ischemia was produced by introducing agents known to cause platelet aggregation (arachidonic acid, adenosine diphosphate, and collagen) into the extracranial arterial circulation. Arachidonic acid caused seizures, adenosine diphosphate caused severe postural hypotension, and only collagen fibrils produced a picture resembling a transient ischemic attack. We propose a theory that intravascular activation of the prostaglandin cascade by chemical initiation may result in the pathophysiologic changes of transient cerebral ischemia.
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PMID:Pathogenesis of transient ischemic attacks and stroke in baboons. 292 78

We tested the antiplatelet effects of low-dose aspirin in patients with occlusive cerebrovascular disease, because conventional dosage aspirin inhibits vascular synthesis of prostacyclin at the same time that it inhibits platelets. The effects on platelet function and thromboxane A2 synthesis of 40 mg of aspirin daily or 40 mg aspirin plus dipyridamole were measured in 23 patients starting within a week after the onset of cerebral ischemia. All patients had normal baseline platelet aggregation responses to four stimuli: arachidonate, epinephrine, adenosine diphosphate and collagen. The generation of thromboxane A2 by platelets, measured as serum thromboxane B2, was also normal. After 3 to 7 days of low dose aspirin therapy, platelet aggregation responses were suppressed to the extent observed with higher dosage aspirin. Serotonin release during platelet aggregation was inhibited by more than 95% and thromboxane B2 levels in clotted blood fell by more than 95%. Responses to aspirin treatment were similar in patients with transient ischemic attacks and in those with stroke and were also similar in both sexes. No differences in platelet responses were observed between patients receiving aspirin alone and aspirin plus dipyridamole. Thus 40 mg aspirin daily inhibited platelet responses as effectively as higher doses of aspirin in patients who had recent cerebral ischemia and showed a cumulative antiplatelet effect.
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PMID:Effects of low dose aspirin on platelet function in patients with recent cerebral ischemia. 396 66

Studies evaluating the static and dynamic characteristics of the common carotid bifurcation are described. Slow motion angiographic frames, real time B-mode images and time position M-mode tracings have demonstrated appreciable vessel wall motion with an increase in distensibility at the carotid bulb compared to the proximal common carotid artery. Histopathological studies suggest that changes in the carotid artery elastin and collagen structure may contribute to the increased distensibility at the carotid bulb. The presence or absence of a cervical bruit did not correlate with the ultrasonic demonstration of plaque or blood flow turbulence. Mechanical factors relating to the development of symptoms of cerebral ischaemia are discussed.
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PMID:Transient ischaemic attacks: the static and dynamic morphology of the carotid artery bifurcation. 708 73

Berberine (Ber) 20 mg.kg-1.d-1 for 1, 3, or 5 d inhibited platelet aggregation induced by ADP, arachidonic acid (AA) and collagen (Coll) in rats with 24 h reversible middle cerebral artery occlusion (MCAO), and the platelet adhesiveness was inhibited as well. Using radioimmunoassay method, the thromboxane B2(TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) contents in rat plasma were measured 24 h after MCAO. The results indicate that the TXB2 levels after drug treatment were lower than those in ischemia control rats, but the 6-keto-PGF1 alpha levels showed no obvious difference between the two groups. The same dose of Ber was also shown to inhibit thrombosis formation. This suggests that the decline of platelet aggregation and decrease of TXB2 content may be one of the important factors involved in the anti-cerebral ischemia effect of Ber.
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PMID:[Effects of berberine on platelet aggregation and plasma levels of TXB2 and 6-keto-PGF1 alpha in rats with reversible middle cerebral artery occlusion]. 778 38

Severe cerebral ischemia was successfully treated in a patient with arteriosclerotic aortic arch syndrome by an iliac-subclavian-internal carotid artery bypass, using an extra-anatomic modified Dacron prosthesis externally coated with collagen. The procedure and material seem suitable for managing high-risk patients who have critically stenotic or occluded branches of the aortic arch and who would not tolerate anatomic, transthoracic repair.
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PMID:Iliac-subclavian-internal carotid artery bypass for cerebral ischemia due to multiple proximal supra-aortic vessel obstruction (aortic arch syndrome). 797 76


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