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

Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enchanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation. Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit. Findings from patients with cerebral infarction were compared against those of three control groups: (1)normals, (2)a stroke control group and(3)a stroke risk factor group. Plasma HMWFC findings were significantly (p less than 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p less than 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha1-antitrypsin and alpha2-macroglobulin also were significiantly higher (p less than 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p less than 0.001), and high HMWFC values were associated with poor clinical outcome. Plasma HMWFC values were significantly higher (p less than 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism. These findings docunment the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.
Stroke
PMID:Blood coagulation and plasma fibrinolytic enzyme system pathophysiology in stroke. 6 Aug 7

The hemodynamic response to slow and rapid defibrination was sutdied in anesthetized beagle dogs, with the following results: 1. Slow defibrination was a benign procedure that had little or no effect on the hemodynamic variables studied. 2. Rapid defibrination induced statistically significant decreases in cardiac output, stroke volume, and mean aortic arterial pressure. 3. Bradycardia, a drop in mean left v"ntricular pressure, cardiac and minute work indices, an increase in pulmonary artery pressure, and a drastic rise in pulmonary and systemic vascular resistances were also observed. Although physiologically apparent, these changes were not statistically significantly different from control levels. 4. Pulmonary capillary wedge pressure, left ventricular end-disatolic pressure, arterial pH, and blood gases were not altered by rapid defibrination. 5. In view of the similarities between the hemodynamic changes observed after rapid defibrination and acute myocardial ischemia, the role of decreasing fibrinogen concentrations and blood viscosity in aucte myocardial infarction and the sudden death syndrome is questioned.
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PMID:Hemodynamic effects of slow and rapid defibrination with defibrizyme, the thrombin-like enzyme from venom of the timber rattlesnake. 23 15

Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.
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PMID:Cerebral and retinal vascular complications of inflammatory bowel disease. 44 68

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
Stroke
PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Studies of 11 patients with haemorrhagic stroke revealed no significant change in kaolin cephalin clotting time, prothrombin time, thrombin time, PF 3 availability, platelet count and factor V and VIII during the first week. Plasma fibrinogen was significantly increased while factors VII + X were decreased (borderline significance). Prolongation of plasma recalcification time and decrease in heparin tolerance reached borderline significance. There was moderate, but significant, increase in serum antithrombin activity and plasma (euglobulin fraction) fibrinolytic activity.
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PMID:Blood coagulation and fibrinolysis in haemorrhagic stroke. 58 May 8

Cerebral thromboembolic stroke in the young is uncommon. Disturbances in the n ormally existing dynamic equilibrium between coagulation and fibrinolysis may play a major role in the pathogenesis of such episodes. In a search for a possible hypercoagulable state platelet adhesiveness by the method of Eastham, plasma fibrinogen and euglobulin clot lysis times were estimated in 46 patients. A group of 15 normal subjects matched for age and sex were also studied for comparison. Significant increase in platelet adhesiveness (P less than 0.001) and plasma fibrinogen (P less than 0.001) was noted in the patients when compared with the normal subjects. Absence of corresponding increases in fibrinolytic activity in the patients suggests disturbed equilibrium between coagulation and fibrinolysis. The possibility of a hypercoagulable state in these cases is discussed.
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PMID:Platelet adhesiveness, plasma fibrinogen, and fibrinolytic activity in young patients with ischaemic stroke. 63 18

Seven calves underwent thoracotomy to study the response of 41 physiologic variables over a 14 day post-operative period for comparison to a recent series of left ventricular bypass pump implants. The experimental protocols were identical to the pump implant protocols except that the sham operated animals did not receive antiplatelet or anticoagulant drugs and the pumps were not implanted. Of the 41 variables studied, 13 changed significantly during the post-operative period. Heart rate, hematocrit, whole blood hemoglobin, and fibrinogen concentration decreased, while fibrinogen survival, stroke volume, cardiac output, arterial blood pH, pCO2 and pO2, plasma sodium concentration, and urinary excretion rates of sodium and potassium increased from the first or second to the fourteenth post-operative day. Heart rate and hematocrit also decreased in the recent series of 18 animals in which left ventricular bypass pumps were implanted. The decrease in heart rate is toward the unoperated control value as the calves recover from the operative stress. The decrease in hematocrit is probably the result of daily removal of blood for the physiologic studies because there was no evidence of hemorrhage or red blood cell destruction.
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PMID:Forty-one variables following thoracotomy in calves. 72 17

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
Stroke
PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Apoproteins from plasma lipoproteins were localized by immunofluorescence techniques in human carotid artery atherosclerotic lesions. These studies were performed in light of the possible importance of these apoproteins in both lipid metabolism and the pathogenesis of atherosclerosis. ApoA-I from high density lipoproteins, apoB from low density lipoproteins, and apoC-III from very low density lipoproteins were localized also as markers for their respective lipoproteins, since the latter cross-react immunologically. The three apoproteins were localized to the same regions of lesions as neutral lipids and, to some extent, fibrinogen. These regions consisted of bands of collagen fibers, usually deeper within the lesion, and the lipid core or atheroma of such advanced lesions. Although the superposition of localization for the three apoproteins and lipid was only 53%, it was suggested that deviation from complete superposition was due to the abrupt changes in lesion structure resulting from the focal nature of the atherosclerotic process. These results suggest that there is a broader specificity than previously implied of the interaction between such lesion components as connective tissue and extracellular lipid accumulations, and apoproteins from plasma lipoproteins. This interaction is believed to result in a net retention within atherosclerotic lesions of human extracranial arteries of these plasma-derived factors, either as free apoproteins or as native lipoproteins.
Stroke
PMID:Localization of apo-lipoproteins in human carotid artery plaques. 117 63

Forty out of 76 patients (53%) who had suffered a cerebrovascular accident developed deep venous thrombosis of the paralysed leg, as detected with the 125I-fibrinogen technique. A further five also had thrombosis in the non-paralysed leg. A study of many predisposing risk factors provided no help either in elucidating the cause of venous thromboembolism or in identifying patients at risk of DVT as a complication of cerebrovascular accidents.
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PMID:Deep venous thrombosis of the legs after strokes. Part I--incidence and predisposing factors. 126 14


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